艾滋病病毒在大脑内的复制 - 中国病毒学论坛|我们一直在坚持！

"This shows that viral replication and inflammation can occur early in infection with the concern being that the damage caused could be irreversible," says study virologist Ronald Swanstrom, PhD, Director of the University of North Carolina's Center for AIDS Research (CFAR) and Professor of Biochemistry and Biophysics at UNC's School of Medicine. "HIV and inflammation have the potential to accelerate the aging process and cause neurocognitive impairment, in the extreme case resulting in HIV-associated dementia."

One-third of people not taking antiretroviral therapy (ART) to control their HIV will eventually develop HIV-associated dementia, Swanstrom says. For him, the study's results in these newly infected people stress the importance of routine HIV testing to catch the infection as early as possible to allow the prompt initiation antiretroviral therapy.

"This is yet another reason we want people on ART right away to limit the possibility of replication and inflammation in the brain," Swanstrom says.

Future studies could focus on whether or not damage to the brain caused by this early replication and inflammation is reversible. Swanstrom collaborated on the study with senior author and neurologist Serena Spudich, MD, Division Chief of Neurological Infections & Global Neurology and Associate Professor of Neurology at Yale School of Medicine, and neurologist Richard Price, MD, Professor of Neurology at the University of California San Francisco School of Medicine. The first author on the study was a UNC graduate student in the Department of Microbiology and Immunology, Christa Sturdevant, who is now a postdoctoral fellow at Duke University. The study was funded by the National Institute of Mental Health.

Early HIV-1 CNS replication likely provides a foundation for brain injury and a potentially important tissue reservoir. To explore the character and timing of emergence of early HIV-1 CNS replication, we examined paired cerebrospinal fluid (CSF) and blood samples from 72 ART-naïve adults, with one-half having longitudinal samples, during the first two years following HIV-1 subtype B infection. In a cross sectional analysis over the first two years of infection, 10–25% of subjects had evidence of either local viral replication in the CNS, defined by the presence of CSF compartmentalization, or a robust inflammatory response, and in approximately 16% of subjects this CNS involvement persisted over time. In some subjects, one of two transmitted viruses replicated predominantly within the CNS, providing insight into how HIV-1 can establish independently replicating populations early in different parts of the body. Based on their entry phenotype, all viruses were selected for replication in CD4+ T cells, although this phenotype was slightly altered in the compartmentalized virus. Overall, we suggest four states to model the nature of HIV-1 CNS infection, which imply distinct mechanisms of virus/host interaction within the CNS during early infection.

HIV's double strike at the brain: neuronal toxicity and compromised neurogenesis