NYU Langone Medical Center, U. Rochester Medical Center and research groups from France have worked together for five years to look into the role of SAMHD1 in contracting AIDS.

Most recently, they discovered building blocks of HIV virus disappeared when the anti-viral protein SAMHD1 was placed in an AIDS-infected cell. As a result, DNA components of the virus replicated slower or stopped replicating.

Nathaniel Landau, an NYU professor and one of the main researchers of the study, said the discovery will lead to new understandings of HIV.

“It may lead to mechanisms or ways to boost the immune systems response,” he said. “It will not cure somebody, but it will allow the immune system to control the violence [of AIDS].”

But Landau said these new findings cannot be seen as a cure for HIV.

“This tells us how the immune system tries to fight the virus and how the virus tries to escape from the immune system,” he said. “Now we have to think about how to prevent the virus from escaping. A cure for HIV will not be coming up soon.”

However, Landau said the group will research further to understand the idea of attacking the HIV infection.

Pablo Tebas, director of the adult AIDS Clinical Trials Unit research site at the University of Pennsylvania, said the study is an interesting mechanism to fight against viral infection.

“The cells of the body have developed multiple mechanisms to fight viral infections and prevent the virus for taking over,” Tebas said. “It seems that the investigators identified another protein that is part of that system.”

Sita Awasthi, a researcher of Infectious Disease Division at Penn, said finding the function in relation to HIV infection was groundbreaking.

“[The] HIV-1 field will [now] be exploring therapeutic potential of this [SAMHD1] finding in controlling HIV-1 infections,” she said.