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These studies found that >95% of CD4 T cells die because of abortive HIV infection. [9] These dying cells are resting and thus are nonpermissive for productive HIV infection. Full viral replication was limited to the ~5% of activated CD4 T cells present in these tissues; these cells die by apoptosis. [10]
HIV is a retrovirus that primarily infects components of the human immune system such as CD4 + T cells, macrophages and dendritic cells. It directly and indirectly destroys CD4 + T cells. [88] HIV is a member of the genus Lentivirus, [89] part of the family Retroviridae. [90] Lentiviruses share many morphological and biological characteristics.
The pathophysiology of HIV/AIDS involves, upon acquisition of the virus, that the virus replicates inside and kills T helper cells, which are required for almost all adaptive immune responses. There is an initial period of influenza-like illness, and then a latent, asymptomatic phase.
The following month, on October 28, 1994, in a press conference at a Greensboro, North Carolina hotel, Willner jabbed his finger with blood he said was from an HIV-infected patient. [ 1 ] [ 2 ] Willner was heavily influenced by the research of AIDS denialist Peter Duesberg , which has been discredited by the scientific community.
HIV-1 is the most common and most pathogenic strain of the virus. As of 2022, approximately 1.3 million such infections occur annually. [4] [5] Scientists divide HIV-1 into a major group (group M) and two or more minor groups, namely groups N, O and possibly a group P.
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HIV-2 carries a slightly lower risk of transmission than HIV-1 and infection tends to progress more slowly to AIDS. [7] In common usage HIV usually implies HIV-1. [8] HIV-1 protease is one of the best known aspartic proteases, and an attractive target for the treatment of AIDS. [9]
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