Researchers from Loyola University Chicago has discovered bicaudal D2 protein, which helps the virus to travel so fast. They found that virus could be detected by the viral defense system when the virus becomes stranded in the cytoplasm. The depletion of the protein results in the virus to become stranded in the cytoplasm. The study was published in the Proceedings of the National Academy of Sciences.
Edward M. Campbell, the corresponding author of the study, said, "By preventing its normal movement, we essentially turned HIV-1 into a sitting duck for cellular sensors." Including T cells and macrophages, HIV-1 infects and kills immune system cells, which were used in the study. Common bacteria, viruses, and other pathogens those are usually harmless in people with healthy immune systems.
However, this cripples the immune system, making the patient vulnerable to common bacteria, viruses, and other pathogens. HIV-1 should work its way through the cytoplasm to the nucleus, after entering a cell. HIV-1 takes control of the cell and makes additional copies of HIV-1, inside the nucleus. However, getting through the cytoplasm is not easy. Cytoplasm consists of fluid that is thick with proteins and structures such as mitochondria.
Campbell said, "Something the size of a virus cannot just diffuse through the cytoplasm." He added, "It would be like trying to float to the bathroom in a very crowded bar. You need to have a plan." Tubular tracks called microtubules, via these tracks, HIV-1 can get to the nucleus quickly. The virus attaches itself to a molecular motor called dynein, which moves down the microtubule like a train car on tracks.
The investigators discovered a protein called bicaudal D2. This protein acts, as a "ticket" for virus needs to get on the train. HIV-1 binds to bicaudal D2, which employees the dynein molecular motor. This study raises the possibility of developing a drug that would prevent HIV-1 from binding to bicaudal D2, thus stranding the virus in the cytoplasm. This would not only prevent infection; however, it also provides cell time to turn on antiviral agents.