College and primary school students hold a giant red ribbon they made for an event to raise awareness of HIV/AIDS on   World AIDS Day  in Fuyang, Anhui province, China, on Dec. 1. (Reuters)

In the places where HIV has hit the hardest, the virus may also be relatively quickly mutating to become less infectious.

In a matter of decades, the HIV virus has changed in such a way that its ability to replicate in the body is weakened and as a result, it progresses to AIDS more slowly, according to a new study.

The finding could mean two important, and promising, things. A virus that replicates more slowly means that the rate of infections may eventually slow. And over time, as weaker versions of the virus become more prevalent, people who are infected progress to full-blown illness much later -- opening a wider window for treatment.

Scientists have long believed that over time, in order for viruses to survive in their hosts, they must become less virulent or cause less disease.  In the case of HIV, the virus in most cases kills its host eventually. So over time, scientists would expect natural selection to favor mutations of the virus that allow the host to survive longer.

The research published  Monday in the journal Proceedings of the National Academy of Sciences suggests that this process is at work with HIV as well. And surprisingly, these changes are being observed in a relatively short period of time -- decades since the virus began spreading rapidly among humans.

"I'm totally amazed that you can see these effect so quickly," said Phillip Goulder, the study's lead scientist and a professor a the University of Oxford. "You wouldn't expect an effect like this to be evident in an incredibly small amount of time. This difference is happening so quickly in the locations where you have the greatest impact of the virus."

In some humans, a type of protein called HLA-B-57 is effective at giving the body some protection against the HIV virus. But the virus adapts to that protective protein by mutating to survive. Those mutations, however, damage the virus, changing its ability to replicate.

"The parts of the virus that it targets are the parts of the virus that can't really change without losing some ability to replicate efficiently,"  Goulder said.  "What B-57 is doing is creating a virus that is relatively crippled."

As the crippled HIV virus proliferates in the human population, the protective benefit of HLA B-57 is also greatly diminished. Despite the trade-off, a less potent virus can have a powerful, positive impact on the HIV population at large.

The study compared HIV samples from populations in Botswana and in South Africa, two places where the virus has ravaged the population. In Botswana, HIV was introduced to the population earlier than in South Africa. And Botswana has been a notable early  and aggressive adopter of antiretroviral therapies that researchers suspect could help to accelerate the process of weakening the virus.

They found that the Botswana population had lower viral loads and no protective effect of the HLA B-57 protein compared to South Africa, where the HIV virus has been present for a shorter period of time and where antiretroviral use began relatively recently.

"The normal time to AIDS is about 10 years, and this difference in the ability of the virus to cause disease probably means that there's a 25 percent increase in the amount of time to AIDS. So it probably means about 12 years," said Goulder.

A two-year difference from infection to the onset of disease may not seem like much, but over time, it can add up. Coupled with the more widespread and targeted use of antiretroviral treatments and vaccines, it could aid the global effort to combat AIDS.

"By and large, if the virus is less efficient at replicating, generally it doesn't transmit as well," Goulder noted. "Secondly, if you have a virus that replicates more slowly, the viral load is definitely lower. It's very clear that the risk of transmission is strongly related to the viral load." And a higher viral load makes transmission far easier.

Changes in the way the virus affects humans can have downsides. In the U.S. alone, 1 in 7 people infected with HIV don't know know that they contracted the virus. And in low and middle income countries around the world, most people living with HIV don't know their status, according to the World Health Organization.

A longer road from infection to disease could mean that people might not know their status for even longer and as a result, might not get the treatment that they need.

"That's a problem that I guess comes along with any sort of piece of good news about HIV and any benefit that comes from an intervention," Goulder acknowledged. "If people's behavior changes as a consequence -- it becomes more risky or their desire to get treated or tested is reduced -- that disadvantage might outweigh the benefits that come from something like this."

For now, aid organizations could help speed the mutation process by targeting antiretroviral therapy programs to focus on people who exhibit rapidly replicating, stronger forms of the virus. Goulder's research suggests that this strategy could help suppress the spread of more aggressive strains among humans, leaving more of the weaker virus.

A weaker HIV won't eliminate the virus among humans, but it might help slow its spread and help science catch up.

"It does help to buy us a bit of time. It means that there will be less disease than there would be without it," Goulder said. "It is quite a good thing to have and it probably will have quite a bearing, given that we can't reach all infected people with antiretroviral therapy and a vaccine isn't going to materialize anytime soon."