HIV is able to evade the host immune system to cause infection. In particular, HIV downregulates CD4+ immune T cell function, which might aid infection, but the mechanisms underlying this phenomenon are unknown. In a study appearing online on July 7 in advance of print publication of the August 1 issue of the Journal of Clinical Investigation, Yechiel Shai and colleagues from the Weizmann Institute examine the fusion peptide (FP) of HIV.
The researchers show that the FP plays two roles in HIV infection – it works with other domains to mediate fusion of the virus with the cell membrane, while also downregulating the T cell responses that normally would block infection.
The authors show that the HIV FP can co-localize with CD4 and T cell receptor in T cells, and inhibits antigen-specific T cell proliferation. This data highlights a potential immunosuppressive activity specific to HIV infection.
The authors then extend their findings by exploiting the activity of FP and show that it ameliorates the autoimmune disease adjuvant arthritis in rats. This study not only adds to our understanding of the mechanisms of HIV pathogenesis, but it also shows that the FP molecule, independent of HIV, may provide a novel way to decrease undesirable immune responses.
Title: HIV-1 Fusion Peptide Targets the TCR and Inhibits Antigen-Specific T-Cell Activation
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