Scientists at the Yerkes National Primate Research Center, Emory University, have newly published results that support a straightforward explanation for the backfire effect. According to the study, the vaccination may increase the number of immune cells that serve as viral targets.
In a nonhuman primate model of HIV transmission, higher levels of viral target cells in gateway mucosal tissues were associated with an increased risk of infection.
"One of the reasons why it has been so difficult to make an AIDS vaccine is that the virus infects the very cells of the immune system that any vaccine is supposed to induce," says senior author Guido Silvestri, chief of microbiology and immunology at Yerkes National Primate Research Center.
A large part of the vaccine effort has been focused on developing vaccines that stimulate antiviral T cells.
T cells come in two main categories, defined by the molecules found on their surfaces.
CD8 is a marker for "killer" cells, while CD4 is a marker for "helper" cells. CD4+ T cells are known to be primary targets for HIV and SIV infection, while several studies have proposed that CD8+ T cells could be valuable in controlling infection.
"This study shows that if a vaccine induces high levels of activated CD4+ T cells in mucosal tissues, any potential protective effect of the vaccine may be hampered," he explains.
The study emphasizes the unique challenges that HIV poses in terms of vaccine development, and the importance of pursuing vaccine concepts and products that elicit strong antiviral immune responses without increasing the number of CD4+ T cells in the
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