Serosurveillance for pandemic influenza A (H1N1) 2009 virus infection in domestic elephants, Thailand.

Weena Paungpin,Nareerat Sangkachai,Ekasit Tiyanun,Pilaipan Puthavathana,Witthawat Wiriyarat,Kridsada Chaichoun,Don Changsom,Parntep Ratanakorn,Kanaporn Poltep,Florian Krammer

doi:10.1371/journal.pone.0186962

Weena Paungpin, Nareerat Sangkachai + Show 8 more

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https://doi.org/10.1371/journal.pone.0186962

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Abstract

The present study conducted serosurveillance for the presence of antibody to pandemic influenza A (H1N1) 2009 virus (H1N1pdm virus) in archival serum samples collected between 2009 and 2013 from 317 domestic elephants living in 19 provinces situated in various parts of Thailand.To obtain the most accurate data, hemagglutination-inhibition (HI) assay was employed as the screening test; and sera with HI antibody titers ≥20 were further confirmed by other methods, including cytopathic effect/hemagglutination based-microneutralization (microNT) and Western blot (WB) assays using H1N1pdm matrix 1 (M1) or hemagglutinin (HA) recombinant protein as the test antigen. Conclusively, the appropriate assays using HI in conjunction with WB assays for HA antibody revealed an overall seropositive rate of 8.5% (27 of 317). The prevalence of antibody to H1N1pdm virus was 2% (4/172) in 2009, 32% (17/53) in 2010, 9% (2/22) in 2011, 12% (1/8) in 2012, and 5% (3/62) in 2013. Notably, these positive serum samples were collected from elephants living in 7 tourist provinces of Thailand. The highest seropositive rate was obtained from elephants in Phuket, a popular tourist beach city. Young elephants had higher seropositive rate than older elephants.The source of H1N1pdm viral infection in these elephants was not explored, but most likely came from close contact with the infected mahouts or from the infected tourists who engaged in activities such as elephant riding and feeding. Nevertheless, it could not be excluded that elephant-to-elephant transmission did occur.

Highlights

The outbreak of the 2009 pandemic influenza was initially reported in the Mexican town of La Gloria, Veracruz, in mid-February of 2009 [1]
The data suggested that the NT antibody detected might be the result of H1N1pdm virus infection, the cross-reactive antibody induced by the other influenza virus strains, or a false positive result due to the neutralizing activity of serum inhibitor(s)
Another obstacle is the lack of anti-species Ig-conjugate needed as the secondary detector in enzyme-linked immunosorbent assay (ELISA) or Western blot (WB) assay

Summary

Introduction

The outbreak of the 2009 pandemic influenza was initially reported in the Mexican town of La Gloria, Veracruz, in mid-February of 2009 [1]. The disease spread and led to the announcement of the pandemic phase by the World Health Organization on 11th June 2009 This pandemic influenza A (H1N1) 2009 virus (H1N1pdm virus) is shown to be a quadruple reassortant whose genome was derived from 4 origins: the hemagglutinin (HA), nucleoprotein (NP) and nonstructural (NS) genomic segments from classical swine virus; the neuraminidase (NA) and matrix (M) segments from Eurasian avian-like swine virus; the polymerase basic protein 2 (PB2) and polymerase acidic protein (PA) segments from North American avian virus; and the polymerase basic protein 1 (PB1) segment from human H3N2 virus [2]. Epidemiological study and molecular characterization suggested that the pandemic influenza viruses originated mostly from animals, in particular, pigs and birds [4]

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