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HIV-1 Vif: Multiple ways to outsmart the body’s defences?

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17.09.2004

The way that HIV disables the body’s natural defences against retroviruses is not as well understood as recent studies suggest, according to new research published in the Open Access journal Retrovirology. Klaus Strebel and his colleagues from NIH found that the HIV encoded Vif protein does not need to destroy the enzyme APOBEC3G within infected cells to disable it. This latest finding has serious implications for the design of antivirals to fight HIV.

APOBEC3G is one of the most recently identified ways that the body fights off unwanted attacks by retroviruses such as HIV. APOBEC3G is a cellular enzyme with the ability to chemically modify viral genomes and to change their genetic code. The changes to the HIV genome effectively neutralize it and prevent it from spreading to uninfected cells.

Recent research has shown that HIV has found a way to outsmart the body’s attempts to prevent it from replicating. HIV’s viral infectivity factor, or Vif, can prevent the packaging of APOBEC3G into the virus particles, stopping the enzyme from damaging the viral genome. The most popular current working model proposes that Vif does this by destroying APOBEC3G in infected cells.

Strebel and colleagues from the National Institutes of Health analyzed the coexpression of Vif and APOBEC3G in single-cells. They found that Vif can inactivate APOBEC3G without eliminating it from the virus producing cells. In their system, APOBEC3G was expressed at high levels even in the presence of Vif; yet, viruses produced in the presence of Vif were fully infectious.

These findings have important implications as they question the current working model proposing the efficient elimination of APOBEC3G from Vif-expressing cells. The authors do not question the validity of previously published data reporting on the destruction of APOBEC3G by Vif. Instead, they claim that destruction of APOBEC3G by Vif is not essential for the virus to multiply, and propose that the HIV Vif protein may have acquired the ability to target APOBEC3G on multiple levels to ensure that this protein is not packaged into viral particles. Understanding the exact mechanism of how Vif inhibits APOBEC3G will be essential for the design of antivirals targeting Vif.

This press release is based on the following article: Production of Infectious Human Immunodeficiency Virus Type 1 Does Not Require Depletion of APOBEC3G from Virus-Producing Cells Sandra Kao, Eri Miyagi, Mohammad A Khan, Hiroaki Takeuchi, Sandrine Opi, Ritu Goila-Gaur and Klaus Strebel Retrovirology 2004, 1:27 To be published 17 September 2004 Upon publication, this article will be available free of charge according to Retrovirology’s Open Access policy at: http://www.retrovirology.com/content/1/1/27

Grace Baynes | Source: Press BioMed Central
Further information: www.retrovirology.com/content/1/1/27
www.biomedcentral.com
www.niaid.nih.gov

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