Being Alive 1992 Nov 5: 5
We have been hearing about tat inhibitors for some time. Early studies
continue to show promise.
Unlike the current generation of antivirals, tat inhibitors do work in
chronically infected cells. In order to make new virus, HIV requires
the presence of the tat gene. Tat is like the "master switch" of HIV;
without it, very little if any new HIV can be made by a chronically
infected cell. Also, tat released from infected cells seems to play a
role in causing latent HIV in other infected cells to activate.
This antiviral is potentially a giant leap forward in our fight
against HIV. A person infected with HIV may have thousands of cells
with HIV in the nucleus and AZT, ddI, ddC cannot touch them. The tat
inhibitor will ensure that no new virus can be made.
Several companies are working on tat inhibitors. Test tube studies
have shown no resistance developing even after a year, so there is
hope of avoiding the rapid development of resistance seen, for
example, with the "L" drugs. The tat inhibitors have also been shown
to be effective against AZT-resistant strains of HIV.
Human studies are now under way at the University of California, San
Diego. A group of 18 people in the 50-500 T-cell range are taking one
of three doses of tat inhibitor. Six people are taking either AZT or
ddI. This is only a 12 week study so results should be known by the
end of the year. We can only hope for good news about efficacy and
lack of resistance and side effects. We need the next generation of
antivirals to become the current generation as quickly as possible.