The HIV--?1 protein Vpr is highly conserved across all known lentiviruses, yet HIV mutants lacking vpr are capable of replicating in most cell culture models with little or no defect. The contrast between the evolutionary pressure to maintain indicate that in cultures of monocyte--?derived macrophages a vpr--? vpr and its relative inconsequence in vitro has not been fully explained. Our earlier findings null mutant displays restricted virion production and Env expression. Additionally C--? type lectin expressed in macrophages that is known to bind the Env subunit our preliminary data suggest this restriction is dependent on mannose receptor, a gp120. Our proposed studies aim to determine how Env and virions are targeted and to confirm the identity of the restriction factor responsible for the defects we have observed. Successful completion of the project will provide insight into innate immunity and viral mechanisms of evasion.
HIV, a global health pandemic that continues to infect over 2 million people per year (UNAIDS, 2013), infects a variety of cell types within the body. One cell type that can be infected is macrophages, which are an important part of the immune system and have several defenses against viruses (Mashiba & Collins, 2013). We plan to study the ways that the HIV protein Vpr overcomes these defenses in the hope that we will be able to develop treatments that reduce infection of macrophages.
