An untreated HIV infection will kill 60% of children within two and a half years, but the equivalent infection in monkeys is not fatal.
The findings could lead to new immune-based therapies for HIV infection.
The virus eventually wipes out the immune system, leaving the body vulnerable to other infections, what is known as acquired human immunodeficiency syndrome (Aids).
The researchers analysed the blood of 170 children from South Africa who had HIV, had never had antiretroviral therapy and yet had not developed Aids.
Tests showed they had tens of thousands of human immunodeficiency viruses in every millilitre of their blood.
Their immune system is ignoring the virus as far as possible
“Waging war against the virus is in most cases the wrong thing to do.”
Counter-intuitively, not attacking the virus seems to save the immune system.
HIV kills white blood cells – the warriors of the immune system.
And when the body’s defences go into overdrive, even more of them can be killed.
Immune systems that avoid the HIV trap survives.
HIV progression at a standstill
Although most people that get infected with HIV develop AIDS, rare individuals maintain immune function in the presence of virus, a phenomenon also seen in natural hosts of the closely related SIV. Muenchhoff et al. describe a cohort of pediatric HIV patients who have normal CD4 T cell counts, despite high viremia and lack of antiviral treatment. These children have low immune activation, including less chemokine receptor CCR5 expression on central memory CD4 T cells, similar to sooty mangabeys infected with SIV. The immune mechanisms described in these patients shed light on HIV pathogenesis, which may help develop future treatments.
Disease-free infection in HIV-infected adults is associated with human leukocyte antigen–mediated suppression of viremia, whereas in the sooty mangabey and other healthy natural hosts of simian immunodeficiency virus (SIV), viral replication continues unabated. To better understand factors preventing HIV disease, we investigated pediatric infection, where AIDS typically develops more rapidly than in adults. Among 170 nonprogressing antiretroviral therapy–naïve children aged >5 years maintaining normal-for-age CD4 T cell counts, immune activation levels were low despite high viremia (median, 26,000 copies/ml). Potent, broadly neutralizing antibody responses in most of the subjects and strong virus-specific T cell activity were present but did not drive pediatric nonprogression. However, reduced CCR5 expression and low HIV infection in long-lived central memory CD4 T cells were observed in pediatric nonprogressors. These children therefore express two cardinal immunological features of nonpathogenic SIV infection in sooty mangabeys—low immune activation despite high viremia and low CCR5 expression on long-lived central memory CD4 T cells—suggesting closer similarities with nonpathogenetic mechanisms evolved over thousands of years in natural SIV hosts than those operating in HIV-infected adults.