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Usually dendritic cells hanging out in the epithelial or mucosal tissue where the virus entered the body, capture the virus and migrate to the lymph nodes, where a lot of immune cells live, and the R5 strain of HIV essentially has a field day, infecting T-helper cells, macrophages, and more dendritic cells, which leads to a big spike in HIV ...
HIV is the cause of the spectrum of disease known as HIV/AIDS. 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]
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]
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.
P24 is a structural protein that plays a crucial role in the formation and stability of the viral capsid, which protects the viral RNA. p24 capsid protein's roles in the HIV replicative process are summarized as follows: [citation needed] Fusion: HIV replication cycle begins when HIV fuses with the surface of the host cell.
The B cell waits for a helper T cell (T H) to bind to the complex. This binding will activate the T H cell, which then releases cytokines that induce B cells to divide rapidly, making thousands of identical clones of the B cell. These daughter cells either become plasma cells or memory cells. The memory B cells remain inactive here; later, when ...
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