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.2024.05.019 | DOI Listing |
Respiratory syncytial virus (RSV) is a leading cause of respiratory infection, hospitalization and death in infants worldwide. No fully effective RSV therapy using direct antivirals is marketed. Since clinical efficacy data from naturally infected patients for such antivirals are not available yet, animal studies are indispensable to predict therapeutic intervention.
View Article and Find Full Text PDFMicrobiol Spectr
January 2025
NHC Key Laboratory of Systems Biology of Pathogens and Christophe Mérieux Laboratory, National Institute of Pathogen Biology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Respiratory syncytial virus (RSV) causes lower respiratory tract infections in infants and young children, leading to a pathogenesis-associated imbalance in CD4 T-cell subsets and monocyte subsets. To investigate whether RSV affects the imbalance of CD4 T-cells through monocytes, we examined the effects of the RSV-infected monocyte subset on CD4 T-cell subsets, namely, Th1, Th2, Th17, and regulatory T (Treg) subsets, on proliferation and identified key monocyte-derived cytokines. We found that RSV efficiently infects CD16 monocytes, but not CD16 monocytes, cocultures of CD4 T-cells with RSV-infected CD16 monocytes, inhibits Treg cell proliferation and increases Th2 cell frequency, suggesting that RSV causes an imbalance in the CD4 T-cell subset by primarily infecting CD16 monocytes.
View Article and Find Full Text PDFJ Med Virol
November 2024
Research Center in Infectious Diseases, CHU de Québec and Laval University, Québec City, Québec, Canada.
We looked at the interactions between viral loads, coinfection rates and disease severity for children infected with two pneumoviruses: human metapneumovirus (HMPV) and respiratory syncytial virus (RSV). The HMPV RNA load in nasopharyngeal swabs of hospitalized children was significantly higher in mono-infections compared to coinfections but this was not the case for RSV, which could be explained by different innate immune responses. Also, the viral load of neither of the two viruses was associated with disease severity although RSV-infected children had higher severity scores than HMPV-infected children.
View Article and Find Full Text PDFBMC Infect Dis
November 2024
Coordinating Centre for Epidemiology, University of Debrecen Clinical Centre, Debrecen, Hungary.
Background: Severe acute respiratory infection (SARI) is a major cause for hospital admission and associated with high mortality among children worldwide. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), influenza viruses and respiratory syncytial virus (RSV) are the most frequently identified pathogens in children with SARI. The duration of care can be affected by the type of infection and patient characteristics.
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