We often cite the fact that tuberculosis (TB) fueled the spread of HIV in southern Africa, said Diane Havlir, MD, of the University of California at San Francisco and co-Chair of the 2012 International AIDS Conference (IAC). But AIDS also shaped the enormous spread of TB seen in southern Africa during the late 80s and ’90s as a sweeping increase in HIV/AIDS occurred simultaneously, she said.
We were asleep at the wheel early on in the co-epidemic, Havlir told an audience of scientists, program managers and TB/HIV advocates at a co-infection IAC pre-conference. She attributed the slow early response to the epidemics to factors that included enormous scientific gaps like difficulty diagnosing TB in HIV-infected persons and the still novel administration of antiretroviral therapy (ART), as well as the politics of funding silos for HIV and TB, limited access to TB drugs, and overburdened TB and HIV care infrastructures.
But in the early 2000s things started to change, she said. When Mark Dybul was head of the Office of the U.S. Global AIDS Coordinator he allocated specific funding to respond HIV-TB co-infection in sub-Saharan Africa. “I cannot tell you how important that was to the response,” Havlir said. Policy, funding investment, advocacy, research support and visibility were key drivers of progress in this time period.
HIV testing rates of TB patients in the Afro region increased from 38 percent in 2007 to 71 percent in 2011, Havlir said. According to data from the World Health Organization, thanks to putting into place increases in testing and treatment and other interventions, an estimated 1 million lives were saved between 2005 and 2010.
Still, she said, more needs to be done.
“It is absolutely unacceptable that this number of individuals – hundreds of thousands of people – are still dying of HIV-TB when we know and understand and have the tools in hand to prevent these deaths from occurring.“
Havlir hinted at new study data that will be released at a late-breaker IAC session this week showing that isoniazid preventive therapy (IPT) for TB can add to the protective benefit HIV-infected persons experience when on ART. She also mentioned data from a study in Malawi that demonstrated a decrease in new TB rates as ART access was ramped up. The protective effect was not just limited to people with low CD4 cell counts, she said, but was experienced across a range of CD4 counts. “We still see broad protection against TB with ART,” she said, and mentioned the “unappreciated” finding from the HIV Prevention Trial Network (HPTN) 052 study results that came out in May of 2011 that demonstrated a 40 percent reduction in probability of death or AIDS in TB patients on ART.
Moving forward, Havlir said we must conduct drug interaction studies earlier with new TB drugs and ART, and include HIV patients in new TB drug clinical trials – citing the failure of recent breakthrough studies of Hepatitis C drugs that excluded HIV-infected patients and now need to be studied in that population, delaying their access to these novel Hepatitis C drugs.