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"We think that the new replication mechanism we have found could provide a target for drugs designed to eliminate infection," says David Levy. (Credit: Dominic Alves/Flickr)


Team uncovers HIV’s secret survival trick

HIV, the virus that causes AIDS, has an alternate way to replicate, researchers have discovered.

“Although this is not the virus’ main method for replicating, having this option available can help HIV survive,” says David N. Levy, an associate professor of science and craniofacial biology at the New York University College of Dentistry.

“These new findings suggest one mechanism by which HIV may be surviving in the face of antiviral drugs, and suggests new avenues for research into eliminating infection,” adds Levy, who led the research published in the Journal of Virology.

For decades, scientists have been confident that HIV-1, the virus that causes AIDS, must insert its genetic material into a cell’s DNA in order to reproduce. This process, called “integration,” makes the virus a permanent part of the cell.

Some of these infected cells can remain as long as the person is alive, and this is one reason why HIV+ individuals must remain on anti-HIV drugs for life.

HIV-1 can sometimes skip this integration step entirely, the researchers discovered.

The integration step is highly inefficient and actually fails up to 99 percent of the time, leaving most viruses stranded outside of the safe harbor of cell’s DNA. The assumption was that these stranded, or “unintegrated”, viruses were unable to reproduce, but Levy’s team has found that if the conditions are right, they can generate new viruses that infect new cells.

The unintegrated viruses can survive for many weeks in cells, allowing HIV to “hide out” in a dormant state. The ability of HIV-1 to go dormant helps it avoid elimination by antiviral drugs and immune responses.

“There is intense interest by researchers in the idea that new drugs might be developed to help to completely eliminate the virus from infected individuals,” says Levy. “We think that the new replication mechanism we have found could provide a target for drugs designed to eliminate infection.”

The National Institutes of Health supported the work.

Source: New York University

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