introduction
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HIV
Sunday, February 1, 2009/ 12:18 AM
Human Immunodeficiency Virus
The two human Lentiviruses, HIV-1 and HIV-2, cause the well-known disease called AIDS (Acquired Immunodeficiency Syndrome). Although both HIV-1 and HIV-2 cause AIDS in people, HIV-2 is not as serious a pathogen. The latent period before disease develops is longer, the virus is not as easily transmissible, and it has not spread as extensively as has HIV-1. It is HIV-1 that is responsible for the vast majority of AIDS in people, and HIV-1 has correspondingly been much more exhaustively studied.
The primary cellular targets of HIV in infected humans are macrophages and CD4+ T cells. These cells express CD4, the primary receptor for all primate Lentiviruses, as well as chemokine coreceptors that are also required for entry of the virus.The infection of macrophages and of CD4+ T cells differs in several important respects. HIV can replicate in fully differentiated, non-dividing macrophages, but infection of macrophages does not lead to extension cytopthology. Efficient infection of CD4+ T cells, in contrast, require that the T cell be activated and results in the death of the cell. Strains of HIV are known that infect macrophages (M-tropic virus) or T cells (T-tropic) more efficiently, which is a function of the env gene of the virus.
Primary infection may be asymptomatic (most infected people do not see a doctor on primary infection) or accompanied by nonspecific symptoms that appear 3-6 weeks after infection. Symptoms may include rash, fever, diarrhea, arthralgia, myalgia, nausea, sore throat, lethargy, headache, or stiff neck. The number of CD4+ T cells declines during this phase. An immune response is mounted that includes both CD8+ cytotoxic T cells (CTLs) and antibody production. This reduces the amount of virus in the blood, the number of CD4+ T cells recovers but does not reach preinfection levels, and symptoms of disease ameliorate. However, clearance of the virus is not complete, and a long period of clinical latency ensues. During this period, even though the infected individual is often asymptomatic, the virus continues to replicate actively, especially in lymph nodes, and the immune system continues to fight the infection. It has been estimated that during this clinically quiescent period 10^8 to 10^9 virus particles per day are released into the peripheral blood supply (and cleared). During this time the turnover of CD4+ lymphocytes is also 10^8 to 10^9 cells per day.
In untreated individuals, the continuing replication of virus results in a steady decline in the number of CD4+ T cells and the continuing appearance of mutations in the virus. In the Env protein, the rate of change in the amino acid sequence average about 2.5% per year, with a large fraction of changes occurring in certain hyper-variable regions. It seems clear that this accumulation of mutations is driven, at least in part, by immune selection.
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