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Home / Equine Research Bank / Virus Genes / Horses naturally infected with EIAV harbor 2 distinct SU pop...
Virus genes2016; 52(1); 71-80; doi: 10.1007/s11262-015-1280-z

Horses naturally infected with EIAV harbor 2 distinct SU populations but are monophyletic with respect to IN.

Abstract: Equine infectious anemia virus (EIAV) causes lifelong infections ranging from acutely fatal, to chronic, to asymptomatic. Within infected animals, EIAV is found as a quasispecies. Many experimental studies on EIAV, carried out in the U.S. over the past 70 years, have used either the highly virulent Wyoming (EIAVWYO) field strain or various derivatives of that strain. These infections have provided insights into the variety of genetic changes that accumulate in the env gene and LTR in experimentally infected horses. In the current study, we obtained EIAV sequences from blood samples collected from naturally infected Texas horses between 2000 and 2002. We found surface (SU) and long terminal repeat (LTR) sequences clearly related to EIAVWYO and its cell culture-adapted derivatives. Some blood samples yielded SU or LTR sequences belonging to 2 discrete clusters. In these cases, SU and LTR variation between animals was no greater than sequence variation within animals. In contrast, a portion of integrase (IN) was more homogeneous within animals than between animals. These results suggest that specific selective pressures are applied to SU and LTR sequences, potentially driving generation of two distinct sequence clusters within a horse. We speculate that viruses in one cluster may be more highly expressed and easily transmitted while those in the second cluster support long-term inapparent infection. The presence of homogeneous IN sequences within a horse supports the hypothesis that SU and LTR sequences diverged after the initial infection.
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Publication Date: 2016-01-06 PubMed ID: 26739458DOI: 10.1007/s11262-015-1280-zGoogle Scholar: Lookup
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Summary

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The article discusses a research study conducted on horses naturally infected with Equine Infectious Anemia Virus (EIAV) in Texas between 2000 and 2002. The researchers found that infected horses harbor two distinct SU populations and are monophyletic with respect to IN.

Background and Purpose of the Research

  • The equine infectious anemia virus (EIAV) is known to cause lifelong infections in horses that can range from being acutely fatal to chronic and sometimes asymptomatic.
  • The virus is found as a quasispecies within infected animals, and many experiments on it have been conducted over the past 70 years.
  • The study aimed to examine blood samples collected from naturally infected Texas horses. It sought to offer insights into the variety of genetic changes that accumulate in the env gene and long terminal repeats (LTR) in infected horses.

Findings of the Research

  • The examination of the blood samples revealed surface (SU) and long terminal repeat (LTR) sequences that are closely related to the highly virulent Wyoming field strain of EIAV.
  • The research uncovered that SU and LTR sequences from some blood samples belonged to two different clusters. The sequence variation between animals was found to be no greater than the variation within animals themselves.
  • However, a portion of integrase (IN) was found to be more homogeneous within animals than between them, contradicting the variance found in SU and LTR samples.
  • The results indicate that specific selective pressures could be applied to SU and LTR sequences, potentially leading to the creation of two distinct sequence clusters within a horse.

Implications and Hypotheses

  • The researchers speculate that viruses in one cluster might be more highly expressed and easy to transmit, while the viruses in the second cluster could support long-term inapparent infection.
  • The presence of homogeneous IN sequences within a horse backs the hypothesis that SU and LTR sequences diverged following the initial infection. This means that these parts of the virus may mutate and diverge differently post-infection, impacting the course and expression of the illness within the host.

Cite This Article

APA
Cervantes DT, Ball JM, Edwards J, Payne S. (2016). Horses naturally infected with EIAV harbor 2 distinct SU populations but are monophyletic with respect to IN. Virus Genes, 52(1), 71-80. https://doi.org/10.1007/s11262-015-1280-z

Publication

Virus genes
ISSN: 1572-994X
NlmUniqueID: 8803967
Country: United States
Language: English
Volume: 52
Issue: 1
Pages: 71-80

Researcher Affiliations

Cervantes, Diana T
  • Texas Department of State Health Services, HSR 2/3 1301 S. Bowen Rd., Ste 200, Arlington, TX, 76013, USA.
Ball, Judith M
  • Texas A&M University, College Station, TX, USA.
Edwards, John
  • Texas A&M University, College Station, TX, USA.
Payne, Susan
  • Texas A&M University, College Station, TX, USA. spayne@cvm.tamu.edu.

MeSH Terms

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Equine Infectious Anemia / virology
  • Genetic Variation
  • Genome, Viral
  • Horses
  • Infectious Anemia Virus, Equine / classification
  • Infectious Anemia Virus, Equine / enzymology
  • Infectious Anemia Virus, Equine / genetics
  • Integrases / chemistry
  • Integrases / genetics
  • Molecular Sequence Data
  • Phylogeny
  • Sequence Alignment
  • Texas

References

This article includes 28 references
  1. Capomaccio S, Cappelli K, Cook RF, Nardi F, Gifford R, Marenzoni ML, Passamonti F. Geographic structuring of global EIAV isolates: a single origin for New World strains?. Virus Res 2012 Feb;163(2):656-9.
    pubmed: 22119901doi: 10.1016/j.virusres.2011.11.011google scholar: lookup
  2. 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.
    pubmed: 14963146doi: 10.1128/jvi.78.5.2478-2485.2004google scholar: lookup
  3. Capomaccio S, Willand ZA, Cook SJ, Issel CJ, Santos EM, Reis JK, Cook RF. Detection, molecular characterization and phylogenetic analysis of full-length equine infectious anemia (EIAV) gag genes isolated from Shackleford Banks wild horses.. Vet Microbiol 2012 Jun 15;157(3-4):320-32.
    pubmed: 22310073doi: 10.1016/j.vetmic.2012.01.015google scholar: lookup
  4. Craigo JK, Li F, Steckbeck JD, Durkin S, Howe L, Cook SJ, Issel C, Montelaro RC. Discerning an effective balance between equine infectious anemia virus attenuation and vaccine efficacy.. J Virol 2005 Mar;79(5):2666-77.
    pubmed: 15708986doi: 10.1128/JVI.79.5.2666-2677.2005google scholar: lookup
  5. Coggins L. Development of the Coggins test.. Cornell Vet 1994 Jan;84(1):3-5.
    pubmed: 8313705
  6. Payne SL, Rausch J, Rushlow K, Montelaro RC, Issel C, Flaherty M, Perry S, Sellon D, Fuller F. Characterization of infectious molecular clones of equine infectious anaemia virus.. J Gen Virol 1994 Feb;75 ( Pt 2):425-9.
    pubmed: 8113766doi: 10.1099/0022-1317-75-2-425google scholar: lookup
  7. Mealey RH, Fraser DG, Oaks JL, Cantor GH, McGuire TC. Immune reconstitution prevents continuous equine infectious anemia virus replication in an Arabian foal with severe combined immunodeficiency: lessons for control of lentiviruses.. Clin Immunol 2001 Nov;101(2):237-47.
    pubmed: 11683583doi: 10.1006/clim.2001.5109google scholar: lookup
  8. 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.
    pubmed: 9371627doi: 10.1128/JVI.71.12.9627-9639.1997google scholar: lookup
  9. Mealey RH, Leib SR, Pownder SL, McGuire TC. Adaptive immunity is the primary force driving selection of equine infectious anemia virus envelope SU variants during acute infection.. J Virol 2004 Sep;78(17):9295-305.
    pubmed: 15308724doi: 10.1128/JVI.78.17.9295-9305.2004google scholar: lookup
  10. Quinlivan M, Cook F, Kenna R, Callinan JJ, Cullinane A. Genetic characterization by composite sequence analysis of a new pathogenic field strain of equine infectious anemia virus from the 2006 outbreak in Ireland.. J Gen Virol 2013 Mar;94(Pt 3):612-622.
    pubmed: 23175240doi: 10.1099/vir.0.047191-0google scholar: lookup
  11. Taylor SD, Leib SR, Carpenter S, Mealey RH. Selection of a rare neutralization-resistant variant following passive transfer of convalescent immune plasma in equine infectious anemia virus-challenged SCID horses.. J Virol 2010 Jul;84(13):6536-48.
    pubmed: 20392850doi: 10.1128/JVI.00218-10google scholar: lookup
  12. Kobayashi K, Kono Y. Serial passages of equine infectious anemia virus in horse leukocyte culture.. Natl Inst Anim Health Q (Tokyo) 1967 Spring;7(1):1-7.
    pubmed: 4293211
  13. Kobayashi K, Kono Y. Propagation and titration of equine infectious anemia virus in horse leukocyte culture.. Natl Inst Anim Health Q (Tokyo) 1967 Spring;7(1):8-20.
    pubmed: 4293214
  14. Payne SL, La Celle K, Pei XF, Qi XM, Shao H, Steagall WK, Perry S, Fuller F. Long terminal repeat sequences of equine infectious anaemia virus are a major determinant of cell tropism.. J Gen Virol 1999 Mar;80 ( Pt 3):755-759.
    pubmed: 10092016doi: 10.1099/0022-1317-80-3-755google scholar: lookup
  15. Cook RF, Leroux C, Issel CJ. Equine infectious anemia and equine infectious anemia virus in 2013: a review.. Vet Microbiol 2013 Nov 29;167(1-2):181-204.
    pubmed: 24183747doi: 10.1016/j.vetmic.2013.09.031google scholar: lookup
  16. Mealey RH, Zhang B, Leib SR, Littke MH, McGuire TC. Epitope specificity is critical for high and moderate avidity cytotoxic T lymphocytes associated with control of viral load and clinical disease in horses with equine infectious anemia virus.. Virology 2003 Sep 1;313(2):537-52.
    pubmed: 12954220doi: 10.1016/s0042-6822(03)00344-1google scholar: lookup
  17. Craigo JK, Zhang B, Barnes S, Tagmyer TL, Cook SJ, Issel CJ, Montelaro RC. Envelope variation as a primary determinant of lentiviral vaccine efficacy.. Proc Natl Acad Sci U S A 2007 Sep 18;104(38):15105-10.
    pubmed: 17846425doi: 10.1073/pnas.0706449104google scholar: lookup
  18. Hammond SA, Cook SJ, Lichtenstein DL, Issel CJ, Montelaro RC. Maturation of the cellular and humoral immune responses to persistent infection in horses by equine infectious anemia virus is a complex and lengthy process.. J Virol 1997 May;71(5):3840-52.
    pubmed: 9094660doi: 10.1128/JVI.71.5.3840-3852.1997google scholar: lookup
  19. Payne SL, Qi XM, Shao H, Dwyer A, Fuller FJ. Disease induction by virus derived from molecular clones of equine infectious anemia virus.. J Virol 1998 Jan;72(1):483-7.
    pubmed: 9420249doi: 10.1128/JVI.72.1.483-487.1998google scholar: lookup
  20. Maury W, Thompson RJ, Jones Q, Bradley S, Denke T, Baccam P, Smazik M, Oaks JL. Evolution of the equine infectious anemia virus long terminal repeat during the alteration of cell tropism.. J Virol 2005 May;79(9):5653-64.
    pubmed: 15827180doi: 10.1128/JVI.79.9.5653-5664.2005google scholar: lookup
  21. 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.
    pubmed: 11312327doi: 10.1128/JVI.75.10.4570-4583.2001google scholar: lookup
  22. Payne SL, Fuller FJ. Virulence determinants of equine infectious anemia virus.. Curr HIV Res 2010 Jan;8(1):66-72.
    pubmed: 20210781doi: 10.2174/157016210790416352google scholar: lookup
  23. Lichtenstein DL, Issel CJ, Montelaro RC. Genomic quasispecies associated with the initiation of infection and disease in ponies experimentally infected with equine infectious anemia virus.. J Virol 1996 Jun;70(6):3346-54.
    pubmed: 8648664doi: 10.1128/JVI.70.6.3346-3354.1996google scholar: lookup
  24. 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.
    pubmed: 19843328doi: 10.1186/1742-4690-6-95google scholar: lookup
  25. Kakinuma S, Motokawa K, Hohdatsu T, Yamamoto JK, Koyama H, Hashimoto H. Nucleotide sequence of feline immunodeficiency virus: classification of Japanese isolates into two subtypes which are distinct from non-Japanese subtypes.. J Virol 1995 Jun;69(6):3639-46.
    pubmed: 7745712doi: 10.1128/JVI.69.6.3639-3646.1995google scholar: lookup
  26. 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.
    pubmed: 20955830doi: 10.1016/j.vaccine.2010.10.003google scholar: lookup
  27. Maury W, Oaks JL, Bradley S. Equine endothelial cells support productive infection of equine infectious anemia virus.. J Virol 1998 Nov;72(11):9291-7.
    pubmed: 9765477doi: 10.1128/JVI.72.11.9291-9297.1998google scholar: lookup
  28. Sponseller BA, Sparks WO, Wannemuehler Y, Li Y, Antons AK, Oaks JL, Carpenter S. Immune selection of equine infectious anemia virus env variants during the long-term inapparent stage of disease.. Virology 2007 Jun 20;363(1):156-65.
    pubmed: 17328936doi: 10.1016/j.virol.2007.01.037google scholar: lookup

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