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Journal of Undergraduate Research

Keywords

vitro activation, FDC, immunodeficiency virus infection, follicular dendritic cells

College

Physical and Mathematical Sciences

Department

Chemistry and Biochemistry

Abstract

HIV is known to survive on follicular dendritic cells (FDCs) for many months and is believed to contribute to persisting HIV infection. FDCs protect HIV from degradation, thereby prolonging the infectivity of the virus. Moreover, when virus is trapped on FDCs, it escapes the ability of neutralizing antibodies (NtAb) to block infection of CD4+ T cells and subsequent removal of virus from the body. We postulate that FDC CD32 and/or CD21 contribute to maintaining virus infectivity and permitting infection in the presence of NtAb. Furthermore, when HIV forms an immune complex with antibodies and binds to CD32 and/or CD21, the FDC becomes activated. FDC activation increases its expression of FDC CD32 and CD21, thereby permitting more viruses to be trapped and we reason to better escape the blocking effects from NtAb. If our hypothesis that FDC CD32 and CD21 play a role in increasing the infectivity of HIV on FDCs is correct, then we may be able to block the actions of these two receptors, thereby inhibiting the spread of infection.

Included in

Chemistry Commons

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