HIV is a retrovirus that exhibits a variety of structural and nonstructural proteins that determine the interaction of the virus with the host’s immune system and cellular components. The HIV virus attaches to the host cell by the association of a surface glycoprotein to the CD4 molecule; therefore, it primarily infects CD4+ lymphocytes and macrophages.
Once the virus core enters the cell cytoplasm of the host, viral reverse transcriptase copies viral RNA to the DNA of the host. The viral DNA is then transported into the nucleus and incorporated into the DNA of that cell. If activated, viral expression can result in new viral RNA and proteins. New viral core proteins, enzymes, and viral RNA molecules can induce budding, with additional cell infection. The reduction in cell-mediated immunity and secondary B-cell dysfunction result in the immunocompromised state and in the proliferation of opportunistic infections and malignancies. An elevated level of activation-induced cell death resulting from apoptosis of T cells occurs in patients who are HIV positive.
The CD95/Fas receptor/ligand system is necessary for the apoptosis of T cells, and abnormalities in this system are linked with increased T-cell death in patients who are HIV positive. As the immune status deteriorates, an increase in CD95+ T cells is found; conversely, a low CD95+ T cell count is found in asymptomatic patients who are HIV positive.
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