DC interaction with HIV is relevant to the pathogenesis of AIDS because they are present in the mucosa and skin of humans and are believed to be the first HIV-1 targets following sexual transmission of the virus. Both myeloid DC and plasmacytoid DC possess the receptors for HIV entry ; that is, CD4, CXR4, and CCR5 can be infected but with a lower efficacy than CD4 cells or macrophages. The long-term result of this infection is that DC remains a reservoir for the production and persistence of the HIV-1 virus, and the virus induces several functional impairments and variations in the DC populations. Thus, the number of both myeloid DC (MDC) and peripheral DC (PDC) are significantly decreased in HIV-positive progressors, while remaining unaltered in HIV-positive long-term nonprogression. The destruction of these cells may be a consequence of direct lytic infection or as targets for specific CTL or through a block in DC development from peripheral CD34 stem cells. More recent evidence supports the notion that both midi and pad show impaired functional capacity in HIV-positive patients. Since both DC subsets participate in the initiation of innate and adaptive immune responses, infection, depletion, and dysfunction of DCs may contribute to the immunesuppression seen in HIV disease. Therefore, DCs play a dual role in HIV infection: they trigger both innate and adaptic immune responses to control the infection, but they also represent a viral reservoir for infection of permissive CD4 T cells.
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