An immune response that likely evolved to help fight infections appears to be the mechanism that drives human immunodeficiency virus (HIV) into a latent state, lurking in cells only to erupt anew, researchers at Duke Health report. Publishing Nov. 14 in the journal Nature Microbiology, the research team provides new insights into the vexing process that makes HIV particularly stealthy, but could also play a role in other viral infections.
HIV has proven to be incurable because of a small number of latently HIV-infected T-cells that are untouched by both antiviral drugs and the immune response." Bryan R. Cullen, Ph.
D., senior author, professor, Department Molecular Genetics and Microbiology, Duke University School of Medicine "These cells, which are very long lived, can spontaneously emerge from latency and start producing HIV even years after infection, thus necessitating the life-long use of antiretrovirals," Cullen said. "The origin of these latently infected cells has remained unknown despite considerable effort.
" The findings from Cullen and colleagues offer important insights, pointing to a protein complex called SMC5/6, which is involved in a host cell's chromosome function and repair. HIV enters the body, infects the immune system's CD4+ T-cells, then makes a genome-length DNA molecule that it integrates into a host cell chromosome where it is then copied to generate viral RNAs and proteins. If this so-called DNA provirus is prevented from integrating into the host cel.
