The inrease of methylation that helps the HIV virus replicate

Researchers from the University of California, San Diego School of Medicine, found that HIV infected human immune cells can trigger the significant increase of a chemically modified human viral RNA - methylation, thereby helping the virus replicate. The study published in the February 22 journal Nature Microbiology establishes a new mechanism of the interaction between controlling HIV replication and the host's immune system.

Senior author of the paper, Dr. Tariq Rana, Professor, University of California San Diego School of Medicine, said: "Over the years we have a number of pharmaceutical companies and colleagues have been working on the development of targeted HIV genetic material --RNA drugs, but failed to push it into the clinical now we know the reason - we do not use these modified RNA target sequence to develop drugs, and the reality of RNA are different.”

In human cells, RNA is responsible to a command from the nucleus to the cytoplasm DNA the genetic material to go, in the cytoplasm of cells using these machine instructions to build proteins. In contrast, the entire HIV genome is composed of RNA rather than DNA constructed. The virus hijack the cellular machinery of the host to itself RNA translation into protein.

Cells can be controlled or change its function by chemically modifying RNA. One is referred to as N6- methyl adenosine (m6A) modified in humans and other organisms are common. In 2011, the Chinese chemical biologist Professor He Chuan the first to discover, the first can be reversed most common mRNA methylation modification: N6- methyl adenosine (m6A) of RNA demethylase, certificates and DNA and protein seen as adding and removing the methyl group can significantly affect these messenger RNA, and gene expression. June 2015, Professor He Chuan m6A reveals a new feature: the regulation of messenger RNA (mRNA) translation efficiency. These groundbreaking findings published in the journal Cell. October 2015, Samie R. Jaffrey Cornell University who led the research team published an article that, mRNA 5 'UTR of the RNA methylation (m6A) does not depend on the hat can promote protein translation in the journal Cell.

But until now people for m6A in the human immune system, as well as in our cells and invading pathogens such as HIV interaction between the roles is poorly understood.

In this study, Rana research team first discovered m6A modifications in HIV RNA. They also studied the infection of human immune cells during m6A for HIV RNA and function of the human host.

The first author of the paper, Rana laboratory Gianluigi Lichinchi graduate student, said: "People always thought m6A is a stable cell RNA modification of new studies confirms it is very dynamic, fast response to external stimuli such as viral infections in the future, these studies. The discovery could help improve and enhance HIV / AIDS vaccine design and efficacy."

Rev protein of HIV RNA is encoded by the gene. When constructed Rev protein in the cytoplasm of human host cells, they will return to the nucleus, where, Rev gathered on an HIV RNA known as Rev-responsive element (RRE) is a special site. Rev helped to transport the new generation of HIV RNA transcript into the host cytoplasm. This is an important step in viral replication.

The team is determined; m6A on human and viral RNA modification affects HIV Rev protein and RNA RRE interaction between. When the researchers responsible for silencing removed from the RNA enzyme m6A, HIV replication increases. In contrast, when they were silent m6A add up to the RNA enzyme, HIV replication reduces - the researchers say can be used in pharmacological studies have found that to fight HIV infection.

Rana said, "Such modification in research in the physical structure and HIV RNA genome of HIV field over the past 30 years had been missed. If other viruses having RNA genomes also use this mechanism to escape m6A modified immune surveillance and control them, I wouldn't be surprised. These viruses include influenza virus, hepatitis C virus, Ebola virus and Zika virus and so."

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