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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.
The reason for the preferential loss of mucosal CD4 + T cells is that a majority of mucosal CD4 + T cells express the CCR5 coreceptor, whereas a small fraction of CD4 + T cells in the bloodstream do so. [5] HIV seeks out and destroys CCR5 expressing CD4 + cells during acute infection. A vigorous immune response eventually controls the infection ...
HIV is now known to spread between CD4 + T cells by two parallel routes: cell-free spread and cell-to-cell spread, i.e. it employs hybrid spreading mechanisms. [95] In the cell-free spread, virus particles bud from an infected T cell, enter the blood/extracellular fluid and then infect another T cell following a chance encounter. [95]
As cells reproduce, the HIV DNA inside replicates fast and makes mistakes, creating mutations that can make treatment harder. Antiretroviral therapy, which interrupts the virus’ copy-and-paste ...
Scientists have successfully zapped HIV out of infected cells — raising hopes of a cure for the chronic disease. The team from Amsterdam UMC used gene-editing technology to eliminate all traces ...
The within-host dynamics of HIV infection include the spread of the virus in vivo, the establishment of latency, the effects of immune response on the virus, etc. [6] [7] Early studies used simple models and only considered the cell-free spreading of HIV, in which virus particles bud from an infected T cell, enter the blood/extracellular fluid ...
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