Earlier this year doctors reported that they had cured, for the first time, a child born to an HIV-infected mother after a swiftly administered course of drugs. If the advance holds up to further scrutiny (some wonder if the child was perhaps never infected or is not actually cured), it may be at least partly because the immaturity of a newborn's immune system enables it to cope better with HIV, says Joseph M. McCune, a professor of experimental medicine at the University of California, San Francisco, who was not involved in the research.
Previous work shows that the inflammatory response mounted by an immune system under threat can make the HIV virus multiply more readily. The inflammation brings more immune cells to the site of injury or infection, increases cell division and boosts the production of proteins called cytokines that cells use to communicate. The HIV virus has evolved to take advantage of each of these processes—because the virus spreads from cell to cell, rapid division nearby helps HIV replicate quickly, McCune says.
Inside the womb, a fetus's immune system is set to “calm” because it “doesn't want to make an inflammatory response against the mother,” McCune explains. That “do not respond” signal may hold over to the first few days of the newborn's life, robbing the new HIV infection of additional fuel. The delay, combined with a short course of aggressive treatment, may give the body enough of a head start to eradicate the virus on its own.
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The case, reported in March at the Conference on Retroviruses and Opportunistic Infections in Atlanta, raises multiple questions, and the National Institute of Child Health and Human Development has put out a call for research proposals related to the new findings. “Now people are aware of this and can bring other children to our attention,” says Lynne Mofenson, chief of the institute's Maternal and Pediatric Infectious Disease Branch. “Within a year or two we hope to have better answers.”
