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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 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 ...
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.
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]
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.
An illustration of HIV entry mechanism and mechanisms of action (MOA) of two entry inhibitor, 5-Helix and C37. An HIV virion binds to a CD4+ human cell. The two bottom pictures depict two proposed models of HIV fusion with the cell. They are used in combination therapy for the treatment of HIV infection.
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.
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.
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