Replication ability in vitro and in vivo of equine infectious anemia virus avirulent Japanese strain.
Abstract: An attenuated equine infectious anemia virus (EIAV), V26, was previously prepared by 50 passages of the Japanese virulent strain V70 in primary horse macrophage culture. The horses inoculated with this V26 virus were shown to raise neutralizing antibodies against V70 without any viremia. Here, we investigated the in vitro and in vivo replication ability of V26. Comparison of the long-terminal repeat (LTR) sequences between V26 and V70 revealed a large insertion within the LTR U3 hypervariable region of V26. V26 with the mutation in the LTR showed much higher promoter activity in vitro than V70. This is consistent with the much higher replication rate of V26 in horse primary macrophage cultures compared with V70. In sharp contrast, we failed to identify the V26-specific LTR sequence by PCR, at least in sequential samples of plasma or peripheral blood mononuclear cells derived from three horses until day 62 after V26 inoculation. In contrast, antibody responses to EIAV were observed in all horses. The results suggest that the replication ability of V26 in vivo is extremely low. When one of the horses was subsequently challenged with cell-associated V70, it was found that the horse became PCR positive for EIAV. There was no LTR mutation in EIAV genome in samples periodically prepared from the V70-challenged horse. Thus it was suggested that the LTR mutation in EIAV, which occurs during serial passage in vitro, affects EIAV replication in vitro and in vivo.
Copyright 2000 Academic Press.
Publication Date: 1999-12-29 PubMed ID: 10612667DOI: 10.1006/viro.1999.0076Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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The research article investigates the replication abilities of an attenuated strain of equine infectious anemia virus (EIAV), known as V26, both in vitro (in the laboratory) and in vivo (in the body). The strain V26 is known to produce neutralizing antibodies against EIAV without causing detectable viremia in inoculated horses. The study centered on the large insertion within the long-terminal repeat (LTR) sequences of V26, its promoter activity, and the virus replication rate compared to the virulent strain V70.
Research Methodology
- The scientists started by comparing the long-terminal repeat (LTR) sequences between the V26 and the V70 strains. The LTR is a crucial part of a virus that helps control the replication of the virus. This comparison revealed a significant insertion within the LTR U3 hypervariable region of V26.
- They experimented the in vitro replication rate of V26 by measuring its promoter activity, which is the process that initiates transcription of a gene. Compared to V70, V26 had a much higher promoter activity, indicating a higher replication rate.
- The researchers also studied the virus’s in vivo replication ability. They used a Polymerase Chain Reaction (PCR) to detect the V26-specific LTR sequence in sequential samples of plasma or peripheral blood mononuclear cells collected from horses inoculated with V26.
Findings of the Study
- It was found that V26 had a higher replication rate than V70 in vitro.
- In contrast to the in vitro experiment, the researchers could not detect the V26-specific LTR sequence in any body samples collected from the inoculated horses, suggesting that V26’s replication in vivo was extremely low.
- Despite the low replication ability in vivo, all inoculated horses exhibited antibody responses to EIAV.
- When one inoculated horse was subsequently exposed to V70, it was found to be PCR positive for EIAV, suggesting that the inoculation with V26 did not confer enough immunity to prevent subsequent infection with V70.
Conclusion
- The study concludes that the LTR mutation in EIAV, which occurs during the serial passage in the laboratory, impacts EIAV’s replication ability both in vitro and in vivo. This could have implications for vaccine development strategies against EIAV, especially regarding the use of the V26 strain.
Cite This Article
APA
Zheng YH, Sentsui H, Sugita M, Nakaya T, Kishi M, Hagiwara K, Inoshima Y, Ishihara C, Kono Y, Lu JL, Ikuta K.
(1999).
Replication ability in vitro and in vivo of equine infectious anemia virus avirulent Japanese strain.
Virology, 266(1), 129-139.
https://doi.org/10.1006/viro.1999.0076 Publication
Researcher Affiliations
- Institute of Immunological Science, Hokkaido University, Sapporo, Kita-ku, Japan.
MeSH Terms
- Animals
- Antibodies, Viral / blood
- Base Sequence
- Cells, Cultured
- DNA, Viral / blood
- Equine Infectious Anemia / virology
- Genetic Variation
- Horses
- Infectious Anemia Virus, Equine / immunology
- Infectious Anemia Virus, Equine / pathogenicity
- Infectious Anemia Virus, Equine / physiology
- Japan
- Macrophages / virology
- Molecular Sequence Data
- Promoter Regions, Genetic
- RNA, Viral / blood
- Terminal Repeat Sequences / genetics
- Virulence
- Virus Replication
Citations
This article has been cited 4 times.- Wang XF, Liu Q, Wang YH, Wang S, Chen J, Lin YZ, Ma J, Zhou JH, Wang X. Characterization of Equine Infectious Anemia Virus Long Terminal Repeat Quasispecies In Vitro and In Vivo.. J Virol 2018 Apr 15;92(8).
- 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.
- Qi X, Wang X, Wang S, Lin Y, Jiang C, Ma J, Zhao L, Lv X, Shen R, Wang F, Kong X, Su Z, Zhou J. Genomic analysis of an effective lentiviral vaccine-attenuated equine infectious anemia virus vaccine EIAV FDDV13.. Virus Genes 2010 Aug;41(1):86-98.
- 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.
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