"In earlier studies, we knew that we could interfere with the spread of HIV-1, but we couldn't identify the mechanism that was stopping the process," said Yong-Hui Zheng, Michigan State University (MSU) associate professor and co-author of the study.
"We now know that ERManI is an essential key, and that it has the potential as a antiretroviral treatment," said Zheng.
Antiretroviral treatments are not vaccines; they simply keep HIV in check in low levels in the body.
The next steps will be to test if HIV resistance can be promoted by increasing ERManI levels, said Zheng, who worked on the study with scientists from the Harbin Veterinary Research Institute, the Chinese Academy of Agricultural Sciences and the University of Georgia.
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Most viruses have viral envelopes, or protective skins, that comprise similar building blocks of the host the pathogens are trying to infect.
On the surface of the envelope, there are viral glycoproteins, known as Env spikes, which act as valets, leading viruses to binding sites that allow infections to spread at the molecular level.
Zheng's lab was the first to show that HIV-1 envelope glycoprotein biosynthesis can be specifically inhibited by ERManI, which is a host enzyme to add sugars to proteins.
By identifying ERManI as the target that slows the spread of HIV-1, the team showed a target in which future natural therapies can be developed.
More than 1.2 million people in the US have HIV. In China, doctors diagnosed 104,000 new cases of HIV/AIDS in 2014. The number of infections is rising, though overall the country still has a low rate of infection.
Current drug treatments have to be taken for a lifetime, which causes side effects and many other issues, Zheng said.
"We see a way to treat this disease by helping the body protect itself," he said.
The study was published in the Journal of Biological Chemistry.