WASHINGTON – At the International AIDS conference, reminders that HIV is not just a life-threatening infection, but also a social challenge, are constant.

The conference bag contains, in addition to the abstract book and various announcements, a pack of condoms. The gender choices on the registration form are male, female and transgender. Clothing runs to indigenous designs for those from the developing world, and boots not suits for the Western contingent. And in a sign of the important but not always convenient role activists have played in shaping the HIV agenda, rather than the more typical banning of cameras from the meeting rooms, the organizers have forbidden noisemakers and chains longer than 15 inches.

Nevertheless, Secretary of Health and Human Services Kathleen Sibelius told attendees of the opening plenary session, "science is the reason this conference got started, and it remains the driving force behind our efforts to combat the disease."

And at an overview session on the science of HIV, some of the field's most notable researchers shared their impression of recent scientific advances, and where the field will be heading over the next few years.

Gary Nabel, director of the Vaccine Research Institute at the National Institute of Allergies and Infectious Disease, said that he hopes that by 2020, "we will be in the midst of an efficacy trial for a vaccine candidate that could really work."

Nabel did not sugarcoat where vaccines are – namely, "at least 10 years away under the best of circumstances."

But the science underpinning those vaccines has made strides. After 15 years where the total number of broadly neutralizing antibodies known to the scientific community was four, "we now have hundreds" of such antibodies, as well as ways to identify more of them. (See BioWorld Today, Sept. 4, 2009.)

To date, though, no one has managed to identify an antigen that will reliably stimulate the human immune system to produce such an antibody. And even once such a vaccine is developed, because of the long latency of HIV infection, it will take more than a decade for it to make an appreciable difference in the number of people that actually need to be treated with antiretroviral drugs.

A cure for HIV, of course, would change that. And perhaps nothing has energized the HIV community like the report of the Berlin patient, Timothy Brown, who was apparently cured of his HIV infection through a bone marrow transplant. The bone marrow donor had no functional CCR5 receptor – a co-receptor that HIV needs to enter cells. And so the T cells produced from that bone marrow are immune to HIV infection.

Robert Siliciano, of Johns Hopkins University, described the sea change that this case has brought to the research community. "For a long time," he told the audience, "even the word cure was taboo." And it remains very hard to prove that Brown has truly been cured. But certainly, he has taken no antiretroviral drugs for five years now and has no detectable virus in his system.

Like a vaccine, a cure has a way to go until it becomes practical – if it ever does. Siliciano said that the problem with the approach that appears to have cured Timothy Brown is that it "essentially involves replacing a patient's entire immune system." And that, in turn, necessitates highly toxic therapies. Brown received both chemotherapy and irradiation, and some believe that the reason the transplant was successful at ridding him of HIV was that he had graft-vs.-host disease.

Those treatments were fine for Brown, who had leukemia and needed them anyway. But for a regular HIV patient, justifying highly toxic treatments is not a slam dunk, considering how well highly active antiretroviral therapy works.

Siliciano said that progress in knocking out the CCR5 co-receptor on T cells themselves via genetic means, such as Sangamo Biosciences Inc.'s zinc finger nuclease approach, has been "terrific."

But, he added, "you still have to get rid of all the other cells that are susceptible," because those cells otherwise harbor HIV reservoirs that can allow HIV to stage a comeback.

Eradicating those reservoirs without highly toxic interventions, Siliciano said, "is a problem that remains unsolved." But especially since Brown's proof of principle that HIV can be cured, it is in the crosshairs. Siliciano's prediction for 2020 is that the science will have advanced to the point of testing drugs that can dry up those reservoirs and reverse HIV latency.

In other conference news:

• Gilead Sciences Inc., of Foster City, Calif., reported two-year Phase III results showing that integrase inhibitor elvitegravir dosed once daily is noninferior to Isentress (raltegravir, Merck & Co. Inc.) dosed twice daily in treatment-experienced HIV patients. At 96 weeks of treatment, 48 percent of patients in the elvitegravir group achieved and maintained HIV RNA levels less than 50 copies/mL, compared to 45 percent in the raltegravir group. Rates of adverse events, discontinuations due to adverse events and development of resistance were similar for both drugs, though Grade 2 through Grade 4 diarrhea was more frequent among elvitegravir patients (13 percent) than raltegravir patients (8 percent) (p = 0.02). Gilead reported top-line data from the trial in December 2011, and elvitegravir is under review in both the U.S. and Europe. Gilead also presented full results from a Phase III trial of boosting agent cobicistat, showing that an HIV regimen containing cobistat-boosted protease inhibitor was noninferior to a regimen containing a Norvir (ritonavir, Abbott)-boosted protease inhibitor at 48 weeks of therapy. The study found that 85 percent of patients in the cobicistat arm compared to 87 percent in the ritonavir arm achieved HIV RNA levels less than 50 mg copies/mL. Cobicistat is under review in both the U.S. and Europe. Both elvitegravir and cobicistat also are included in the four-drug tablet Quad, which also includes emtricitabine and tenofovir disoproxil fumarate, which has a PDUFA date of Aug. 27.