Antiretroviral therapy, the common approach in the treatment of HIV, halts replication of the virus and has saved the lives of millions of people. However, for patients the drug cocktail becomes a lifetime necessity because they continue to harbor latent HIV in a small number of immune system cells. In the absence of treatment, HIV can again replicate and rebound into full blown AIDs.
A new study, however, suggests that addition of a single small molecule can rip away the cloak that shields those cells containing HIV and make them susceptible the patient's own antibodies that otherwise are not normally of much use against HIV.
For the study, a team of researchers led by scientists at Yale and the University of Montreal Hospital Research Centre stopped antiretroviral treatment for mice carrying human plasma and blood cells infected with HIV. They then treated the mice with a drug developed at the University of Pennsylvania that mimics receptors of immune T cells called CD4. The CD4-like molecule binds to and exposes vulnerable parts of the viral envelope on infected cells.
The mice experienced either no rebound of infection or long delays before active HIV infection restarted, the researchers report May 20 in the journal Cell Host & Microbe.
Researchers hope one day the new treatment may eliminate the need for long-term antiretroviral treatments.
It's sort of like pawn promotion in the game of chess, said Priti Kumar, associate professor of infectious diseases at Yale School of Medicine and lead author of the study
"These antibodies are like pawns," Kumar said. "There are many of them, but they are useless against the source of virus. But with the right move, they can be promoted to a powerful position and score a decisive victory by eliminating infected cells."
The CD-4 like molecule in the presence of antibodies acts like a "can opener" that allows antibodies to recognize the virus and trigger an immune response.
"The virus can now be recognized by patient antibodies that call the immune system's 'police,' the natural killer cells, to get rid of the infected cells," said Andrés Finzi, co-lead author of the study and professor at the Université de Montréal.
"In this way, a patient's own antibodies and cells that are commonly present can eliminate the viral reservoir and prevent viral rebound," Kumar said. "The hope is one day we might be able to do away with antiretroviral therapies altogether."
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Yale's Richard Flavell and Amos B. Smith of the University of Pennsylvania are also co-corresponding authors of the paper.
Journal
Cell Host & Microbe