IAVI-Report-13(1)
In past years, the opening session of the Conference on Retroviruses and Opportunistic Infections (CROI) has coincided with what would be considered by many to be much bigger events—the Super Bowl or the annual Academy Awards Ceremony. But oftentimes, the conference itself has had a “big event” feel, generating its fair share of publicity. At the 3rd annual CROI in 1996, data showed that the first protease inhibitor, when used along with two other antiretrovirals (ARVs), could substantially boost antiviral activity and control HIV’s furious replication. This, of course, opened the door to effective combination therapy for the treatment of HIV/AIDS. Over the following years, other waves of excitement would sweep over this annual scientific conference as new strides were made in the treatment of HIV infection.
What was remarkable at this year’s 16th annual CROI was not a new advancement in the ability to treat this disease, but rather how undeniably well different combinations of the now more than 20 ARVs work in controlling HIV replication. Granted, after 28 years of battling HIV, there is still a long way to go. Throughout developing countries, access to life-saving ARV therapy still reaches only a fraction of individuals in need, and despite decades of research, condoms and circumcision remain the only effective means of protection against sexual transmission of HIV, the most common route of infection. But as Robert Siliciano of Johns Hopkins University School of Medicine remarked in his delivery of the 14th Bernard Fields Memorial Lecture, “It is now possible to completely stop HIV replication,” with ARV therapy. “It is actually highly active antiretroviral therapy,” he said.
This has led researchers to pursue with a renewed vigor the possibility of eradication—curing an infected individual of HIV infection. By all accounts, this will be no easy task. Latent reservoirs of HIV-infected CD4+ T cells persist in unknown hiding spots in the body (think of them as the virus’s network of terrorist sleeper cells). And now, researchers think there is at least one additional mysterious reservoir of infected cells that is contributing to a continued ongoing low-level viremia seen even in HIV-infected individuals that are on effective ARV therapy.
Given the complexity and challenges relating to eradication, it is no surprise that some of the greatest excitement at this year’s CROI was related to HIV prevention strategies. Results from a Phase IIb trial of the microbicide candidate PRO 2000 offered the first positive microbicide trial results so far, and more promising data from nonhuman primate studies continued fueling optimism that the success of ARVs may extend to their use in pre-exposure prophylaxis. Meanwhile vaccine researchers are mining elite controllers for clues about what a partially effective AIDS vaccine might look like, and some researchers now think that T-cell responses similar to those seen in elite controllers will likely be induced by vaccine candidates in the near future. Wouldn’t all that be better than the Super Bowl?
—Kristen Jill Kresge, Managing Editor