Abstract

The continual emergence of novel influenza A strains from non-human hosts requires constant vigilance and the need for ongoing research to identify strains that may pose a human public health risk. Since 1999, canine H3 influenza A viruses (CIVs) have caused many thousands or millions of respiratory infections in dogs in the United States. While no human infections with CIVs have been reported to date, these viruses could pose a zoonotic risk. In these studies, the National Institutes of Allergy and Infectious Diseases (NIAID) Centers of Excellence for Influenza Research and Surveillance (CEIRS) network collaboratively demonstrated that CIVs replicated in some primary human cells and transmitted effectively in mammalian models. While people born after 1970 had little or no pre-existing humoral immunity against CIVs, the viruses were sensitive to existing antivirals and we identified a panel of H3 cross-reactive human monoclonal antibodies (hmAbs) that could have prophylactic and/or therapeutic value. Our data predict these CIVs posed a low risk to humans. Importantly, we showed that the CEIRS network could work together to provide basic research information important for characterizing emerging influenza viruses, although there were valuable lessons learned.

Highlights

  • In the United States (US), the 2017–2018 influenza season was one of the most severe in recent memory resulting in a total of 171 laboratory-confirmed influenza-associated pediatric deathsCharacterizing canine H3 influenza viruses CEIRS network exercise and over 30,000 confirmed hospitalizations [1]

  • We found that H3 canine H3 influenza A viruses (CIVs) were closest to early H3N2 vaccine strains A/ Hong Kong/1/1968 H3N2 (HK68) and A/Port Chalmers/1/1973 H3N2 (PC73) (Fig 5A)

  • As predicted by Characterizing canine H3 influenza viruses CEIRS network exercise antigenic cartography, vaccination with a contemporary Hong Kong/ 4801/2014 (HK14) H3N2 vaccine had no impact on neutralizing Ab (NAb) titers against CIV-41915 at either site but did increase titers against the human Beth15 H3N2 virus (Fig 7B and 7C). These results demonstrate that vaccination with human seasonal H3N2 vaccines does not change the Ab response to the H3 CIV in patients infected with H3N2 viruses

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Summary

Introduction

In the United States (US), the 2017–2018 influenza season was one of the most severe in recent memory resulting in a total of 171 laboratory-confirmed influenza-associated pediatric deathsCharacterizing canine H3 influenza viruses CEIRS network exercise and over 30,000 confirmed hospitalizations [1]. Dogs infected with H3N2 CIV exhibited respiratory influenza-like symptoms, shed virus through nasal discharge, and the virus was readily transmitted between dogs via direct contact [5] causing several outbreaks throughout the United States [4,6]. This H3N2 CIV is avian in origin [2,4,5,6,7,8,9] but prior to 2015, a separate CIV strain derived from equine H3N8 influenza viruses, circulated in the United States [10]

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