Influence of long terminal repeat and env on the virulence phenotype of equine infectious anemia virus.
Abstract: The molecular clones pSPeiav19 and p19/wenv17 of equine infectious anemia virus (EIAV) differ in env and long terminal repeats (LTRs) and produce viruses (EIAV(19) and EIAV(17), respectively) of dramatically different virulence phenotypes. These constructs were used to generate a series of chimeric clones to test the individual contributions of LTR, surface (SU), and transmembrane (TM)/Rev regions to the disease potential of the highly virulent EIAV(17). The LTRs of EIAV(19) and EIAV(17) differ by 16 nucleotides in the transcriptional enhancer region. The two viruses differ by 30 amino acids in SU, by 17 amino acids in TM, and by 8 amino acids in Rev. Results from in vivo infections with chimeric clones indicate that both LTR and env of EIAV(17) are required for the development of severe acute disease. In the context of the EIAV(17) LTR, SU appears to have a greater impact on virulence than does TM. EIAV(17SU), containing only the TM/Rev region from the avirulent parent, induced acute disease in two animals, while a similar infectious dose of EIAV(17TM) (which derives SU from the avirulent parent) did not. Neither EIAV(17SU) nor EIAV(17TM) produced lethal disease when administered at infectious doses that were 6- to 30-fold higher than a lethal dose of the parental EIAV(17). All chimeric clones replicated in primary equine monocyte-derived macrophages, and there was no apparent correlation between macrophage tropism and virulence phenotype.
Publication Date: 2004-02-14 PubMed ID: 14963146PubMed Central: PMC369206DOI: 10.1128/jvi.78.5.2478-2485.2004Google Scholar: Lookup
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- P.H.S.
Summary
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The research article is focused on investigating the role of long terminal repeats (LTRs) and env in influencing the virulence phenotype of the equine infectious anemia virus (EIAV). The study found both elements to be important in the development of severe acute disease.
Investigation of Virulence Phenotypes
- The study used two different molecular clones of the equine infectious anemia virus (EIAV) named pSPeiav19 and p19/wenv17. These two clones differ in their env and long terminal repeats (LTRs), resulting in viruses of sharply different virulence phenotypes, referred to as EIAV(19) and EIAV(17) respectively.
- These constructs were utilized to generate a range of chimeric clones for testing the individual contributions of the LTR, surface (SU), and transmembrane (TM)/Rev regions to the high virulence potential of EIAV(17).
Key Findings
- Results from the conducted in vivo infections with the created chimeric clones revealed that both LTR and env of EIAV(17) are required for developing a severe acute disease.
- The research further clarified that within the context of the EIAV(17) LTR, SU seemingly has a greater influence on virulence compared to TM.
- The study also noted that while EIAV(17SU) (which contained only the TM/Rev region from the avirulent parent) led to acute disease in two tested animals, a similar infectious dose of EIAV(17TM) (which derives the SU from the avirulent parent) did not.
- Furthermore, neither EIAV(17SU) nor EIAV(17TM) resulted in lethal disease when administered at infectious doses that were between 6- and 30-fold higher than a lethal dose of the parental EIAV(17).
Further Observations
- All of the chimeric clones created for the study were observed to replicate in primary equine monocyte-derived macrophages.
- The research found no apparent correlation between macrophage tropism (the tendency of specific pathogens to infect specific cell types) and the virulence phenotype of the virus.
Cite This Article
APA
Payne SL, Pei XF, Jia B, Fagerness A, Fuller FJ.
(2004).
Influence of long terminal repeat and env on the virulence phenotype of equine infectious anemia virus.
J Virol, 78(5), 2478-2485.
https://doi.org/10.1128/jvi.78.5.2478-2485.2004 Publication
Researcher Affiliations
- Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas 77843-4467, USA. spayne@cvm.tamu.edu
MeSH Terms
- Amino Acid Sequence
- Animals
- Base Sequence
- Genome, Viral
- Genotype
- Horses / virology
- Infectious Anemia Virus, Equine / genetics
- Infectious Anemia Virus, Equine / pathogenicity
- Infectious Anemia Virus, Equine / physiology
- Molecular Sequence Data
- Phenotype
- Terminal Repeat Sequences / genetics
- Viral Envelope Proteins / genetics
- Viral Envelope Proteins / metabolism
- Virulence / genetics
Grant Funding
- R01 CA059278 / NCI NIH HHS
- CA-59278 / NCI NIH HHS
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