Following an HIV-1 infection, the virus is usually very quick and efficient in trafficking itself into the nucleus of host cells for integration of its genome. Imagine however, if there was a way to stop the integration of the virus’s genome, or a way to significantly prolong the trafficking of the virus through the cytoplasm so that the immune response could begin to fight the virus off before it even begun replication. Well, it turns out that recently, a study from Loyola University of Chicago has found that a protein called bicaudal D2 is responsible for binding HIV-1 virions to a dynein, which helps traffic the HIV-1 virions through microtubules into the nucleus. Bicaudal D2 moreover, was found to bind to HIV capsid tubes via its CC3 domain. Campbell and his fellow peers also observed an increase in the stimulation of interferon genes when bicaudal D2 was significantly depleted in a monocytic cell line THP-1. All of the evidence found in the study point us to the conclusion that bicaudal D2 should be a target for novel development of drugs.
The development of a drug that specifically targeted the bicaudal D2 protein would hypothetically be effective in stopping HIV in the cytoplasm, where it would be left stranded and vulnerable to our immune response. This discovery is a big step in our battle against this speedy intruder that has no chill, but it is reasonable to assume that the development of any drugs is still a far ways off, and the testing of drugs in clinical trials will be tedious process.
Sources:
- -Daniel Gutierrez
0 Komentar