Abstract

BackgroundWe performed a longitudinal study of viral etiology in samples collected in New York City during May 2009 to May 2010 from outpatients with fever or respiratory disease symptoms in the context of a pilot respiratory virus surveillance system.MethodsSamples were assessed for the presence of 13 viruses, including influenza A virus, by MassTag PCR.ResultsAt least one virus was detected in 52% of 940 samples analyzed, with 3% showing co-infections. The most frequently detected agents were rhinoviruses and influenza A, all representing the 2009 pandemic H1N1 strain. The incidence of influenza H1N1-positive samples was highest in late spring 2009, followed by a decline in summer and early fall, when rhinovirus infections became predominant before H1N1 reemerged in winter. Our study also identified a focal outbreak of enterovirus 68 in the early fall of 2009.ConclusionMassTag multiplex PCR affords opportunities to track the epidemiology of infectious diseases and may guide clinicians and public health practitioners in influenza-like illness and outbreak management. Nonetheless, a substantial proportion of influenza-like illness remains unexplained underscoring the need for additional platforms.

Highlights

  • We performed a longitudinal study of viral etiology in samples collected in New York City during May 2009 to May 2010 from outpatients with fever or respiratory disease symptoms in the context of a pilot respiratory virus surveillance system

  • Samples were tested by MassTag PCR [10] for the presence of 13 viruses including influenza A (FLUAV), influenza B (FLUBV), human rhinoviruses (HRV), human enteroviruses (HEV), human metapneumovirus (HMPV), human parainfluenza virus (HPIV) 1-4, human coronaviruses (HCoV) 229E and OC43, and respiratory syncytial virus (RSV) A and B

  • Influenza A virus was detected in the majority of samples collected from May through June 2009, and again during November 2009 to January 2010, whereas rhinoviruses predominated during August through October 2009 and February to May 2010, when influenza A virus activity was low (Figure 2)

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Summary

Introduction

We performed a longitudinal study of viral etiology in samples collected in New York City during May 2009 to May 2010 from outpatients with fever or respiratory disease symptoms in the context of a pilot respiratory virus surveillance system. The first cases were reported in March and April 2009, initially from the Veracruz region of Mexico, immediately followed by reports from California and Texas in the United States (US) [6,7]. By late April 2009 over half of the total confirmed US cases were from New York City (NYC) [8]. In response to the outbreak, the NYC Department of Health and Mental Hygiene (DOHMH) implemented an enhanced citywide influenza surveillance program focusing on cases of severe influenza and influenza-like illness (ILI)

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