Editor’s note: This article is part of WRAL Local Tech Wire’s highlighting of research at universities across the Carolinas and Georgia.

RALEIGH, N.C. — In a surprising finding, researchers at North Carolina State University have discovered that HIV can cause portions of the body’s innate immune system, when stimulated, to actually increase the virus’ replication. The finding could lead to a change in therapeutic strategies for HIV patients.

Dr. Gregg Dean, professor of immunopathology at NC State, led the research team. Dr. Shila Nordone, a research assistant professor in Dean’s lab, collaborated on the study, which was published in the journal AIDS Research and Human Retroviruses.

There are two "arms" to the human immune system: adaptive and innate. The adaptive immune system can be "trained" to recognize a particular pathogen by either experience or vaccination. It identifies and responds to specific threats, such as certain strains of flu.

The innate immune system, on the other hand, is designed to recognize broad categories of pathogens – such as viruses, bacteria, or fungi – and to respond when these pathogens invade the body. Specialized molecules known as Toll-like receptors (TLRs) act as the body’s alarm system and send the signal to produce antibodies when triggered by a particular pathogen. Scientists have identified and numbered TLRs according to the type of pathogens to which they respond.

Dean and his team looked at certain Toll-like receptors to determine how HIV affected their function. They discovered that HIV impairs the function of a specific TLR, which might explain why AIDS patients suffer from recurrent bacterial infections. The researchers also found that the virus exploited the receptors so that when they signaled the immune system to respond to a threat, it resulted in the production of more HIV.

"This goes to a long-standing question about HIV and its interaction with the immune system: does it shut down the toll receptor’s ability to recognize pathogens, resulting in a patient contracting more illnesses, or does it ‘hijack’ the toll receptor and cause it to replicate the HIV virus?" Dean says.

"We found that the answer wasn’t necessarily one or the other, but that both scenarios can and do occur. On the one hand, the HIV can inhibit toll receptor function, but on the other, stimulation of the toll receptor can activate HIV replication."

The team’s findings have implications for HIV patients’ treatment strategies.

"A lot of research has focused on getting the human immune system to respond better to the HIV virus," Dean says. "Our findings indicate that we want to be careful about utilizing drugs that stimulate the activation of TLRs, because we may accidentally stimulate viral replication."