AI Article Synopsis

  • - Respiratory syncytial virus (RSV) is a leading cause of lower respiratory infections and hospitalizations in infants, but the immune response in this age group is not fully understood.
  • - Research revealed that antibody responses to RSV proteins differ significantly as children age, with maternal antibodies present in the first 3 months followed by a vulnerable period, and development of immunity after 6 months.
  • - Hospitalized infants showed lower levels of specific antibodies and, as their illness improved, they developed broader and more effective immune responses to RSV, indicating key aspects of protective immunity are not solely dependent on age.

Article Abstract

Respiratory syncytial virus (RSV) is among the most common causes of lower respiratory tract infection (LRTI) and hospitalization in infants. However, the mechanisms of immune control in infants remain incompletely understood. Antibody profiling against attachment (G) and fusion (F) proteins in children less than 2 years of age, with mild (outpatients) or severe (inpatients) RSV disease, indicated substantial age-dependent differences in RSV-specific immunity. Maternal antibodies were detectable for the first 3 months of life, followed by a long window of immune vulnerability between 3 and 6 months and a rapid evolution of FcγR-recruiting immunity after 6 months of age. Acutely ill hospitalized children exhibited lower G-specific antibodies compared with healthy controls. With disease resolution, RSV-infected infants generated broad functional RSV strain-specific G-responses and evolved cross-reactive F-responses, with minimal maternal imprinting. These data suggest an age-independent RSV G-specific functional humoral correlate of protection, and the evolution of RSV F-specific functional immunity with disease resolution.

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http://dx.doi.org/10.1016/j.immuni.2024.05.019DOI Listing

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Article Synopsis
  • Infants have an immature immune system and narrower airways, making them more vulnerable to severe respiratory syncytial virus (RSV) infections.
  • A study by Zhao et al. found that airway cells from children are more susceptible to damage from RSV than those from adults, due to poor STAT3 activation.
  • Enhancing STAT3 activation and using apoptosis inhibitors in neonatal mice showed promise in reducing virus spread, indicating potential therapeutic strategies for treating RSV in infants.
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