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Archives of virology1989; 106(1-2); 159-164; doi: 10.1007/BF01311048

Origin of the hemagglutinin on A/Equine/Johannesburg/86 (H3N8): the first known equine influenza outbreak in South Africa.

Abstract: A severe influenza outbreak occurred in horses in South Africa in 1986. The causative agent was identified as an influenza virus [A/Equine/Johannesburg/86 (H3N8)]. Antigenic analyses of the hemagglutinin (HA) with ferret antisera and monoclonal antibodies showed that the Eq/Johannesburg/86 virus is similar to recent equine H3 viruses. The nucleotide sequence analysis on the HA genes of Eq/Johannesburg/86 and other equine H3 influenza viruses, together with the epidemiological data, clearly demonstrated that the Eq/Johannesburg/86 virus was derived from a virus that had been circulating in horses in the United States in 1986-87. The epidemiological information suggests that the unusually severe influenza outbreak in South Africa may be due to the lack of immunity to these viruses in the horse population.
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Publication Date: 1989-01-01 PubMed ID: 2548457DOI: 10.1007/BF01311048Google Scholar: Lookup
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  • Comparative Study
  • Journal Article
  • Research Support
  • Non-U.S. Gov't
  • Research Support
  • U.S. Gov't
  • P.H.S.

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This research explores the origins of an influenza outbreak in horses in South Africa in 1986. It was found that the outbreak was caused by a virus—specifically A/Equine/Johannesburg/86 (H3N8)—that had previously been circulating in equine populations in the United States.

Analysis and Identification of the Virus

  • The outbreak of influenza in horses in South Africa was severe and the causing agent of the epidemic was identified as the influenza virus A/Equine/Johannesburg/86 (H3N8).
  • Through antigenic analysis of the hemagglutinin (HA) using ferret antisera and monoclonal antibodies, it was found that the Eq/Johannesburg/86 virus is similar to other recent equine H3 viruses.
  • The researchers employed nucleotide sequence analysis on the HA genes of Eq/Johannesburg/86 and other equine H3 influenza viruses. This analysis further supported their earlier antigenic observations and confirmed the similarity of the Eq/Johannesburg/86 virus to other equine H3 viruses.

Origins and Epidemiology of the Virus

  • Further studies, combining the results from the nucleotide sequence analysis with epidemiological data, demonstrated that the Eq/Johannesburg/86 virus likely originated from a virus circulating in horse populations in the United States in 1986-87.
  • The virus, therefore, was not unique to the South African outbreak but instead part of a wider circulation of similar viruses in global equine populations.

Severity of the Outbreak and Lack of Immunity

  • The epidemiological information gathered during the research suggested a possible explanation for the unusually severe outbreak in South Africa: a lack of immunity to these viruses in the South African horse population.
  • This implies that the South African horses had not been previously exposed or had not built sufficient immunity to this strain of influenza virus. As a result, when the virus was introduced, it caused a severe epidemic.

Conclusion

  • The study concludes that the severity of the outbreak in South Africa in 1986 was due to a lack of immunity in the horse population and identifies the virus that caused the outbreak as a strain of influenza that was also circulating in the United States around the same time.

Cite This Article

APA
Kawaoka Y, Webster RG. (1989). Origin of the hemagglutinin on A/Equine/Johannesburg/86 (H3N8): the first known equine influenza outbreak in South Africa. Arch Virol, 106(1-2), 159-164. https://doi.org/10.1007/BF01311048

Publication

Archives of virology
ISSN: 0304-8608
NlmUniqueID: 7506870
Country: Austria
Language: English
Volume: 106
Issue: 1-2
Pages: 159-164

Researcher Affiliations

Kawaoka, Y
  • Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, Tennessee.
Webster, R G

    MeSH Terms

    • Amino Acids / analysis
    • Animals
    • Disease Outbreaks / veterinary
    • Hemagglutination Inhibition Tests / veterinary
    • Hemagglutinins, Viral / genetics
    • Hemagglutinins, Viral / immunology
    • Horse Diseases / immunology
    • Horse Diseases / microbiology
    • Horses
    • Influenza A Virus, H3N8 Subtype
    • Influenza A virus / immunology
    • Orthomyxoviridae Infections / epidemiology
    • Orthomyxoviridae Infections / immunology
    • Orthomyxoviridae Infections / veterinary
    • South Africa

    Grant Funding

    • AI52586 / NIAID NIH HHS
    • CA 21765 / NCI NIH HHS

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    Citations

    This article has been cited 8 times.
    1. Oladunni FS, Oseni SO, Martinez-Sobrido L, Chambers TM. Equine Influenza Virus and Vaccines. Viruses 2021 Aug 20;13(8).
      doi: 10.3390/v13081657pubmed: 34452521google scholar: lookup
    2. Jang Y, Seo T, Seo SH. Higher virulence of swine H1N2 influenza viruses containing avian-origin HA and 2009 pandemic PA and NP in pigs and mice. Arch Virol 2020 May;165(5):1141-1150.
      doi: 10.1007/s00705-020-04572-zpubmed: 32222822google scholar: lookup
    3. Murcia PR, Wood JL, Holmes EC. Genome-scale evolution and phylodynamics of equine H3N8 influenza A virus. J Virol 2011 Jun;85(11):5312-22.
      doi: 10.1128/JVI.02619-10pubmed: 21430049google scholar: lookup
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      doi: 10.1017/s0950268800001552pubmed: 8870635google scholar: lookup
    5. Binns MM, Daly JM, Chirnside ED, Mumford JA, Wood JM, Richards CM, Daniels RS. Genetic and antigenic analysis of an equine influenza H 3 isolate from the 1989 epidemic. Arch Virol 1993;130(1-2):33-43.
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    7. Webster RG, Bean WJ, Gorman OT, Chambers TM, Kawaoka Y. Evolution and ecology of influenza A viruses. Microbiol Rev 1992 Mar;56(1):152-79.
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    8. Endo A, Pecoraro R, Sugita S, Nerome K. Evolutionary pattern of the H 3 haemagglutinin of equine influenza viruses: multiple evolutionary lineages and frozen replication. Arch Virol 1992;123(1-2):73-87.
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