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Journal of virology1986; 57(1); 71-80; doi: 10.1128/JVI.57.1.71-80.1986

Rapid emergence of novel antigenic and genetic variants of equine infectious anemia virus during persistent infection.

Abstract: Previous results from our laboratory have demonstrated that equine infectious anemia virus displays structural variations in its surface glycoproteins and RNA genome during passage and chronic infections in experimentally infected Shetland ponies (Montelaro et al., J. Biol. Chem. 259:10539-10544, 1984; Payne et al., J. Gen. Virol. 65:1395-1399, 1984). The present study was undertaken to obtain an antigenic and biochemical characterization of equine infectious anemia virus isolates recovered from an experimentally infected pony during sequential disease episodes, each separated by intervals of only 4 to 8 weeks. The virus isolates could be distinguished antigenically by neutralization assays with serum from the infected pony and by Western blot analysis with a monoclonal antibody against the major surface glycoprotein gp90, thus demonstrating that novel antigenic variants of equine infectious anemia virus predominate during each clinical episode. The respective virion glycoproteins displayed different electrophoretic mobilities on sodium dodecyl sulfate-polyacrylamide gels, indicating structural variation. Tryptic peptide and glycopeptide maps of the viral proteins of each virus isolate revealed biochemical alterations involving amino acid sequence and glycosylation patterns in the virion surface glycoproteins gp90 and gp45. In contrast, no structural variation was observed in the internal viral proteins pp15, p26, and p9 from any of the four virus isolates. Oligonucleotide mapping experiments revealed similar but unique RNase T1-resistant oligonucleotide fingerprints of the RNA genomes of each of the virus isolates. Localization of altered oligonucleotides for one virus isolate placed two of three unique oligonucleotides within the predicted env gene region of the genome, perhaps correlating with the structural variation observed in the envelope glycoproteins. Thus these results support the concept that equine infectious anemia virus is indeed capable of relatively rapid genomic variations during replication, some of which result in altered glycoprotein structures and antigenic variants which are responsible for the unique periodic disease nature observed in persistently infected animals. The findings of envelope specific differences in isolates of visna virus and of human T-cell lymphotropic virus III (acquired immune deficiency syndrome-related virus) suggest that this variation may be a common characteristic of the subfamily Lentivirinae.
Publication Date: 1986-01-01 PubMed ID: 3001367PubMed Central: PMC252700DOI: 10.1128/JVI.57.1.71-80.1986Google Scholar: Lookup
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  • Journal Article
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  • Non-U.S. Gov't
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  • 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.

The research demonstrates that equine infectious anemia virus (EIAV), which is a virus causing infection in horses, presents novel genetic and antigenic variations during the persistence of the infection, resulting in different symptoms in different infectious phases.

Study Background

  • This study builds on previous findings of the same laboratory which had shown structural variations in the EIAV’s surface proteins and RNA genome during its passage in the host and during chronic infections.
  • The focus of this particular research was to explore antigenic and biochemical characterization of EIAV recovered from infected ponies experiencing different disease episodes.

Methodology and Findings

  • For their experiment, the researchers used disease infections in ponies that were separated by intervals of 4 to 8 weeks.
  • Applying neutralization assays and Western blot analyses, they discovered that the virus isolates could be antigenically differentiated, suggesting that new antigenic variants of EIAV were predominant in each clinical episode.
  • The researchers observed a structural variation in the virus isolates, citing different electrophoretic mobilities of the viruses’ surface proteins on the sodium dodecyl sulfate-polyacrylamide gels.
  • Through tryptic peptide and glycopeptide maps of the virus isolates’ proteins, the researchers detected biochemical changes involving alteration in the amino acid sequence and the glycosylation patterns of the virion surface proteins.
  • However, no structural variation was identified in the internal viral proteins of the virus isolates.
  • Oligonucleotide mapping experiments revealed unique oligonucleotide fingerprints for each virus isolate’s RNA genome with altered oligonucleotides placed within the predicted env gene region of the genome.

Implications of Findings

  • The study supports the idea that EIAV can result in considerable genomic variations during replication, causing altered glycoprotein structures and antigenic variants responsible for unique disease characters in persistently infected ponies.
  • The researchers also hint that variation in envelope-specific differences observed in isolates of visna virus and human T-cell lymphotropic virus III might be a common feature of Lentivirinae, the subfamily to which these viruses belong.

Cite This Article

APA
Salinovich O, Payne SL, Montelaro RC, Hussain KA, Issel CJ, Schnorr KL. (1986). Rapid emergence of novel antigenic and genetic variants of equine infectious anemia virus during persistent infection. J Virol, 57(1), 71-80. https://doi.org/10.1128/JVI.57.1.71-80.1986

Publication

ISSN: 0022-538X
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 57
Issue: 1
Pages: 71-80

Researcher Affiliations

Salinovich, O
    Payne, S L
      Montelaro, R C
        Hussain, K A
          Issel, C J
            Schnorr, K L

              MeSH Terms

              • Animals
              • Antibodies, Monoclonal / immunology
              • Antibodies, Viral / immunology
              • Antigens, Surface / genetics
              • Antigens, Surface / immunology
              • Antigens, Viral / genetics
              • Chronic Disease
              • Equine Infectious Anemia / microbiology
              • Glycoproteins / genetics
              • Glycoproteins / immunology
              • Horses / microbiology
              • Infectious Anemia Virus, Equine / genetics
              • Infectious Anemia Virus, Equine / immunology
              • Infectious Anemia Virus, Equine / isolation & purification
              • Neutralization Tests
              • Oligonucleotides / analysis
              • Peptides / analysis
              • RNA, Viral / genetics
              • Viral Proteins / genetics
              • Viral Proteins / immunology

              Grant Funding

              • CA-38851 / NCI NIH HHS

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