New technology shows promise for cure of HIV

Friday researchers from the University of Arizona and Louisiana State University met to discuss the hurdles they've recently over come in the race to defeat HIV.

The scientists have been formulating therapies and antiviral drugs for HIV patients and are progressing through the intricate work with protease inhibitors, to block the spread of the disease.

Ron Luftig, a professor at LSU's medical school, presented a slide show Friday at the Arizona Health Sciences Center on his staff's recent success on treating HIV with the inhibitors.

"Protease inhibitors are very important in killing HIV infected cells," Luftig said. "We need to try to develop more types of protease inhibitors that differ in how they block enzymes."

HIV is propagated when enzymes break down the information in infected cells causing a higher rate of transmission to uninfected cells.

Protease inhibitors developed for different enzymes would create a cocktail of multiple drugs, so there would be a less likely chance of resistance building up, Luftig said.

Protease inhibitors have enjoyed a 50 percent success rate in the study, but are very expensive, Luftig said.

Nafees Ahmad, an assistant professor and virologist at the University of Arizona, shares a common thread with Luftig through research on the mechanism that transmits HIV from mother to infant.

"If we can understand the molecular basis of how the virus is spread from mother to infant, then we can develop molecular strategies to develop therapy," Ahmad said.

Ahmad's 12-year research project is the only HIV investigation being conducted in Arizona.

Through his research Ahmad found that small amounts of one strain of HIV are passed to an in utero infant.

"If we can block that one subtype, then we can stop transmission through drugs, preventative vaccines or any other prenatal antibodies," he said.

Ahmad and his associates have gained national notoriety for the identification of HIV subtypes genetically relayed to infants.

AZT therapy can reduce up to 50 percent of HIV cells present in the mother, but the resistant virus can still be passed on to the child, Ahmad said. The AZT therapy interferes with an infected cell's ability to replicate.

Although AZT halts replication of HIV cells, the enzyme responsible for DNA replication eventually mutates and builds up a resistance to the effects of AZT, Ahmad said.

In his presentation, Luftig contended that clone cells from HIV populations have an abundance of a molecule called GP 120 and kill unaffected healthy cells much more efficiently.

"Protease inhibitors block protease cleavage (the break down of large molecules) by binding to active sites on enzymes that break unaffected healthy cells down," Luftig said.

Luftig believes the answer to the HIV problem will involve the integration of many different solutions.

"The best way eventually is to treat AIDS in different pathways. Antiviruses, drugs that block the HIV virus and vaccines, autoimmune responses, are two possible methods," Luftig said.

DNA vaccines could work, Luftig said, but scientists are still far away from understanding the complete biology and immunology needed to implement vaccines.

"We don't understand the details in individual's as to why the nuances of the HIV virus remain dormant for eight to 10 years before exploding," Luftig said.