Researchers discover HIV vulnerability
 

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posted Friday, February 17, 2012 - Volume 40 Issue 07

Researchers discover HIV vulnerability
by Mike Andrew - SGN Staff Writer

An international team of researchers has discovered that some human cells can repel HIV infections by 'starving' the virus of the necessary raw materials of life.

The study, published in the journal Nature Immunology, shows how macrophages and dendritic cells resist HIV infections.

It remains to be seen if these new findings have practical application in treatment of HIV infections, the researchers said.

Viruses like HIV cannot replicate on their own. They attach themselves to other cells, using material from them to produce more viruses. HIV attaches to cells involved in the human immune system, weakening it and inviting secondary infections.

Not all parts of the immune system are easily subverted by the virus, however. Macrophages and dendritic cells, which have important roles in orchestrating the immune response, seem to be more resistant.

Last year researchers identified the protein SAMHD1 as being a critical part of this resistance. Now they believe they know how it works.

The new research shows that SAMHD1 breaks down the building blocks of DNA.

When a cell needs to replicate itself it will have a pool of these building blocks - deoxynucleoside triphosphates, or dNTPs - which make new copies of the DNA.

The same dNTPs are also used by viruses like HIV.

The latest study shows that SAMHD1 lowers the levels of dNTPs below what is needed to build viral DNA, and therefore helps to prevent infection. When researchers removed SAMHD1, cells had higher levels of dNTPs and were infected by HIV.

'By depleting the pool of available dNTPs, SAMHD1 effectively starves the virus of a building block that is central to its replication strategy,' the report says.

Macrophages and dendritic cells can produce the SAMHD1 protein because they are 'mature cells' which do not go on to produce new cells, and therefore do not need to conserve dNTPs.

'It makes sense that a mechanism like this is active in macrophages,' Professor Baek Kim, one of the researchers from the University of Rochester Medical Center, said.

'Macrophages literally eat up dangerous organisms, and you don't want those organisms to have available the cellular machinery needed to replicate and macrophages themselves don't need it, because they don't replicate.

'So macrophages have SAMHD1 to get rid of the raw material those organisms need to copy themselves. It's a great host defense.'

Dr. Jonathan Stoye, virologist at the Medical Research Council National Institute for Medical Research in England, was part of the team that determined the chemical structure of SAMHD1 last year, and predicted that it would attack dNTPs.

'We hypothesized that it works in this fashion and the paper tells us we were right. It is depleting cells of these dNTPs, in cells which are not proliferating,' he told BBC News.

The downside, Stoye said, is that some cells - CD4 cells, which are prime targets for HIV infection - actually do need to replicate and boost their numbers as part of the immune defense.

'Cells which are proliferating would be in trouble if we took dNTPs away,' Stoye said.

'How we can use the anti-retroviral action of this protein is not clear to me,' he added.



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