New research from the Gladstone Institutes for the first time provides strong evidence that HIV latency is controlled not by infected host cells, but by the virus itself. This fundamentally changes how scientists perceive latency, presenting it as an evolutionarily advantageous phenomenon rather than a biological accident.

Viral latency is one of the premier challenges in developing a cure for HIV. Latency causes the virus to go into hibernation, enabling it to escape eradication by currently available antiretroviral therapies. The prevailing view has been that latency is an unintended byproduct of the host cell's natural life cycle; the infected immune cell naturally "relaxes" into a resting state, incidentally causing the virus to be suppressed.

However, a pair of articles published in the journal Cell turn this model on its head, proposing that the virus itself -- not the body's immune cells -- controls when HIV is in the latent or active state. What's more, the researchers suggest that latency is a naturally selected tactic employed by the virus to increase infection rates.

"Latency has been seen as an accident, a lucky break for HIV that allows the virus to avoid eradication by modern drug therapies," says Leor Weinberger, PhD, an associate investigator at the Gladstone Institutes and senior author on the two papers. "These 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."