Insertions, duplications and substitutions in restricted gp90 regions of equine infectious anaemia virus during febrile episodes in an experimentally infected horse.
Abstract: We have studied a horse which exhibited typical clinical signs of disease when experimentally infected with a non-adapted virulent strain of equine infectious anaemia virus (EIAV), designated V70. Five viruses (F1V, F2V, F3V, F4V and F5V) were recovered during periodic febrile episodes. Cross-neutralization tests revealed that all of these variants and the parental V70 were antigenically distinct. Sequencing of their full-length env gp90 genes and gp45 5' sequences revealed novel mutations at a limited number of nucleotide positions, consisting of insertions and duplications in the gp90 principal neutralizing domain (PND) in F1V, F3V and F5V. Parts or all of small units (6, 9 and 12 nucleotides) located just before the insertion site were used for the duplications. Furthermore, amino acid substitutions in the env PND and hypervariable region were also observed in all five viruses. These mutations may contribute to the generation of serial variants. Consequently, the full-length gp90 sequences showed close relationships between V70, F2V and F4V, and between F1V, F3V and F5V. In addition to the two domains (PND and hypervariable region), a comparison of these viruses with the reported env gp90 sequences revealed four additional variable domains, although these four domains were highly conserved among the five variants.
Publication Date: 1997-04-01 PubMed ID: 9129653DOI: 10.1099/0022-1317-78-4-807Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This research investigated the evolution of mutations in the equine infectious anaemia virus (EIAV) during its infection cycle in a horse. The study found that during periods of fever, new variants of the virus emerged, each with unique aspects to their genetic makeup.
Research Context and Methodology
- Scientists experimentally infected a horse with EIAV and periodically gathered samples of the virus during the horse’s febrile episodes.
- For this research, they used the particularly virulent V70 strain of EIAV.
- From these samples, they isolated five different virus variants, named F1V through F5V.
Virus Variations
- Through cross-neutralization tests (tests used to compare antigen-antibody reactions across different viruses), they found that each virus variant and the original V70 strain were antigenically distinct, meaning that they were recognized differently by the immune system.
- The team then used sequencing methods to analyze these virus variants, with particular attention given to their full-length env gp90 genes and the 5′ end of their gp45 sequences.
Findings Regarding Mutations
- The study identified novel mutations at a number of nucleotide positions within the env genes. These mutations included insertions, duplications, and amino acid substitutions.
- In the gp90 principal neutralizing domain (PND) of the F1V, F3V, and F5V variants, they discovered insertions and duplications. It was noted that small sections of nucleotides located before the insertion site were used in these duplications.
- Amino acid substitutions were also noted in the env PND and the hypervariable region of all five virus variants. The team hypothesizes that these mutations could be factors in the generation of new virus variants.
- The gp90 sequences showed close relationships between V70, F2V, and F4V, and a separate grouping between F1V, F3V, and F5V.
- The research further identified four additional variable domains within the gp90 sequences. However, these domains appeared to be highly conserved among the five virus variants.
Implications
- The study provides insights into the ongoing evolution of the EIAV virus within an infected host, which could be valuable for developing treatments or vaccines. It offers a clear picture of how subtle changes in the virus’s genetic makeup can lead to antigenically distinct variants.
Cite This Article
APA
Zheng YH, Nakaya T, Sentsui H, Kameoka M, Kishi M, Hagiwara K, Takahashi H, Kono Y, Ikuta K.
(1997).
Insertions, duplications and substitutions in restricted gp90 regions of equine infectious anaemia virus during febrile episodes in an experimentally infected horse.
J Gen Virol, 78 ( Pt 4), 807-820.
https://doi.org/10.1099/0022-1317-78-4-807 Publication
Researcher Affiliations
- Section of Serology, Hokkaido University, Sapporo, Japan.
MeSH Terms
- Amino Acid Sequence
- Animals
- Base Sequence
- Equine Infectious Anemia / virology
- Glycoproteins
- Horses / virology
- Infectious Anemia Virus, Equine / genetics
- Molecular Sequence Data
- Mutation
- Sequence Analysis
- Viral Envelope Proteins / genetics
Citations
This article has been cited 17 times.- Ahmad I, Li S, Li R, Chai Q, Zhang L, Wang B, Yu C, Zheng YH. The retroviral accessory proteins S2, Nef, and glycoMA use similar mechanisms for antagonizing the host restriction factor SERINC5.. J Biol Chem 2019 Apr 26;294(17):7013-7024.
- Schwartz EJ, Nanda S, Mealey RH. Antibody escape kinetics of equine infectious anemia virus infection of horses.. J Virol 2015 Jul;89(13):6945-51.
- Qian L, Han X, Liu X. Structural insight into equine lentivirus receptor 1.. Protein Sci 2015 May;24(5):633-42.
- Liu C, Cook SJ, Craigo JK, Cook FR, Issel CJ, Montelaro RC, Horohov DW. Epitope shifting of gp90-specific cellular immune responses in EIAV-infected ponies.. Vet Immunol Immunopathol 2014 Oct 15;161(3-4):161-9.
- Craigo JK, Montelaro RC. Lessons in AIDS vaccine development learned from studies of equine infectious, anemia virus infection and immunity.. Viruses 2013 Dec 2;5(12):2963-76.
- Craigo JK, Ezzelarab C, Cook SJ, Chong L, Horohov D, Issel CJ, Montelaro RC. Envelope determinants of equine lentiviral vaccine protection.. PLoS One 2013;8(6):e66093.
- Craigo JK, Ezzelarab C, Montelaro RC. Development of a high throughput, semi-automated, infectious center cell-based ELISA for equine infectious anemia virus.. J Virol Methods 2012 Nov;185(2):221-7.
- Wang X, Wang S, Lin Y, Jiang C, Ma J, Zhao L, Lv X, Wang F, Shen R, Zhou J. Unique evolution characteristics of the envelope protein of EIAV(LN₄₀), a virulent strain of equine infectious anemia virus.. Virus Genes 2011 Apr;42(2):220-8.
- Cappelli K, Capomaccio S, Cook FR, Felicetti M, Marenzoni ML, Coppola G, Verini-Supplizi A, Coletti M, Passamonti F. Molecular detection, epidemiology, and genetic characterization of novel European field isolates of equine infectious anemia virus.. J Clin Microbiol 2011 Jan;49(1):27-33.
- Craigo JK, Barnes S, Cook SJ, Issel CJ, Montelaro RC. Divergence, not diversity of an attenuated equine lentivirus vaccine strain correlates with protection from disease.. Vaccine 2010 Nov 29;28(51):8095-104.
- Craigo JK, Barnes S, Zhang B, Cook SJ, Howe L, Issel CJ, Montelaro RC. An EIAV field isolate reveals much higher levels of subtype variability than currently reported for the equine lentivirus family.. Retrovirology 2009 Oct 20;6:95.
- Boissin-Quillon A, Piau D, Leroux C. In silico segmentations of lentivirus envelope sequences.. BMC Bioinformatics 2007 Mar 21;8:99.
- Payne SL, Pei XF, Jia B, Fagerness A, Fuller FJ. Influence of long terminal repeat and env on the virulence phenotype of equine infectious anemia virus.. J Virol 2004 Mar;78(5):2478-85.
- Howe L, Leroux C, Issel CJ, Montelaro RC. Equine infectious anemia virus envelope evolution in vivo during persistent infection progressively increases resistance to in vitro serum antibody neutralization as a dominant phenotype.. J Virol 2002 Nov;76(21):10588-97.
- Leroux C, Craigo JK, Issel CJ, Montelaro RC. Equine infectious anemia virus genomic evolution in progressor and nonprogressor ponies.. J Virol 2001 May;75(10):4570-83.
- Leroux C, Issel CJ, Montelaro RC. Novel and dynamic evolution of equine infectious anemia virus genomic quasispecies associated with sequential disease cycles in an experimentally infected pony.. J Virol 1997 Dec;71(12):9627-39.
- Zheng YH, Sentsui H, Nakaya T, Kono Y, Ikuta K. In vivo dynamics of equine infectious anemia viruses emerging during febrile episodes: insertions/duplications at the principal neutralizing domain.. J Virol 1997 Jul;71(7):5031-9.
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