AI Article Synopsis
- Recent research explored the anti-viral effects of the HIV-1 resistance factor (HRF) on CD4 T cells, demonstrating its role in blocking the NF-kappaB/DNA complex crucial for HIV gene expression.
- HRF was tested on primary macrophages and shown to inhibit HIV-1 replication while also promoting HRF-like activity in these immune cells.
- The study concluded that HRF disrupts NF-kappaB binding in macrophages triggered by HIV-1 and bacterial components, leading to reduced inflammatory responses against these pathogens.
Article Abstract
We have recently described the molecular basis of HIV-1 resistance factor (HRF)-mediated anti-viral activity in primary and transformed CD4 T cells. HRF+ cell culture supernatants or partially purified HRF were found to incapacitate the formation of the NF-kappaB/DNA complex, which is indispensable for long terminal promoter-driven transcription of virus genes. In this study, we tested whether HRF might have much broader activity against other organisms whose pathogenesis is linked to NF-kappaB activation. Specifically, we tested the effects of HRF on the NF-kappaB-mediated responses of primary macrophages to HIV-1 or several bacterial antigens. We found that exposure to HRF inhibited HIV-1 expression in macrophages and also induced the production of HRF-like activity by macrophages, which prevented replication of virus in HIV-1-infected peripheral blood lymphocytes cultured in the adjacent compartment. We investigated the mechanism of this inhibition and found that HRF impeded NF-kappaB/DNA binding in macrophages induced by either HIV-1 or lipopolysaccharide from several bacteria species, resulting in impaired tumor necrosis factor-alpha responses to these organisms.
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| http://dx.doi.org/10.1038/sj.icb.7100092 | DOI Listing |
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