Abstract

The surveillance of swine influenza A viruses in France revealed the emergence of an antigenic variant following deletions and mutations that are fixed in the HA-encoding gene of the European human-like reassortant swine H1N2 lineage. In this study, we compared the outcomes of the parental (H1huN2) and variant (H1huN2Δ14–147) virus infections in experimentally-inoculated piglets. Moreover, we assessed and compared the protection that was conferred by an inactivated vaccine currently licensed in Europe. Three groups of five unvaccinated or vaccinated piglets were inoculated with H1huN2 or H1huN2Δ14–147 or mock-inoculated, respectively. In unvaccinated piglets, the variant strain induced greater clinical signs than the parental virus, in relation to a higher inflammatory response that involves TNF-α production and a huge afflux of granulocytes into the lung. However, both infections led to similar levels of virus excretion and adaptive (humoral and cellular) immune responses in blood. The vaccinated animals were clinically protected from both infectious challenges and did not exhibit any inflammatory responses, regardless the inoculated virus. However, whereas vaccination prevented virus shedding in H1huN2-infected animals, it did not completely inhibit the multiplication of the variant strain, since live virus particles were detected in nasal secretions that were taken from H1huN2Δ14–147-inoculated vaccinated piglets. This difference in the level of vaccine protection was probably related to the poorer ability of the post-vaccine antibodies to neutralize the variant virus than the parental virus, even though post-vaccine cellular immunity appeared to be equally effective against both viruses. These results suggest that vaccine antigens would potentially need to be updated if this variant becomes established in Europe.

Highlights

  • Swine influenza is an acute respiratory infection of pigs that is characterized by fever, loss of appetite, lethargy, dyspnea, nasal discharge, and coughing

  • All of the animals showed hyperthermia at D1 (41.1 ± 0.5 ◦ C and 40.5 ± 0.5 ◦ C on average for H1N2var and H1N2 groups, respectively) and a decrease in food consumption which resulted in reduced rate of weight gain during the post-inoculation week as compared to control animals (p = 0.01)

  • The first objective of this work was to study the clinical, virological, and immunological responses of pigs infected with the variant 212/13 virus strain (H1N2var group), as compared to those that were observed in pigs infected with the parental 415/11 virus strain (H1N2 group)

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Summary

Introduction

Swine influenza is an acute respiratory infection of pigs that is characterized by fever, loss of appetite, lethargy, dyspnea, nasal discharge, and coughing. Swine influenza A viruses (swIAV), the etiological agents of the disease, are widespread around the world. Four distinct genetic lineages are enzootic in pig herds in Europe: the “avian-like swine. H1N2” (H1hu N2), and the “human-like reassortant swine H3N2” (H3N2) [1]. Given the impact of swIAV in terms of animal health and public health due to zoonotic potential, monitoring the circulation and evolution of virus strains has been encouraged in many countries after the last influenza pandemic in 2009. In France, swIAV surveillance highlighted the emergence in 2012 of a new antigenic variant of H1N2 subtype, which results from a genetic drift in the H1hu N2 virus circulating since the ‘90s (“Scotland/94” lineage; HA clade 1B.1.2.3) [2,3]. The proportion of new variant H1hu N2∆146–147 strains that were detected over the country among the H1hu N2 viruses increased until reaching 50% in

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