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Respiratory syncytial virus infection may be associated with higher risk for bacterial pneumonia

Two common and sometimes dangerous respiratory diseases, a viral one caused by (RSV), and a bacterial one caused by may be linked, suggests a study published in . Daniel Weinberger, from , and colleagues, analyzed US hospitalization data to investigate a possible association between RSV activity and pneumonia in children under two, and found that infection with RSV may increase the risk of pneumonia caused by S. pneumoniae, especially in infants.

For their analysis, the researchers used data collected between 1992 and 2009 on more than 700,000 hospitalizations for RSV and more than 16,000 hospitalizations for (caused by Streptococcus pneumoniae) among young children. They show that periods with high numbers of RSV hospitalizations were also associated with significant increases in . Among children under one year old, 20.3% of cases were associated with high RSV activity. Following the introduction of routine vaccination against S. pneumoniae in 2000, there was a significant decline in hospitalizations for RSV among children under one year old.

Associations cannot prove that one infection causes increased susceptibility to the other, and because the researches only had overall numbers for hospitalizations linked to either pathogen, they also could not check whether children had actually been infected with both RSV and S. pneumoniae. Nonetheless, the results point to possible interaction between the two diseases, and suggest that RSV infection may increase the risk for pneumococcal pneumonia, particularly in young infants.


Weinberger DM, Klugman KP, Steiner CA, Simonsen L, Viboud C (2015) Association between Respiratory Syncytial Virus Activity and Pneumococcal Disease in Infants: A Time Series Analysis of US Hospitalization Data. PLoS Med, doi:10.1371/journal.pmed.1001776, published 6 January 2015.

DMW and CV were supported by the Division of International Epidemiology and Population Studies, Fogarty International Center, US National Institutes of Health. DMW is supported by the Claude D. Pepper Older Americans Independence Center at Yale University School of Medicine (#P30AG021342NIH/NIA), the Yale Center for Clinical Investigation (UL1 TR000142), and the Bill & Melinda Gates Foundation. LS acknowledges support from the RAPIDD (Research and Policy for Infectious Disease Dynamics) program of the Science and Technology Directorate, Department of Homeland Security, and the Fogarty International Center. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

DMW has received research support for other projects from an investigator initiated research grant from Pfizer to Yale University. LS and KPK have previously received research support from Pfizer. DMW has received consulting fees from Merck. KPK is a member of the Editorial Board of PLOS Medicine. The other authors have declared that no competing interests exist.