New discovery could hold key to HIV cure

Since researchers first identified AIDS in the early 1980s, 35 million people around the world have died of the disease, according to the World Health Organization. More than three decades later, nearly 37 million people are infected with the HIV virus.

There is no cure for AIDS, but in two recent independent studies a team of researchers from Italy and Switzerland and another from the University of Massachusetts Medical School have discovered cellular mechanisms that may lead to treatments that can prevent the HIV-1 virus from reproducing. HIV-1 is the most predominate form of the virus and accounts for 95 percent of all HIV infections worldwide.

The discovery involves three different types of proteins. Two of them, SERINC5 and SERINC3 are the good guys. They block the ability of the HIV-1 virus to infect new cells. The third protein, Nef, is the bad guy. It disables the action of the two SERINC proteins and facilitates the development of AIDS.

Scientists have known for 20 years that Nef is responsible for making HIV-1 such a deadly virus, but until now they didn’t know how it worked.

The HIV-1 virus consists of only nine genes. It cannot reproduce those genes by itself—it needs the assistance of a host cell. Once the virus invades a cell, it takes over certain processes that enable it to replicate. Infected cells then produce new, mature forms of the virus and propel them out of the cell, where they search for new host cells to invade and use for further replication. It is this cycle of infection the researchers believe they can circumvent now that they understand the process.

“Disrupting this mechanism could be a very powerful strategy for treating HIV and similar viruses that express the Nef protein,” Heinrich Gottlinger, University of Massachusetts Medical School researcher, said in a statement.

In the current studies, researchers discovered the activity of the SERINC proteins is so robust it can reduce the ability of the HIV-1 virus to infect other cells by more than 100 fold. When Nef is not present, the two SERINC proteins latch onto the surface of the viral cell, referred to then as a virion, as it leaves its host cell. The SERINC proteins do not prevent the virion from attaching itself to a new potential host cell, but they do prevent it from releasing its genes into the cell, blocking it from replicating. But when Nef is present, it blocks the SERINC proteins from reaching the surface of the cell and renders them ineffective.

The researchers hope their discovery may have even broader applications.

“These findings demonstrate that the SERINC proteins probably inhibit the infectivity of all retroviruses, even those most distantly related to HIV-1,” said Jeremy Luban from the University of Massachusetts Medical School. “The anti-retroviral effect of SERINC therefore seems to extend across all retroviruses and may turn out to be universal.”