When HIV-1 infects an immune cell, the virus travels to the nucleus so rapidly there’s not sufficient time to set off the cell’s alarm system.
Now, a Loyola University Chicago examine has found the protein that helps the virus journey so quick. Researchers discovered that with out this protein, the virus grew to become stranded in the cytoplasm, the place it was detected by the viral protection system. (The cytoplasm is the portion of the cell outdoors the nucleus.)
“By preventing its normal movement, we essentially turned HIV-1 into a sitting duck for cellular sensors,” stated Edward M. Campbell, PhD, corresponding creator of the examine, printed in the Proceedings of the National Academy of Sciences. Campbell is an affiliate professor in the Department of Microbiology and Immunology of Loyola University Chicago Stritch School of Medicine.
HIV-1 infects and kills immune system cells, together with T cells and macrophages that had been used in the examine. This cripples the immune system, making the affected person susceptible to widespread micro organism, viruses and different pathogens which can be normally innocent in folks with wholesome immune methods.
After HIV-1 enters a cell, it has to work its way by means of the cytoplasm to the nucleus. Once contained in the nucleus, HIV-1 takes management of the cell and makes further HIV-1 copies. But getting by means of the cytoplasm will not be simple. Cytoplasm consists of fluid that’s thick with proteins and constructions corresponding to mitochondria. “Something the size of a virus cannot just diffuse through the cytoplasm,” Campbell stated. “It would be like trying to float to the bathroom in a very crowded bar. You need to have a plan.”
HIV-1 is ready to get to the nucleus rapidly through tubular tracks referred to as microtubules. The virus attaches itself to a molecular motor referred to as dynein, which strikes down the microtubule like a prepare automobile on tracks.
Campbell and colleagues found the “ticket” HIV-1 wants to get on the prepare — a protein referred to as bicaudal D2. HIV-1 binds to bicaudal D2, which recruits the dynein molecular motor. The dynein then transports HIV-1 in the direction of the nucleus.
The discovering raises the potential of creating a drug that may stop HIV-1 from binding to bicaudal D2, thus stranding the virus in the cytoplasm. This wouldn’t solely stop an infection, but in addition give the cell time to activate antiviral genes that may shield it and neighboring cells from an infection.
Materials offered by Loyola University Health System. Note: Content could also be edited for type and size.