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Viral Complementation Allows HIV-1 Replication Without Integration, Research Shows

July 11, 2008 — Vital 'cooperation' is shown to be a mode of retroviral replication, which allows the survival of viruses that would otherwise be 'lost' because of a failure to integrate with a host's DNA.


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Weak HIV viruses piggyback onto stronger ones, raising the possibility that the human body may harbor many more HIV viruses capable of replicating and contributing to the development of AIDS than previously thought, a New York University College of Dentistry AIDS research team has found.

It's widely known that only about one in every 100 HIV viruses can successfully complete the process of integrating its DNA with the DNA of the human cell -- a step that every virus must successfully complete before it can reproduce. But a new study led by Dr. David N. Levy, an Assistant Professor of Basic Science and Craniofacial Biology at the NYU College of Dentistry, has revealed a mechanism that enables some of the other 99 percent of HIV viruses also to replicate and play a potential role in the development of AIDS.

"We've observed a new mode of HIV replication that involves cooperative interaction between viruses," said Dr. Levy, who recently published his findings.

According to Dr. Levy, HIV functions as a community, with those viruses that successfully integrate with the DNA in human cells rescuing the viruses that fail to integrate by providing them with the proteins they need to reproduce. In fact, the viruses that were once thought to be lost because they don't integrate may have an advantage over the others because they can skip several steps in their replication cycle and reproduce faster.

"Cooperation between different viruses is yet another one of the many tricks that HIV uses to survive, and raises the possibility that there are more active viruses in the body than was previously thought. Understanding how viruses interact with each other is a key to understanding how HIV evolves and survives the body's immune responses, which we hope could ultimately lead to the development of new ways to treat HIV infection."

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The above story is reprinted from materials provided by New York University, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Huub C Gelderblom, Dimitrios N Vatakis, Sean A Burke, Steven D Lawrie, Gregory C Bristol and David N Levy. Viral complementation allows HIV-1 replication without integration. Retrovirology, July 9, 2008 [link]
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