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HIV lymphadenopathy, early phase with follicular hyperplasia, medium power microscopic.

HIV lymphadenopathy is seen here microscopically in the early phase with follicular hyperplasia at medium power.Lymphoid interstitial pneumonitis (LIP) is a condition involving the lung that can be seen in AIDS in children. By chest radiograph, bilateral reticulonodular interstitial pulmonary infiltrates are seen. The earliest pathologic finding is a hyperplasia of bronchial associated lymphoid tissue with aggregates of lymphocytes and plasma cells in a bronchovascular distribution. Later lesions demonstrate diffuse lung round cell infiltrates, and lymphoid aggregates can be present.

Progressive multifocal leukoencephalopathy (PML) JC viral particles in nucleus, electron micrograph.

Progressive multifocal leukoencephalopathy is caused by infection with the JC papovavirus. Here, small round dark JC viral particles appear in the nucleus of an infected oligodendrocyte in this electron micrograph.Lymphoid interstitial pneumonitis (LIP) is a condition involving the lung that can be seen in AIDS in children. By chest radiograph, bilateral reticulonodular interstitial pulmonary infiltrates are seen. The earliest pathologic finding is a hyperplasia of bronchial associated lymphoid tissue with aggregates of lymphocytes and plasma cells in a bronchovascular distribution. Later lesions demonstrate diffuse lung round cell infiltrates, and lymphoid aggregates can be present.

Progressive multifocal leukoencephalopathy (PML), high power microscopic.

Microscopically, PML lesions appear with perivascular monocytes, astrocytosis with bizarre or enlarged astrocytes (with occasional mitotic figures), and central lipid-laden macrophages. At the periphery of the lesions are large "ballooned" oligodendrocytes infected with JC virus that have enlarged dark pink "ground glass" nuclei containing viral antigen.Lymphoid interstitial pneumonitis (LIP) is a condition involving the lung that can be seen in AIDS in children. By chest radiograph, bilateral reticulonodular interstitial pulmonary infiltrates are seen. The earliest pathologic finding is a hyperplasia of bronchial associated lymphoid tissue with aggregates of lymphocytes and plasma cells in a bronchovascular distribution. Later lesions demonstrate diffuse lung round cell infiltrates, and lymphoid aggregates can be present.

Progressive multifocal leukoencephalopathy (PML), Luxol fast blue stain, low power microscopic.

Progressive multifocal leukoencephalopathy (PML) affects oligodendrocytes, and cell lysis results in lesions that demonstrate demyelination, as shown here by the Luxol fast blue (LFB) stain in white matter.Lymphoid interstitial pneumonitis (LIP) is a condition involving the lung that can be seen in AIDS in children. By chest radiograph, bilateral reticulonodular interstitial pulmonary infiltrates are seen. The earliest pathologic finding is a hyperplasia of bronchial associated lymphoid tissue with aggregates of lymphocytes and plasma cells in a bronchovascular distribution. Later lesions demonstrate diffuse lung round cell infiltrates, and lymphoid aggregates can be present.

Progressive multifocal leukoencephalopathy (PML), gross.

Progressive multifocal leukoencephalopathy (PML) appears grossly as irregular areas of granularity in white matter which bear some resemblance to the plaques of demyelination with multiple sclerosis.Lymphoid interstitial pneumonitis (LIP) is a condition involving the lung that can be seen in AIDS in children. By chest radiograph, bilateral reticulonodular interstitial pulmonary infiltrates are seen. The earliest pathologic finding is a hyperplasia of bronchial associated lymphoid tissue with aggregates of lymphocytes and plasma cells in a bronchovascular distribution. Later lesions demonstrate diffuse lung round cell infiltrates, and lymphoid aggregates can be present.

Lymphoid interstitial pneumonitis (LIP) of lung, high power microscopic.

Lymphoid interstitial pneumonitis (LIP) is seen here in lung at high power. The mononuclear cells are not malignant.Lymphoid interstitial pneumonitis (LIP) is a condition involving the lung that can be seen in AIDS in children. By chest radiograph, bilateral reticulonodular interstitial pulmonary infiltrates are seen. The earliest pathologic finding is a hyperplasia of bronchial associated lymphoid tissue with aggregates of lymphocytes and plasma cells in a bronchovascular distribution. Later lesions demonstrate diffuse lung round cell infiltrates, and lymphoid aggregates can be present.

Lymphoid interstitial pneumonitis (LIP) of lung, medium power microscopic.

Lymphoid interstitial pneumonitis (LIP) is seen here in lung at medium power. LIP can appear as interstitial infiltrates of mononuclear cells or as aggregates.Lymphoid interstitial pneumonitis (LIP) is a condition involving the lung that can be seen in AIDS in children. By chest radiograph, bilateral reticulonodular interstitial pulmonary infiltrates are seen. The earliest pathologic finding is a hyperplasia of bronchial associated lymphoid tissue with aggregates of lymphocytes and plasma cells in a bronchovascular distribution. Later lesions demonstrate diffuse lung round cell infiltrates, and lymphoid aggregates can be present.

Lymphoid interstitial pneumonitis (LIP) of lung, low power microscopic.

Lymphoid interstitial pneumonitis (LIP) is seen here in lung at medium power. LIP is not seen in adults with AIDS.Lymphoid interstitial pneumonitis (LIP) is a condition involving the lung that can be seen in AIDS in children. By chest radiograph, bilateral reticulonodular interstitial pulmonary infiltrates are seen. The earliest pathologic finding is a hyperplasia of bronchial associated lymphoid tissue with aggregates of lymphocytes and plasma cells in a bronchovascular distribution. Later lesions demonstrate diffuse lung round cell infiltrates, and lymphoid aggregates can be present.

Lymphoid interstitial pneumonitis (LIP) of lung, low power microscopic.

Lymphoid interstitial pneumonitis (LIP) is seen here in lung at low power. LIP can appear in children with AIDS.Lymphoid interstitial pneumonitis (LIP) is a condition involving the lung that can be seen in AIDS in children. By chest radiograph, bilateral reticulonodular interstitial pulmonary infiltrates are seen. The earliest pathologic finding is a hyperplasia of bronchial associated lymphoid tissue with aggregates of lymphocytes and plasma cells in a bronchovascular distribution. Later lesions demonstrate diffuse lung round cell infiltrates, and lymphoid aggregates can be present.

Malignant lymphoma, brain, high power microscopic.

At high magnification, this non-Hodgkin's lymphoma infiltrating the cerebrum is composed of large lymphocytes with occasional mitoses.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Malignant lymphoma, brain, low power microscopic.

Non-Hodgkin's lymphomas seen in the central nervous system with AIDS are essentially clonal expansions of Epstein-Barr virus infected lymphocytes. These lymphomas are high grade (immunoblastic) and agressive, with a poor prognosis. Seen here is the edge of such a lymphoma infiltrating the cerebrum.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Malignant lymphoma, small intestine, high power microscopic.

Malignant lymphoma is typically high grade in AIDS. Seen here in small intestine are cells of a large cell lymphoma infiltrating the mucosa.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Malignant lymphoma, liver, gross.

Extranodal malignant lymphoma in AIDS is often multifocal. Seen here in liver are two mass lesions on the cut surface. The color can range from white to tan to red, often intermixed.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Malignant lymphoma, small intestine, gross.

Malignant lymphoma is typically extranodal in AIDS. Seen here in small intestine are two mass lesions on the mucosal surface.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Malignant lymphoma, lymph node, gross.

Cut sections of this enlarged lymph node involved with high-grade non-Hodgkin's lymphoma in AIDS reveal a "strawberry sundae" appearance with swirls and globs of red in white. This can also be seen with extra-nodal AIDS lymphomas.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Kaposi's sarcoma, liver, gross.

Visceral involvement with Kaposi's sarcoma in AIDS is common. Here are multiple reddish irregular masses in the liver.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Kaposi's sarcoma, stomach, gross.

Visceral involvement with Kaposi's sarcoma in AIDS is common. Here are multiple reddish nodules seen over the gastric mucosa.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Kaposi's sarcoma, oral cavity, immunohistochemical with antibody to CD34, microscopic.

Kaposi's sarcoma can also be highlighted with the use of an immunohistochemical stain with antibody to CD34, which stains the cells forming the vascular slits.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Kaposi's sarcoma, skin, hyaline globules, PAS stain, microscopic.

Kaposi's sarcoma characteristically has hyaline globules, as seen here stained with PAS.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Kaposi's sarcoma, skin, hemosiderin and hyaline globules, microscopic.

Kaposi's sarcoma characteristically has deposits of hemosiderin granules and faint, pale pink hyaline globules, as seen here.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Kaposi's sarcoma, skin, extravasation of RBC's, microscopic.

Kaposi's sarcoma microscopically produces slit-like vascular spaces in the dermis of the skin with extravasation of red blood cells.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Kaposi's sarcoma, skin, nodule, microscopic.

Kaposi's sarcoma microscopically produces slit-like vascular spaces in the dermis of the skin, seen here as a nodule.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Kaposi's sarcoma, skin, patch stage, microscopic.

Kaposi's sarcoma microscopically produces slit-like vascular spaces in the dermis of the skin, seen here in the patch stage of KS.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Kaposi's sarcoma, skin, gross.

Kaposi's sarcoma typically produces one or more reddish purple nodules on the skin, as seen here grossly.Kaposi's sarcoma (KS) produces reddish purple patches, plaques, or nodules over the skin and can be diagnosed with skin biopsy. Visceral organ involvement eventually occurs in 3/4 of patients with KS. Malignant lymphomas seen with AIDS are typically of a high grade and extranodal, often in the brain. They are very aggressive and respond poorly to therapy.

Isospora belli, stool specimen, AFB stain, microscopic.

A cyst of Isospora belli is present in this acid fast stained preparation from a stool specimen.Cryptosporidium, Microsporidium, and Isospora are all capable of producing a voluminous watery diarrhea in patients with AIDS. Diagnosis can be made by examination of stool specimens and/or intestinal biopsy.

Cryptosporidia, electron micrograph.

Cryptosporidia are seen along the brush border of the intestinal mucosa in this electron micrograph.Cryptosporidium, Microsporidium, and Isospora are all capable of producing a voluminous watery diarrhea in patients with AIDS. Diagnosis can be made by examination of stool specimens and/or intestinal biopsy.

Cryptosporidiosis, stool specimen, AFB stain,microscopic.

Cryptosporidia are best seen in a stool specimen with acid fast staining.Cryptosporidium, Microsporidium, and Isospora are all capable of producing a voluminous watery diarrhea in patients with AIDS. Diagnosis can be made by examination of stool specimens and/or intestinal biopsy.

Cryptosporidiosis, small intestine, H and E stain, microscopic.

Small blue cryptosporidia line the surface of the small intestinal epithelium shown here.Cryptosporidium, Microsporidium, and Isospora are all capable of producing a voluminous watery diarrhea in patients with AIDS. Diagnosis can be made by examination of stool specimens and/or intestinal biopsy.

Gastrointestinal protozoa, diagram.

The major gastrointestinal protozoa (Cryptosporidium, Microsporidium, and Isospora organisms) are compared morphologically in this diagram.Cryptosporidium, Microsporidium, and Isospora are all capable of producing a voluminous watery diarrhea in patients with AIDS. Diagnosis can be made by examination of stool specimens and/or intestinal biopsy.

Herpes simplex virus, esophagus, microscopic.

Herpes simplex virus, seen here in the esophagus, infects the squamous epithelium and manifests with multinucleated cells and inclusions.Herpes simplex virus infection with AIDS is most likely to involve the gastrointestinal tract, mainly the esophagus and the perianal region. Herpes zoster infection of the skin can also occur prior to the onset of clinical AIDS. Herpes infections are rarely life-threatening.

Herpes simplex virus, esophagus, microscopic.

Herpes simplex virus often produces sharply demarcated ulcerations in oral, esophageal, or perianal regions. Here is the edge of an ulcer seen microscopically.Herpes simplex virus infection with AIDS is most likely to involve the gastrointestinal tract, mainly the esophagus and the perianal region. Herpes zoster infection of the skin can also occur prior to the onset of clinical AIDS. Herpes infections are rarely life-threatening.

Herpes simplex virus, diagram.

Herpes simplex virus morphology is diagrammed here.Herpes simplex virus infection with AIDS is most likely to involve the gastrointestinal tract, mainly the esophagus and the perianal region. Herpes zoster infection of the skin can also occur prior to the onset of clinical AIDS. Herpes infections are rarely life-threatening.

Toxoplasma gondii, lung, immunohistochemical stain, microscopic.

The free tachyzoites of Toxoplasma gondii are difficult to distinguish by H and E staining, so an immunohistochemical stain can be very helpful. Tachyzoites are seen here in lung.Toxoplasma gondii is a protozoan parasite that most often leads to infection of the brain with AIDS. The lesions are usually multiple and have the appearance of abscesses. Less commonly, T gondii infection is disseminated to other organs.

Toxoplasma gondii, myocardium, microscopic.

Toxoplasma gondii infection can also occur in the heart. Here a pseudocyst appears in myocardium.Toxoplasma gondii is a protozoan parasite that most often leads to infection of the brain with AIDS. The lesions are usually multiple and have the appearance of abscesses. Less commonly, T gondii infection is disseminated to other organs.

Toxoplasma gondii, pseudocysts, microglial nodule, microscopic.

Toxoplasma gondii infection can result in the formation of pseudocysts, which have the infected cell forming the cyst wall, and the cysts contain bradyzoites. Pseudocysts are seen here in cerebrum in a microglial nodule.Toxoplasma gondii is a protozoan parasite that most often leads to infection of the brain with AIDS. The lesions are usually multiple and have the appearance of abscesses. Less commonly, T gondii infection is disseminated to other organs.

Toxoplasma gondii, diagram.

Toxoplasma gondii morphology is diagrammed here.Toxoplasma gondii is a protozoan parasite that most often leads to infection of the brain with AIDS. The lesions are usually multiple and have the appearance of abscesses. Less commonly, T gondii infection is disseminated to other organs.

Toxoplasma gondii, organizing cerebral abscess, gross.

Toxoplasma gondii infection is most often manifested in the central nervous system. Multiple abscesses that are ring-enhancing with CT scans can be seen. Older abscesses can organize, as shown here grossly in brain.Toxoplasma gondii is a protozoan parasite that most often leads to infection of the brain with AIDS. The lesions are usually multiple and have the appearance of abscesses. Less commonly, T gondii infection is disseminated to other organs.

Coccidioides immitis, liver, H&E stain, microscopic.

Spherules of Coccidioides immitis are seen here in liver with H and E staining. Note the thick wall of the sperules containing endospores. One spherule is rupturing to release the endospores, the yeast phase which grows at body temperature.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Coccidioides immitis, lung, H&E stain, microscopic.

Coccidioides immitis infection can often be disseminated to multiple organs, though pneumonia is often present because the infection is acquired via the respiratory tract. Spherules are seen here in lung with H and E staining.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Coccidioides immitis, diagram.

Coccidioides immitis morphology is diagrammed here.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Histoplasma capsulatum, liver, PAS stain, microscopic.

Histoplasma capsulatum organisms in macrophages are seen in liver with PAS stain.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Histoplasma capsulatum, liver, H and E stain, microscopic.

Histoplasma capsulatum is often a disseminated infection, and the macrophages containing small yeasts appear in multiple organs, particularly those of the mononuclear phagocyte system (lymph node, liver, spleen, marrow). Here the organisms are seen in liver with H and E stain.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Histoplasma capsulatum, granulomas in liver, gross.

Histoplasma capsulatum may lead to formation of visible granulomas, but they are often small, as shown here in the liver. More often, involvement is diffuse, leading only to organomegaly.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Histoplasma capsulatum, diagram.

Histoplasma capsulatum morphology is diagrammed here, with appearances by both GMS and PAS staining.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Cryptococcus neoformans, India ink preparation of cerebrospinal fluid, microscopic.

In cerebrospinal fluid obtained via lumbar puncture, Cryptococcus neoformans organisms are highligted by their surrounding capsule, which is white, with a central rounded pale nucleus. Two cryptococcal organisms are seen here.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Cryptococcus neoformans (without capsules), meninges, GMS stain, microscopic.

Cryptococcus neoformans organisms often lack a capsule, but the nucleus stains well with GMS staining as seen here microscopically in the meninges in a case of cryptococcal meningitis.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Cryptococcus neoformans (with capsules), H&E stain, microscopic.

Cryptococcus neoformans often produces a pneumonia, because infection is acquired via the respiratory tract. Here, C neoformans organisms have a clear capsule surrounding the pale blue nucleus with H and E staining.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Cryptococcus neoformans, diagram.

Cryptococcus neoformans morphology is diagrammed here.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Candida albicans, invasive in esophagus, GMS stain, microscopic.

Candida albicans is seen here as an invasive process in the esophagus with GMS staining.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Candida albicans, invasive in esophagus, PAS stain, microscopic.

Candida albicans is seen here as an invasive process in the esophagus with PAS staining.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Candida albicans, invasive in bronchus, H&E stain, microscopic.

Candida albicans is seen here as an invasive process in a bronchus with H and E staining.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Candida albicans, diagram.

Candida albicans morphology is diagrammed here.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Candida albicans, lung, gross.

Candida infections are common with AIDS, but most often appear as oral thrush, which is a nuisance but not life-threatening. Disseminated infections are uncommon, but here is a rare Candida pneumonia, which resembles a bacterial bronchopneumonia.There are many types of fungi that can complicate the course of AIDS. One of the most frequent (though uncommonly life-threatening) is Candida. Oral candidiasis is often seen with HIV infection and may presage the progression to AIDS. Candida can occasionally produce invasive infections in esophagus, upper respiratory tract, and lung. Infections with the pathogenic fungi Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitis are more serious infections that are often widely disseminated. C neoformans often produces pneumonia and meningitis.

Mycobacterium avium complex (MAC), macrophages filled with mycobacteria, spleen, AFB stain, microscopic.

Mycobacterium avium complex (MAC) with acid fast stain often has the characteristic appearance shown here with numerous mycobacteria filling macrophages. Such macrophages may be distributed diffusely or in clusters.Mycobacterial infections are frequently seen with AIDS. Mycobacterium tuberculosis has been increasing in frequency since the start of the AIDS epidemic. The appearance of M tuberculosis with AIDS is similar to that of non-AIDS patients, with granulomatous pulmonary disease, though the infection may be more extensive or may be disseminated to other organs. Mycobacterium avium complex (MAC) infection is more unique to AIDS and is characterized by involvement mostly of the organs of the mononuclear phagocyte system (lymph node, spleen, liver, marrow). MAC infections are less likely to produce visible granulomas, and the lesions often consist of clusters of macrophages filled with numerous mycobacteria. Definitive diagnosis of mycobacterial disease is made by culture.

Mycobacterium avium complex (MAC), diagram.

Mycobacterium avium complex (MAC) morphology is diagrammed here.Mycobacterial infections are frequently seen with AIDS. Mycobacterium tuberculosis has been increasing in frequency since the start of the AIDS epidemic. The appearance of M tuberculosis with AIDS is similar to that of non-AIDS patients, with granulomatous pulmonary disease, though the infection may be more extensive or may be disseminated to other organs. Mycobacterium avium complex (MAC) infection is more unique to AIDS and is characterized by involvement mostly of the organs of the mononuclear phagocyte system (lymph node, spleen, liver, marrow). MAC infections are less likely to produce visible granulomas, and the lesions often consist of clusters of macrophages filled with numerous mycobacteria. Definitive diagnosis of mycobacterial disease is made by culture.

Mycobacterium avium complex (MAC), mesenteric lymph nodes, gross.

Mycobacterium avium complex (MAC) may produce a grossly visible yellowish-tan cut surface, as seen here in these mesenteric lymph nodes, because the mycobacteria are so numerous.Mycobacterial infections are frequently seen with AIDS. Mycobacterium tuberculosis has been increasing in frequency since the start of the AIDS epidemic. The appearance of M tuberculosis with AIDS is similar to that of non-AIDS patients, with granulomatous pulmonary disease, though the infection may be more extensive or may be disseminated to other organs. Mycobacterium avium complex (MAC) infection is more unique to AIDS and is characterized by involvement mostly of the organs of the mononuclear phagocyte system (lymph node, spleen, liver, marrow). MAC infections are less likely to produce visible granulomas, and the lesions often consist of clusters of macrophages filled with numerous mycobacteria. Definitive diagnosis of mycobacterial disease is made by culture.

Mycobacterium avium complex (MAC), spleen with miliary granulomas, gross.

Mycobacterium avium complex (MAC) may produce grossly visible granulomas, as seen here in the spleen. However, often there is organ enlargement, but no visible granulomas.Mycobacterial infections are frequently seen with AIDS. Mycobacterium tuberculosis has been increasing in frequency since the start of the AIDS epidemic. The appearance of M tuberculosis with AIDS is similar to that of non-AIDS patients, with granulomatous pulmonary disease, though the infection may be more extensive or may be disseminated to other organs. Mycobacterium avium complex (MAC) infection is more unique to AIDS and is characterized by involvement mostly of the organs of the mononuclear phagocyte system (lymph node, spleen, liver, marrow). MAC infections are less likely to produce visible granulomas, and the lesions often consist of clusters of macrophages filled with numerous mycobacteria. Definitive diagnosis of mycobacterial disease is made by culture.

Mycobacterium tuberculosis, lung, AFB stain, microscopic.

Mycobacterium tuberculosis infection of lung is shown here with numerous red rods seen with acid fast staining.Mycobacterial infections are frequently seen with AIDS. Mycobacterium tuberculosis has been increasing in frequency since the start of the AIDS epidemic. The appearance of M tuberculosis with AIDS is similar to that of non-AIDS patients, with granulomatous pulmonary disease, though the infection may be more extensive or may be disseminated to other organs. Mycobacterium avium complex (MAC) infection is more unique to AIDS and is characterized by involvement mostly of the organs of the mononuclear phagocyte system (lymph node, spleen, liver, marrow). MAC infections are less likely to produce visible granulomas, and the lesions often consist of clusters of macrophages filled with numerous mycobacteria. Definitive diagnosis of mycobacterial disease is made by culture.

Mycobacterium tuberculosis, lung, gross.

Mycobacterium tuberculosis infection of lung, with upper lung field granulomatous and cavitary disease shown here, is similar to florid cases in non-AIDS patients.Mycobacterial infections are frequently seen with AIDS. Mycobacterium tuberculosis has been increasing in frequency since the start of the AIDS epidemic. The appearance of M tuberculosis with AIDS is similar to that of non-AIDS patients, with granulomatous pulmonary disease, though the infection may be more extensive or may be disseminated to other organs. Mycobacterium avium complex (MAC) infection is more unique to AIDS and is characterized by involvement mostly of the organs of the mononuclear phagocyte system (lymph node, spleen, liver, marrow). MAC infections are less likely to produce visible granulomas, and the lesions often consist of clusters of macrophages filled with numerous mycobacteria. Definitive diagnosis of mycobacterial disease is made by culture.

Cytomegalovirus pneumonitis, immunohistochemical stain, medium and high power microscopic.

Immunoperoxidase staining may reveal CMV in some cases where the inclusions are not numerous or characteristic.Cytomegalovirus (CMV) is the most frequent disseminated opportunistic infection seen with AIDS. It causes the most serious disease as a pneumonia in the lung, but it can also cause serious disease in the brain and gastrointestinal tract. It is also a common cause for retinitis and blindness in persons with AIDS. CMV is identified by the presence of very large cytomegalic cells with enlarged nuclei that contain a violaceous intranuclear inclusion surrounded by a clear halo. Sometimes, basophilic stippling is present in the cytoplasm.

Cytomegalovirus, liver, microscopic.

CMV can often be disseminated and involve a variety of organs, though the degree of organ failure from such involvement varies greatly. Seen here is a characteristic inclusion in liver.Cytomegalovirus (CMV) is the most frequent disseminated opportunistic infection seen with AIDS. It causes the most serious disease as a pneumonia in the lung, but it can also cause serious disease in the brain and gastrointestinal tract. It is also a common cause for retinitis and blindness in persons with AIDS. CMV is identified by the presence of very large cytomegalic cells with enlarged nuclei that contain a violaceous intranuclear inclusion surrounded by a clear halo. Sometimes, basophilic stippling is present in the cytoplasm.

Cytomegalovirus adrenalitis, microscopic.

CMV most often involves the adrenal, but this uncommonly leads to major clinical signs or symptoms. Inclusions can appear in medulla and cortex.Cytomegalovirus (CMV) is the most frequent disseminated opportunistic infection seen with AIDS. It causes the most serious disease as a pneumonia in the lung, but it can also cause serious disease in the brain and gastrointestinal tract. It is also a common cause for retinitis and blindness in persons with AIDS. CMV is identified by the presence of very large cytomegalic cells with enlarged nuclei that contain a violaceous intranuclear inclusion surrounded by a clear halo. Sometimes, basophilic stippling is present in the cytoplasm.

Cytomegalovirus pneumonia, microscopic.

CMV inclusions in lung are seen here microscopically.Cytomegalovirus (CMV) is the most frequent disseminated opportunistic infection seen with AIDS. It causes the most serious disease as a pneumonia in the lung, but it can also cause serious disease in the brain and gastrointestinal tract. It is also a common cause for retinitis and blindness in persons with AIDS. CMV is identified by the presence of very large cytomegalic cells with enlarged nuclei that contain a violaceous intranuclear inclusion surrounded by a clear halo. Sometimes, basophilic stippling is present in the cytoplasm.

Cytomegalovirus pneumonia, microscopic.

CMV inclusions in lung are seen here microscopically. A cell can have more than one inclusion.Cytomegalovirus (CMV) is the most frequent disseminated opportunistic infection seen with AIDS. It causes the most serious disease as a pneumonia in the lung, but it can also cause serious disease in the brain and gastrointestinal tract. It is also a common cause for retinitis and blindness in persons with AIDS. CMV is identified by the presence of very large cytomegalic cells with enlarged nuclei that contain a violaceous intranuclear inclusion surrounded by a clear halo. Sometimes, basophilic stippling is present in the cytoplasm.

Cytomegalovirus pneumonia, microscopic.

CMV can often produce a pneumonia. Here are CMV inclusions in lung.Cytomegalovirus (CMV) is the most frequent disseminated opportunistic infection seen with AIDS. It causes the most serious disease as a pneumonia in the lung, but it can also cause serious disease in the brain and gastrointestinal tract. It is also a common cause for retinitis and blindness in persons with AIDS. CMV is identified by the presence of very large cytomegalic cells with enlarged nuclei that contain a violaceous intranuclear inclusion surrounded by a clear halo. Sometimes, basophilic stippling is present in the cytoplasm.

Cytomegalovirus, appearance of organisms, diagram.

The morphologic appearances of cytomegalovirus are diagrammed here. The cell is so large that in histologic sections, the plane of section may not reveal all or part of the nucleus in every cytomegalic cell, and the cytoplasmic inclusions, though characteristic for CMV, are not always present.Cytomegalovirus (CMV) is the most frequent disseminated opportunistic infection seen with AIDS. It causes the most serious disease as a pneumonia in the lung, but it can also cause serious disease in the brain and gastrointestinal tract. It is also a common cause for retinitis and blindness in persons with AIDS. CMV is identified by the presence of very large cytomegalic cells with enlarged nuclei that contain a violaceous intranuclear inclusion surrounded by a clear halo. Sometimes, basophilic stippling is present in the cytoplasm.

Pneumocystis jiroveci pneumonia, interstitial fibrosis, medium power microscopic.

Pneumocystis carinii may have a variety of "atypical" features, including scant foamy exudate and interstitial fibrosis, as seen here microscopically.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci, exudate with calcification, medium power microscopic.

Pneumocystis carinii, often when disseminated and sometimes in the lung as shown here, can produce large areas of the foamy pink exudate that can calcify.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci, disseminated, spleen, CT scan.

Disseminated of Pneumocystis carinii has led to splenomegaly, and the masses of exudate produce the lucent areas in spleen seen here with CT scan.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci, disseminated, gross.

With dissemination to extrapulmonary sites, Pneumocystis carinii tends to produce foci with prominent calcification, as seen in the kidney here grossly.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci pneumonia, lung, microscopic, immunohistochemical stain.

With immunohistochemical stain with antibody to Pneumocystis carinii at high magnification, the brown-red reaction produce is seen highlighting the exudates.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci pneumonia, microscopic, bronchoalveolar lavage, cytologic smear, Pap stain.

Pap staining of fluid obtained from bronchoalveolar lavage, bronchial washing, or sputum may reveal a characteristic "foamy body" seen here, which represents the alveolar exudate in Pneumocystis carinii infection.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci pneumonia, microscopic, bronchoalveolar lavage, cytologic smear, Giemsa stain.

The giemsa stain demonstrates the faint bluish dot-like intracystic bodies of Pneumocystis carinii in this cytologic preparation from a bronchoalveolar lavage. This staining technique works best with cytologic smears.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci pneumonia, microscopic, bronchoalveolar lavage, cytologic smear, Giemsa stain.

With giemsa stain at high magnification, the faint bluish dot-like intracystic bodies of Pneumocystis carinii in lung are seen in this cytologic preparation from a bronchoalveolar lavage.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci pneumonia, high power microscopic, GMS stain.

With Gomori methenamine silver stain at high magnification, the cysts of Pneumocystis carinii in lung have the appearance of crushed ping-pong balls.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci pneumonia, medium power microscopic, GMS stain.

With Gomori methenamine silver stain, Pneumocystis carinii in lung is demonstrated by the appearance of brown to black cysts in the alveolar exudate.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci pneumonia, low power microscopic.

At low magnification, note the appearance of Pneumocystis carinii in lung with exudate in nearly every alveolus.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci pneumonia with cavitary change, gross.

In rare cases, Pneumocystis carinii pneumonia may produce cavitary change, as shown here grossly in lung.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci pneumonia, gross.

The appearance of Pneumocystis carinii grossly in lung is shown here. Note that this is an extensive pneumonia.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Pneumocystis jiroveci, appearance of organisms, diagram.

The appearance of Pneumocystis carinii with the Gomori methenamine silver (GMS) stain (which stains the capsule) and the Giemsa stain (which stains up to eight intracystic bodies but not the capsule) is diagrammed here.Pneumocystis jiroveci (formerly carinii) is the most frequent opportunistic infection seen with AIDS. It commonly produces a pulmonary infection but rarely disseminates outside of lung. The most frequent clinical findings in patients with pneumonia are acute onset of fever, non-productive cough, and dyspnea. Chest radiograph may show perihilar infiltrates. Diagnosis is made histologically by finding the organisms in cytologic (bronchoalveolar lavage) or biopsy (transbronchial biopsy) material from lung, typically via bronchoscopy. The cysts of P jiroveci stain brown to black with the Gomori methenamine silver stain. With Giemsa or Dif-Quik stain on cytologic smears, the dot-like intracystic bodies are seen.

Schematic diagram of CD4 receptor and chemokine coreceptor.

The interaction of HIV gp120 with the CD4 receptor is shown here. The chemokine coreceptor in the cell membrane induces a conformational change in gp41 that allows fusion of virus with cell membrane.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Life cycle of HIV, with the points of pharmacologic agent effectiveness, diagram.

The life cycle of HIV shown with the points at which pharmacologic agents may block the viral life cycle involving the host cell, including points for inhibition of viral entry, reverse transcriptase, integrase, TAT transcription, protease, and maturation, in this diagram.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Human immunodeficiency virus (HIV) subtypes and simian immunodeficiency virus (SIV) phylogeny, diagram.

A schematic representation of the phylogeny of human immunodeficiency virus (HIV) subtypes and simian immunodeficiency virus (SIV) is shown in this diagram. Subtypes of HIV vary in geographic distribution.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Human immunodeficiency virus, schematic diagram of genome.

The genome of the human immunodeficiency virus type 1 (HIV-1) is shown in the schematic diagram above.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Human immunodeficiency virus, process of infection, diagram.

Human immunodeficiency virus is shown crossing the mucosa of the genital tract to infect CD4+ T-lymphocytes. A Langerhans cell in the epithelium is shown in red in this diagram.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Human immunodeficiency virus within lymphoid tissues, diagram.

Human immunodeficiency virus, once it enters the body, is carried to the lymphoid tissues where both CD4+ T-lymphocytes as well as follicular dendritic cells can become infected, as shown in this diagram.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Human immunodeficiency virus, life cycle, diagram.

The life cycle of human immunodeficiency virus is diagrammed here. Note that the reverse transcriptase enzyme makes an HIV proviral DNA that is incorporated into the host cell.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Human immunodeficiency virus, structural components, diagram.

The structural components, including the key antigenic components, of human immunodeficiency virus are diagrammed here.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Human immunodeficiency virus, electron micrograph.

A human immunodeficiency viral particle is seen budding from the infected cell surface at the top, with a complete viral particle at bottom in this high magnification electron micrograph.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Human immunodeficiency virus, electron micrograph.

Human immunodeficiency viral particles are seen at medium magnification in this electron micrograph. Note the central core and the outer envelope.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

Human immunodeficiency virus, electron micrograph.

Human immunodeficiency virus, viral particles are seen at low magnification adjacent to the cell surface in this electron micrograph.Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk. When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released. The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11. In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.

The donor drinks some liquid (here a tube of apple juice) to replace the lost blood volume, eats some cookies, and is on his way in about 10 minutes.

The donor drinks some liquid (here a tube of apple juice) to replace the lost volume, eats some cookies, and is on his way in about 10 minutes. A bandage is in place over the phlebotomy site.

The needle is removed and pressure is applied over the venipuncture site, then a bandage is placed for the next couple of hours.

The needle is removed and pressure is applied over the venipuncture site, then a bandage is placed for the next couple of hours.

Just after the bag has filled, blood from the line is taken to fill several collection tubes for further testing.

Just after the bag has filled, blood from the line is taken to fill several collection tubes for further testing. A red top collection tube is being filled here.

Blood fills the collection bag by gravity in a few minutes. The sealed plastic collection bag contains a blood preservative.

Blood fills the collection bag by gravity in a few minutes. The sealed plastic collection bag contains a blood preservative.

The needle used to draw the blood from the vein is gently inserted.

The needle used to draw the blood from the vein is gently inserted. The needle is attached to plastic tubing to conduct the blood to the collection bag.

The disinfectant is applied to the area around the vein to be used.

The disinfectant is applied to the area around the vein to be used.

The site for drawing blood is selected and disinfected. A prominent vein is chosen for the venipuncture site.

The site for drawing blood is selected and disinfected. A prominent vein has been chosen for the venipuncture site.

The donor sits in a reclining chair. An inflatable cuff on the arm is used to check blood pressure and to maintain venous filling.

The donor sits in a reclining chair. An inflatable cuff on the arm is used to check blood pressure and to maintain venous filling.

The blood is drawn into a capillary tube which is then spun in the small centrifuge (seen in the background) to determine the hematocrit.

The blood is drawn into a capillary tube which is then spun in the small centrifuge (seen in the background) to determine the hematocrit.