1. A deficiency of cellular immunity induced by infection with the human immunodeficiency virus (HIV-1) and characterized by opportunistic diseases, including Pneumocystis jiroveci (formerly carinii) pneumonia, Kaposi sarcoma, oral hairy leukoplakia, cytomegalovirus disease, tuberculosis, Mycobacterium avium complex (MAC) disease, candidal esophagitis, cryptosporidiosis, isoporiasis, cryptococcosis, non-Hodgkin lymphoma, progressive multifocal leukoencephalopathy (PML), herpes zoster, and lymphoma. HIV is transmitted from person to person in cell-rich body fluids (notably blood and semen) through sexual contact, sharing of contaminated needles (as by IV drug abusers), or other contact with infected blood (as in accidental needlesticks among health care workers). Maternal-fetal transmission also occurs. The primary targets of HIV are cells with the CD4 surface protein, including principally helper T lymphocytes. Antibody to HIV, which appears in the serum 6 weeks to 6 months after infection, serves as a reliable diagnostic marker but does not bind or inactivate HIV. Gradual decline in the CD4 lymphocyte count, typically occurring over a period of 10–12 years, culminates in loss of ability to resist opportunistic infections. The appearance of one or more of these infections defines the onset of AIDS. In some patients, generalized lymphadenopathy, fever, weight loss, dementia, or chronic diarrhea occurs much earlier in the course of the infection. Untreated AIDS is uniformly lethal within 2–5 years after the first appearance of an opportunistic infection. Besides prophylaxis against opportunistic infection, standard therapy of HIV infection includes use of nucleoside analogues (didanosine, lamivudine, ribavirin, stavudine, zipovudine), nonnucleoside reverse transcriptase inhibitors (delavirine, efavirenz, nevirapine) and protease inhibitors (atazanavir, crixivan, indinavir, ritonavir, saquinavir).
acquired immunodeficiency syndrome
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