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
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