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HIV speedy mutation beats immunity

PARIS, February 26 – A worldwide team of scientists on Wednesday said the human immunodeficiency virus (HIV) was swiftly evolving to avoid the body’s immune defences, a phenomenon that adds to the challenge of crafting an AIDS vaccine.

Mutations in HIV enable it to rapidly sidestep genetic variations that offer a better natural shield against the deadly pathogen, they said in a study released by the journal Nature.

"Even in the short time that HIV has been in the human population, it is doing an effective job of evading our best efforts at natural immune control of the virus," said Oxford University researcher Philip Goulder.

"This is high-speed evolution that we’re seeing in the space of just a couple of decades."

Goulder’s team analysed the genetic codes and viral strain of 2,800 infected people in North America, the Caribbean, Europe, sub-Saharan Africa, Australia and Japan.

Their big focus was on so-called human leukocyte antigen (HLA) genes.

These control specialised proteins whose job is to act as a signaller against intruders. The proteins present little pieces of HIV to the body’s heavy armour, T cells, which then seek out the virus and kill it.

Since HIV was identified as the cause of AIDS, more than a quarter of a century ago, doctors have learnt that even though no-one appears to be naturally immune to the virus, people progress to the full-blown disease at different rates.

Without antiretroviral drugs, some individuals may develop AIDS as little as a year after infection, while others take as long as two decades.

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The span depends largely on inherited luck, for there are variants of HLA genes that are far better at combating HIV than others. A tiny difference in DNA can make a huge difference in holding back the virus.

Goulder’s team came across some bad news.

They found that the virus is able to mutate when facing the more successful variants of these genes.

This "escape mutation" is then transmitted on to the viral progeny and then handed on to the human population when another person becomes infected.

"Where a favourable HLA gene is present at high levels in a given population, we see high levels of the mutation that enable HIV to resist this particular gene effect," said co-author Rodney Phillips in a press release issued by Oxford University.

"The virus is outrunning human variation, you might say."

The study adds a further complexity in the quest for an HIV vaccine, say the authors.

Vaccine engineers will have to wrestle with different "escape mutations" in HIV that exist in distinct pools of populations.

For instance, a highly favourable variant of HLA is called HLA-B*51. It is common among people in Japan — and, as a result, two-thirds of infected people there have a strain of HIV which features the "escape mutation" for this variant.

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In Britain and Africa, though, HLA-B*51 is far less common. As a result, only between 15 to 25 percent of HIV-infected people have the "escape mutation" in their version of the virus.

So it means that a successful HIV vaccine may have to take these geographical differences into account, as well as the stealthy, slippery mutability of the virus itself.

"The implication is that once we have found an effective vaccine, it would need to be changed on a frequent basis to catch up with the evolving virus, much like we do today with the flu vaccine," said Goulder.

AIDS first emerged in 1981 as a novel disease that destroys immune cells, exposing the body to opportunistic infections. HIV was identified as its source in 1983. Twenty-five million people have died of AIDS and an estimated 33 million people have HIV.

The new paper focuses only on HIV’s ability to sidestep natural immune systems. It did not address the virus’ mutability towards anti-HIV drugs.


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