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The CD8 + T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4 + T cell counts rebound. 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 ...
Depletion of regulatory T cells increases immune activation. Glut1 regulation is associated with the activation of CD4+ T cells, thus its expression can be used to track the loss of CD4+ T cells during HIV. [19] Antiretroviral therapy, the most common treatment for patients with HIV, has been shown to restore CD4+ T cell counts. [20]
The presence of a CD8+ cell noncytotoxic anti-HIV response (CNAR) was first reported in 1986 by researchers in the laboratory of Dr. Jay Levy at the University of California San Francisco (UCSF). [2] It was recognized that CD8+ cells from HIV-infected individuals can suppress HIV replication without directly killing the infected cells. [3]
Optimal CD8 + T cell response relies on CD4 + signalling. [44] CD4 + cells are useful in the initial antigenic activation of naive CD8 T cells, and sustaining memory CD8 + T cells in the aftermath of an acute infection. Therefore, activation of CD4 + T cells can be beneficial to the action of CD8 + T cells. [45] [46] [47]
Activated CD8 + T cells destroy target cells on contact, whereas activated macrophages produce hydrolytic enzymes and, on presentation with certain intracellular pathogens, transform into multinucleated giant cells. The overreaction of the helper T cells and overproduction of cytokines damage tissues, cause inflammation, and cell death.
HIV infection leads to low levels of CD4 + T cells through a number of mechanisms, including pyroptosis of abortively infected T cells, [12] apoptosis of uninfected bystander cells, [13] direct viral killing of infected cells, and killing of infected CD4 + T cells by CD8 + cytotoxic lymphocytes that recognize infected cells. [14]
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