Abstract
A majority of adults without HIV infection and with a low risk of HIV-exposure have plasma IgG antibodies that enhance the rate and magnitude of HIV-induced interferon alpha (IFN-α) production. Fc-dependent IgG-HIV complexes induce IFN-α rapidly and in high titers in response to HIV concentrations that are too low to otherwise stimulate an effective IFN-α response. IFN-α promoting antibody (IPA) counters HIV-specific inhibition of IFN-α production, and compensates for the inherent delay in IFN-α production common to HIV infection and other viruses. Naturally occurring IPA has the potential to initiate a potent IFN-α response early in the course of HIV mucosal invasion in time to terminate infection prior to the creation of a pool of persistently infected cells. The current study adds IPA as a mediator of an Fc-dependent antiviral state capable of preventing HIV infection.
Highlights
Human immunodeficiency virus (HIV) infection is relatively difficult to acquire, and large numbers of unprotected heterosexual exposures are needed to produce a single infection[1,2,3]
Plasma from 41 of 43 reproducibly HIV-seronegative individuals living in a relatively high risk environment in Thailand promoted IFN-αproduction by Plasmacytoid dendritic cell (pDC) exposed to limited numbers of virus particles in the range of an MOI of 0.001–0.01
No measurable IFN-αwas detected in pDC cultures without virus or plasma, or in pDC cultures containing plasma without HIV
Summary
Human immunodeficiency virus (HIV) infection is relatively difficult to acquire, and large numbers of unprotected heterosexual exposures are needed to produce a single infection[1,2,3]. IFN-αis the central mediator of the innate antiviral immune response, its efficacy is limited by slow production and low initial titers[10,11,12]. IgG capable of intensifying the IFN-αresponse has been demonstrated for other viruses to which humans and animals have antibodies as a result of prior infection, immunization or environmental exposure[17,18,19,20,21,22,23]. The current study examines plasma from people without HIV infection and with a low risk of HIV exposure for antibody capable of promoting HIV-induced IFN-αproduction to a degree that could explain how an otherwise, slow initially weak and virus-compromised IFN-αresponse could terminate HIV infection
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