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HIV Continues To Grow In The UK

May 24, 2011

Figures released by the UK's Health Protection Agency today show that, in 2009, an estimated 85,000 people were living with HIV in the UK, a 2.4% percent increase on 2008's figures, with 61,000 people accessing HIV care and one in five of these aged 50 years or over.

While the rate of increase in diagnoses is slowing down, the number of people living with HIV is still growing, with 7% more people accessing HIV care in 2009 than the previous year. Half of these people (52%) were diagnosed late, when they should have already begun treatment for HIV, and a quarter of those living with HIV, 24%, are still undiagnosed, unaware that they are infected.

Sir Nick Partridge, Chief Executive for the UK's leading HIV and sexual health charity, Terrence Higgins Trust, said: "With more people living with HIV than ever before in the UK it's vitally important we invest in targeted HIV prevention and awareness programmes, particularly for gay men who are most at risk. We also need to re-double work to get people to test, to reduce the high numbers of people who don't know that they have HIV for far too long before being tested and prevent needless deaths.

"If you're diagnosed with HIV promptly after being infected there's no reason why you can't live a long and reasonably healthy life into your seventies, as many people with the condition are now doing, but you need to find out early on to get the maximum benefit from treatment. HIV is still the fastest growing incurable sexually transmitted infection in the UK and we must do more locally and nationally to stop HIV in its tracks."

Other key national findings:

- There were 6,630 new HIV diagnoses in 2009 a decline in new diagnoses for the fourth year running

- There has been a steady increase in the number of heterosexual transmissions in the UK, over 1,000 people

- Gay men remain at greatest risk- with 2,760 newly diagnosed in 2009, four out of five acquiring their infection in the UK. One gay man in seven on the London gay scene now has HIV.

- There was a 95% uptake of HIV testing in antenatal clinics and a 77% uptake in sexually transmitted infection (STI) clinics in England

- HIV treatment is of a high standard and makes a rapid improvement to health. Eighty per cent of people were seen in an HIV clinic within one month of diagnosis, 90% of these had an undetectable viral load one year after starting therapy and 93% of those in care for more than a year, had a healthy CD4 (white blood cell) count of above 200..

Terrence Higgins Trust

Tags: UK, HIV Statistics

Finally, An Explanation For How HIV Infection Kills T Cells

May 10, 2011

Researchers appear to have an explanation for a longstanding question in HIV biology: how it is that the virus kills so many CD4 T cells, despite the fact that most of them appear to be "bystander" cells that are themselves not productively infected. That loss of CD4 T cells marks the progression from HIV infection to full-blown AIDS, explain the researchers who report their findings in studies of human tonsils and spleens in the November 24th issue of Cell, a Cell Press publication.

"In [infected] primary human tonsils and spleens, there is a profound depletion of CD4 T cells," said Warner Greene of The Gladstone institute for Virology and Immunology in San Francisco. "In tonsils, only one to five percent of those cells are directly infected, yet 99 percent of them die."

Lymphoid tissues, including tonsils and spleen, contain the vast majority of the body's CD4 T cells and represent the major site where HIV reproduces itself. And it now appears that those dying T cells aren't bystanders exactly.

The HIV virus apparently does invade those T cells, but the cells somehow block virus replication. It is the byproducts of that aborted infection that trigger an immune response that is ultimately responsible for killing those cells.

More specifically, when the virus enters the CD4 T cells that will later die, it begins to copy its RNA into DNA, Greene and his colleague Gilad Doitsh explain. That process, called reverse transcription, is what normally allows a virus to hijack the machinery of its host cell and begin replicating itself. But in the majority of those cells, the new findings show that the process doesn't come to completion.

The cells sense partial DNA transcripts as they accumulate and, in a misguided attempt to protect the body, commit a form of suicide. Greene says that completed viral transcripts in cells that are productively infected probably don't provoke the same reaction because they are so rapidly shuttled into the nucleus and integrated into the host's own DNA.

The researchers narrowed down the precise "death window" of those so-called bystander cells by taking advantage of an array of HIV drugs that act at different points in the viral life cycle. Drugs that blocked viral entry or that prevented reverse transcription altogether stopped the CD4 T cell killing, they report. Those drugs that act later in the life cycle to prevent reverse transcription only after it has already begun did not save the cells from their death.

Those cells don't die quietly either, Greene says. The cells produce ingredients that are the hallmarks of inflammation and break open, spilling all of their contents. That may provide a missing link between HIV and the inflammation that tends to go with it.

"That inflammation will attract more cells leading to more infection," Greene said. "It's a vicious cycle."

The findings also show that the CD4 T cells' demise is a response designed to be protective of the host. All that goes awry in the case of HIV and "the CD4 T cells just get blown away," compromising the immune system.

Greene said that all the available varieties of anti-HIV drugs will still work to fight the infection by preventing the virus from spreading and reducing the viral load.

The findings may lead to some new treatment strategies, however. For instance, it may be possible to develop drugs that would act on the cell sensor that triggers the immune response, helping to prevent the loss of CD 4 T cells. His team plans to explore the identity of that sensor in further studies. They also are interested to find out if the virus has strategies in place to try and prevent the CD4 T cells' death.

"The cell death pathway is really not in the virus's best interest," Greene says. "It precludes the virus from replicating and the virus may have ways to repel it."

Elisabeth Lyons
Cell Press

Tags: UK, HIV Statistics


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