Chimeric viruses containing the N-terminal ectodomains of GP5 and M proteins of porcine reproductive and respiratory syndrome virus do not change the cellular tropism of equine arteritis virus.
Abstract: Equine arteritis virus (EAV) and porcine reproductive and respiratory syndrome virus (PRRSV) are members of family Arteriviridae; they are highly species specific and differ significantly in cellular tropism in cultured cells. In this study we examined the role of the two major envelope proteins (GP5 and M) of EAV and PRRSV in determining their cellular tropism. We generated three viable EAV/PRRSV chimeric viruses by swapping the N-terminal ectodomains of these two proteins from PRRSV IA1107 strain into an infectious cDNA clone of EAV (rMLVB4/5 GP5ecto, rMLVB4/5/6 Mecto and rMLVB4/5/6 GP5&Mecto). The three chimeric viruses could only infect EAV susceptible cell lines but not PRRSV susceptible cells in culture. Therefore, these data unequivocally demonstrate that the ectodomains of GP5 and M are not the major determinants of cellular tropism, further supporting the recent findings that the minor envelope proteins are the critical proteins in mediating cellular tropism (Tian et al., 2012).
Copyright © 2012 Elsevier Inc. All rights reserved.
Publication Date: 2012-06-26 PubMed ID: 22739441DOI: 10.1016/j.virol.2012.05.022Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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The researchers behind this study have been examining how the changing of certain proteins within the Equine arteritis virus (EAV) and the porcine reproductive and respiratory syndrome virus (PRRSV) impacts their ability to infect certain cell types. They found that these changes don’t alter the type of cells these viruses can infect.
Understanding the Research
- The research aimed to investigate how altering specific proteins within the Equine arteritis virus (EAV) and porcine reproductive and respiratory syndrome virus (PRRSV) would change their ability to infect various cells.
- The researchers were interested in how these changes would affect the viruses’ species-specific characteristics and difference in cellular tropism – the types of cells they can infect within cultured cells.
Methodology
- To conduct this research, the researchers created three chimeric, or hybrid, viruses.
- These new viruses were created by taking the ectodomains, or outer layers of the GP5 and M proteins from the PRRSV IA1107 strain and locating them into a cloned EAV virus. This resulted in three new viruses named rMLVB4/5 GP5ecto, rMLVB4/5/6 Mecto, and rMLVB4/5/6 GP5&Mecto.
Findings
- The outcome of the experiment indicated that these three hybrid viruses could only infect the same types of cells that the original EAV could – they could not infect PRRSV susceptible cells.
- This led the researchers to conclude that the outer layers of the GP5 and M proteins are not the key factors determining which cells the viruses can infect.
- This conclusion supports previous research indicating that other, minor envelope proteins may play a more significant role in determining cellular tropism.
Cite This Article
APA
Lu Z, Zhang J, Huang CM, Go YY, Faaberg KS, Rowland RR, Timoney PJ, Balasuriya UB.
(2012).
Chimeric viruses containing the N-terminal ectodomains of GP5 and M proteins of porcine reproductive and respiratory syndrome virus do not change the cellular tropism of equine arteritis virus.
Virology, 432(1), 99-109.
https://doi.org/10.1016/j.virol.2012.05.022 Publication
Researcher Affiliations
- Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546, United States.
MeSH Terms
- Animals
- Cell Line
- DNA, Complementary
- Equartevirus / genetics
- Equartevirus / physiology
- Horses
- Molecular Sequence Data
- Porcine respiratory and reproductive syndrome virus / genetics
- Protein Structure, Tertiary
- Recombination, Genetic
- Sequence Analysis, DNA
- Swine
- Viral Envelope Proteins / genetics
- Viral Envelope Proteins / metabolism
- Viral Matrix Proteins / genetics
- Viral Matrix Proteins / metabolism
- Viral Tropism
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