More than a decade ago, Tom Richardson watched as many of his friends suffered from memory problems, fatigue and dementia before they died because of complications from AIDS.
But a new UCLA discovery may prevent more of the Oregon AIDS Hotline coordinator’s friends from dying because of the HIV virus.
Last Monday, UCLA researchers found that a protein called DC-SIGN can prevent the spread of HIV, said Shen Pang, an associate professor of oral biology and medicine at UCLA.
DC-SIGN can be found on human body cells called dendritic cells, which are part of the immune system.
When HIV infects a dendritic cell, the virus uses a protein, gp120, to attach itself and release part of its own DNA into the host cell. In a normal HIV infection, the host cell replicates and creates multiple copies of the virus’ genes from the cell’s DNA. Then, the new copies of the HIV genes are repackaged into a virus along with the gp120 protein and released.
Now, UCLA researchers have found that the presence of DC-SIGN can make it impossible for the gp120 protein to attach to the host cell in the first place.
By doing so, it effectively prevents the virus from being replicated or released. Instead, as the host cell dies, so too does the HIV virus inside of it.
Since the interaction with DC-SIGN makes the gp120 protein ineffective, DC-SIGN also prevents other host cells in the body from being infected by the virus.
A dozen breakthroughs related to combatting HIV occur every year in the United States, but this discovery from UCLA researchers may indeed have great potential, Richardson said.
Qiuwei Wang, a postgraduate researcher who coauthored the study, was responsible for the research and a notable amount of closing of the sample cells.
“(Wang) worked very, very hard. We can say more than 100 percent effort,” Pang said.
The research was made possible because of funding from the National Institute of Health.
The experiments leading up to the discovery were all in vitro, or outside of a living organism. If the outcomes of those experiments are successful, the protein might be part of a clinical trial within two years. DC-SIGN might then be available through injections or even taken orally by HIV-infected patients, Pang said.
Currently, many of the medications used to control and treat HIV/AIDS have been effective in extending and improving patients’ quality of life.
But they have significant side effects, such as preventing the body from producing red blood cells, Richardson said.
Pang said a treatment using the DC-SIGN protein could be especially significant for HIV patients who are not responding to current treatment options.
Researchers said they hope their discovery will one day become a widely available treatment for AIDS.
Still, Pang said he is cautious about what the new discovery will mean.
“We need more people to think this is a new option, a new hope. … This should be a prevention and a cure. (But) I don’t expect to completely free the patient from HIV,” Pang said.