The work provides a promising route for designing a vaccine effective against a broad range of RSV strains, which cause serious respiratory disease in infants and older adults.
Respiratory syncytial virus (RSV) causes 118,000 deaths in young children each year worldwide and 57,000 hospitalizations of children each year in the United States alone. Attempts to develop a vaccine—at first based on inoculations with inactivated virus, and then targeting a key viral surface protein (RSV F)—have failed. Recent studies, however, suggest that a second viral surface protein (RSV G) is a promising target.
In one earlier study, elevated concentrations of antibodies targeting both RSV F and RSV G were associated with lower clinical disease severity scores, despite a substantially lower absolute abundance of anti-G antibodies. Another study found that higher levels of maternal anti-G antibodies correlated with less severe disease in infants (up to 4-6 months of age), even though anti-G antibodies were again found in lower concentrations.
While the RSV F surface protein allows the virus to enter a host cell, RSV G is what allows the virus to stick to lung cells and distort immune responses. This disruption of the immune response by RSV G might explain why vaccines based on RSV F have failed. Thus, a protective antibody response that blocks RSV G activity could be more effective, but scientists didn’t know how antibodies target RSV G at the molecular level.
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Image: Stanislav Fedechkin and Rebecca DuBois.
Credit: C. Lagattuta/UC Santa Cruz