Scientists have long thought that HIV's tendency to lay dormant within a person for 10 years or more was due to the behavior of the cells it infects or an error in the disease’s programming, but new evidence suggests that this inactivity may be an evolutionary strategy to help the virus to survive and spread. With this knowledge, scientists may be able to better target reservoirs of the virus which exist within the 35 million people around the world infected with HIV, and someday find a way to wipe it completely from their systems.

"This discovery changes our perspective on HIV latency and contributes to our understanding of what it is going to take to cure HIV," Robert Gallo, a biomedical researcher at the University of Maryland School of Medicine who was the first to find that HIV leads to AIDS, said in a statement.

The virus's long hibernation, which can last for decades in people with HIV (human immunodeficiency virus), appears to boost its ability to live and spread within people, researchers have now shown in a pair of studies published in Cell on Thursday. The authors call this latency “the greatest barrier to eradicating HIV in patients” because the virus can dodge the immune system and conventional therapies while dormant.

Until now, experts thought that latency came about because a host immune cell that became infected with HIV would naturally lower its activity level, thereby impeding the virus from taking further hold. "This new data indicate that latency is far from an accident -- it is encoded in the virus's circuitry and is an evolutionarily advantageous strategy, likely increasing the odds of infection by a substantial amount," Leor Weinberger, a coauthor and researcher at the Gladstone Institutes, a nonprofit focused on biomedical research, said in a statement.

When HIV enters the human body, it typically does so by clinging to only a handful of cells attached to a mucous membrane such as those in the genitals or rectum. There, the researchers say, going dormant allows it to bide its time until the infected cells can spread to other tissues more fertile ground. At that point, the virus progresses to AIDS.

To reach this conclusion, scientists honed in on the mechanism which controls the virus’s activity – a protein known as Tat. By playing with the protein, they showed that the virus could be switched on or off separate from the rhythms of its host immune cell, indicating that the two processes were independent of one another.

The research team also created a synthetic version of the virus in a lab and found that toying with Tat completely outside of a host immune cell could also switch it on and off, building on a study published last year which concluded that latency was “hard-wired” into the virus. A computer model based on data from patients with HIV further demonstrated that this hibernation period was evolutionarily advantageous, and could help the virus to survive and spread.