Restriction of retroviral infection of macrophages.

摘要: Primate immunodeficiency viruses are highly specialized lentiviruses that have evolved to successfully infect and persist for the lifetime of host. Despite encountering numerous potent antiviral factors, HIVs SIVs successful pathogens due acquisition equally countermeasures in form accessory genes. The gene Vpx encoded by HIV-2 a subset profound effect on ability non-dividing cells, such as macrophages. Although most virus replication occurs activated CD4+ T myeloid lineage cells natural targets infection play central role transmission, dissemination, persistence. However, poorly sensitive lentiviral partly high-level expression host protein regulates nucleic acid metabolism named SAMHD1. Degradation SAMHD1 is induced eliminate this intrinsic factor. Importantly, has also been implicated negative regulator innate immune response, so interplay between likely significant consequences replication, persistence, control.