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A good CD8 + T cell response has been linked to slower disease progression and a better prognosis, though it does not eliminate the virus. [3] During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4 + T cell depletion, although apoptosis may also be a factor.
HIV is spread primarily by unprotected sex (including anal and vaginal sex), contaminated hypodermic needles or blood transfusions, and from mother to child during pregnancy, delivery, or breastfeeding. [18] Some bodily fluids, such as saliva, sweat, and tears, do not transmit the virus. [19] Oral sex has little risk of transmitting the virus. [20]
HIV is a retrovirus, which comprise a large and diverse family of RNA viruses that make a DNA copy of their RNA genome after infection of a host cell. An essential step in the replication cycle of HIV-1 and other retroviruses is the integration of this viral DNA into the host DNA. The RNA genome of progeny virions and the template for ...
Interestingly, HIV-1 can undergo a tropism switch, where the virus glycoprotein gp120 initially uses CCR5 (mainly on macrophages) as the primary co-receptor for entering the host cell. Subsequently, HIV-1 switches to bind to CXCR4 (mainly on T cells) as the infection progresses, in doing so transitions the viral pathogenicity to a different stage.
In cell-free spread (see figure), virus particles bud from an infected T cell, enter the blood or extracellular fluid and then infect another T cell following a chance encounter. [90] HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread, for which two pathways have been described.
Human Immunodeficiency Virus (HIV) has the capability to enter a latent stage of infection where it exists as a dormant provirus in CD4+ T-cells.Most latently infected cells are resting memory T cells, [1] however a small fraction of latently infected cells isolated from HIV patients are naive CD4 T cells.
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