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The study set the hypothesis that HMGB1 (such as flagellin, CpG-ODN and LPS), in combination with bacterial components, promote HIV-1 replication. In addition, we studied the level of anti-acne protein antibody during HIV-1 infection. method. Long-term HIV-1-infected U1 cells were stimulated with necrotic extracts / recombinant HMGB1 with TLR ligands or individual complexes. At 48-72 hours after stimulation, HIV-1 replication was estimated by culture of the p24 antigen in the culture supernatant. The presence of systemic flagellin IgG was determined by immunoblotting or in vivo ELISA in 51 HIV-1 infected patients and 19 control controls. result. When incubated with necrotic extracts or recombinant HMGB1, Flagellin, LPS and CpG-ODN induce stronger HIV-1 replication, rather than the use of any compound alone. In addition, the stimulating effect of the necrotic extract is inhibited by the consumption of HMGB1. The presence of anti-flagellin antibody levels in plasma from HIV-1 infected patients was significantly reduced and was significantly reduced during 2 years of antiretroviral therapy. in conclusion. Our findings relate to the possible role of HGMB1 bacterial complex as a result of microbial translocation and cell necrosis in the pathogenesis of HIV-1 immune activation. We suggest that flagellin is an important microbial product that regulates viral replication and induces an adaptive immune response in vivo.
Antiretroviral therapy (ART)
Gastrointestinal (GI) immune system