Scientists at Johns Hopkins have found that 1 percent to 2 percent of those infected with HIV in Baltimore apparently suppress the virus to nearly undetectable levels on their own, confounding public health efforts to accurately monitor the pandemic's spread, now in its 20th year.
The city's health department estimated in 2004 that nearly 14,000 residents are infected.
These so-called elite suppressors of the virus are scientifically almost indistinguishable from new cases of the disease, researchers say, because they have low blood concentrations of antibodies to HIV. The scientists note that these low viral blood levels could result from use of antiretroviral therapy or because of genetic variations that give some people especially strong immune systems, which result in lower concentrations of antibody to HIV when the virus is suppressed. Those with weaker immune systems are also more likely to have already died, leaving behind a greater proportion of those with stronger immunity.
The Hopkins study tested blood in 1,549 patients who came to The Johns Hopkins Hospital emergency room between June and August 2001. All were screened for HIV using the current gold standard, serological testing algorithm for recent HIV seroconversion, or STARHS for short. STARHS is widely recommended by the U.S. Centers for Disease Control and Prevention, and the test relies on differentiating newly infected from chronically infected people based on the amount of HIV antibodies present. Normally, the antibody concentration to HIV increases over time during the first six months of infection.
Some 183 tested positive (12 percent), including 35 who did not know they were infected. Of those who tested positive, 11 were identified by STARHS as newly infected because they had low levels of antibodies to HIV. However, when researchers added a second test to measure the strength of antibody-antigen binding in the immune system's response to HIV infection, they found only six new infections. In the second test, called Affinity/Avidity, an immature response from a new infection produces weak binding, whereas a mature infection involves strong binding.