Equine infectious anemia virus replication is upregulated during differentiation of blood monocytes from acutely infected horses.
Abstract: Equine infectious anemia virus is a lentivirus that replicates in mature tissue macrophages of horses. Ponies were infected with equine infectious anemia virus. During febrile episodes, proviral DNA was detectable, but viral mRNA was not detectable. As cultured blood monocytes from these ponies differentiated into macrophages, viral expression was upregulated. In situ hybridization confirmed that viral transcription occurred in mature macrophages.
Publication Date: 1996-01-01 PubMed ID: 8523576PubMed Central: PMC189850DOI: 10.1128/JVI.70.1.590-594.1996Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
- Research Support
- U.S. Gov't
- P.H.S.
Summary
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The study explains that the replication of Equine infectious anemia virus (EIAV), a virus in horses, is heightened during the differentiation of blood monocytes in infected animals.
Overview and Objectives
- The research aimed to understand the behavior of Equine infectious anemia virus (EIAV) during a horse’s immune response, specifically during the differentiation of blood monocytes.
- Given that EIAV replicates in mature tissue macrophages of horses, the scientists were interested in determining whether this process could be detected and observed during varying stages of the immune response.
Methodology
- The study began by infecting ponies with EIAV to study its progression and the ensuing immune response.
- During the ponies’ febrile episodes (fever conditions often associated with an immune response to infection), the team looked for proviral DNA – an indicator of viral replication. They were successful in detecting this.
- Simultaneously, they looked for viral mRNA, a molecule that carries codes from the DNA for protein synthesis, but in this case, they found none.
Results and Findings
- Researchers then shifted focus to the study of blood monocytes from the infected ponies. Monocytes are a type of white blood cell that can differentiate into macrophages and dendritic cells to respond to an infection.
- They observed that as these monocytes transformed into macrophages, there was a significant increase in viral expression (meaning the virus was replicating more during this stage).
- In situ hybridization tests, a form of DNA labeling, were performed to track and confirm these results, which solidified the evidence that viral transcription (the process of making an RNA copy of a gene’s DNA sequence) indeed occurred in the mature macrophages.
Implications
- The results of this research add valuable knowledge about the lifecycle and behavior of EIAV during the stages of monocyte differentiation.
- This understanding could potentially be leveraged in future treatment strategies focused on modulating macrophage responses or preventing monocyte differentiation to slow down or halt EIAV replication.
Cite This Article
APA
Sellon DC, Walker KM, Russell KE, Perry ST, Covington P, Fuller FJ.
(1996).
Equine infectious anemia virus replication is upregulated during differentiation of blood monocytes from acutely infected horses.
J Virol, 70(1), 590-594.
https://doi.org/10.1128/JVI.70.1.590-594.1996 Publication
Researcher Affiliations
- Department of Food Animal and Equine Medicine, North Carolina State University College of Veterinary Medicine, Raleigh 27606, USA.
MeSH Terms
- Acute Disease
- Animals
- Cell Differentiation
- DNA, Viral
- Equine Infectious Anemia / blood
- Equine Infectious Anemia / virology
- Horses
- Infectious Anemia Virus, Equine / isolation & purification
- Infectious Anemia Virus, Equine / physiology
- Monocytes / metabolism
- Monocytes / virology
- RNA, Messenger / metabolism
- RNA, Viral / metabolism
- Up-Regulation
- Virus Replication
Grant Funding
- CA59278 / NCI NIH HHS
- K11-AI00963 / NIAID NIH HHS
References
This article includes 23 references
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Citations
This article has been cited 7 times.- Covaleda L, Fuller FJ, Payne SL. EIAV S2 enhances pro-inflammatory cytokine and chemokine response in infected macrophages.. Virology 2010 Feb 5;397(1):217-23.
- Valas S, Rolland M, Perrin C, Perrin G, Mamoun RZ. Characterization of a new 5' splice site within the caprine arthritis encephalitis virus genome: evidence for a novel auxiliary protein.. Retrovirology 2008 Feb 29;5:22.
- Nunez R, Gomes-Keller MA, Schwarzwald C, Feige K. Assessment of Equine Autoimmune Thrombocytopenia (EAT) by flow cytometry.. BMC Blood Disord 2001;1(1):1.
- Harrold SM, Cook SJ, Cook RF, Rushlow KE, Issel CJ, Montelaro RC. Tissue sites of persistent infection and active replication of equine infectious anemia virus during acute disease and asymptomatic infection in experimentally infected equids.. J Virol 2000 Apr;74(7):3112-21.
- Li F, Leroux C, Craigo JK, Cook SJ, Issel CJ, Montelaro RC. The S2 gene of equine infectious anemia virus is a highly conserved determinant of viral replication and virulence properties in experimentally infected ponies.. J Virol 2000 Jan;74(1):573-9.
- Li F, Puffer BA, Montelaro RC. The S2 gene of equine infectious anemia virus is dispensable for viral replication in vitro.. J Virol 1998 Oct;72(10):8344-8.
- Oaks JL, McGuire TC, Ulibarri C, Crawford TB. Equine infectious anemia virus is found in tissue macrophages during subclinical infection.. J Virol 1998 Sep;72(9):7263-9.
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