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A small proportion of humans show partial or apparently complete innate resistance to HIV, the virus that causes AIDS. [1] The main mechanism is a mutation of the gene encoding CCR5, which acts as a co-receptor for HIV. It is estimated that the proportion of people with some form of resistance to HIV is under 10%. [2]
New World monkeys such as the owl monkey are resistant to HIV-1 infection, possibly because of a genomic fusion of two viral resistance genes. [163] HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the virus, M, N, and O. [164]
The viral DNA can either remain dormant in the nucleus or be transcribed into mRNA and translated by the host cell into the Gag-Pol polyprotein, which would then be cleaved into individual functional proteins (including a newly synthesized HIV-1 PR) by the mature HIV-1 PR. [9]
The genome and proteins of HIV (human immunodeficiency virus) have been the subject of extensive research since the discovery of the virus in 1983. [1] [2] "In the search for the causative agent, it was initially believed that the virus was a form of the Human T-cell leukemia virus (HTLV), which was known at the time to affect the human immune system and cause certain leukemias.
While the mechanisms are not clearly understood for HIV-1 and HIV-2, it is known that they use different pathways and patterns, making the algorithms used to evaluate HIV-1 resistance-associated mutations irrelevant to HIV-2. [34] Each virus can be contracted individually, or they can be contracted together in what is referred to as co-infection.
It is estimated that HIV-1 entered the human population in Africa in the early 1900s, [56] but symptomatic infections were not reported until the 1980s. The HIV-1 epidemic is therefore far too young to be the source of positive selection that drove the frequency of CCR5 Δ32 from zero to 10% in 2000 years. Protection from bubonic plague.
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