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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 The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.
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
Citations
This article has been cited 13 times.- Thieulent CJ, Sarkar S, Carossino M, Bhowmik M, Zhu H, Balasuriya UBR. Cell Surface Vimentin Is an Attachment Factor That Facilitates Equine Arteritis Virus Infection In Vitro. Viruses 2026 Jan 15;18(1).
- Li Y, Wang Y, Pei X, Chen S, Jing Y, Wu Y, Ma Z, Li Z, Zheng Z, Feng Y, Xu L, Liu X, Guo X, Zheng H, Xiao S. A chimeric strain of porcine reproductive and respiratory syndrome virus 2 derived from HP-PRRSV and NADC30-like PRRSV confers cross-protection against both strains. Vet Res 2024 Oct 7;55(1):132.
- Zhang H, Duan K, Du Y, Xiao S, Fang L, Zhou Y. One-Step Assembly of a PRRSV Infectious cDNA Clone and a Convenient CRISPR/Cas9-Based Gene-Editing Technology for Manipulation of PRRSV Genome. Viruses 2023 Aug 26;15(9).
- Su CM, Rowland RRR, Yoo D. Recent Advances in PRRS Virus Receptors and the Targeting of Receptor-Ligand for Control. Vaccines (Basel) 2021 Apr 7;9(4).
- Chaudhari J, Vu HLX. Porcine Reproductive and Respiratory Syndrome Virus Reverse Genetics and the Major Applications. Viruses 2020 Oct 31;12(11).
- Neuman BW, Buchmeier MJ. Supramolecular Architecture of the Coronavirus Particle. Adv Virus Res 2016;96:1-27.
- Han M, Yoo D. Engineering the PRRS virus genome: updates and perspectives. Vet Microbiol 2014 Dec 5;174(3-4):279-295.
- Butler JE, Lager KM, Golde W, Faaberg KS, Sinkora M, Loving C, Zhang YI. Porcine reproductive and respiratory syndrome (PRRS): an immune dysregulatory pandemic. Immunol Res 2014 Aug;59(1-3):81-108.
- Balasuriya UB, Zhang J, Go YY, MacLachlan NJ. Experiences with infectious cDNA clones of equine arteritis virus: lessons learned and insights gained. Virology 2014 Aug;462-463:388-403.
- Yang M, Xiang Q, Zhang X, Li X, Sylla S, Ding Z. RNA interference targeting nucleocapsid protein inhibits porcine reproductive and respiratory syndrome virus replication in Marc-145 cells. J Microbiol 2014 Apr;52(4):333-9.
- Bailey AL, Lauck M, Weiler A, Sibley SD, Dinis JM, Bergman Z, Nelson CW, Correll M, Gleicher M, Hyeroba D, Tumukunde A, Weny G, Chapman C, Kuhn JH, Hughes AL, Friedrich TC, Goldberg TL, O'Connor DH. High genetic diversity and adaptive potential of two simian hemorrhagic fever viruses in a wild primate population. PLoS One 2014;9(3):e90714.
- Balasuriya UB, Go YY, MacLachlan NJ. Equine arteritis virus. Vet Microbiol 2013 Nov 29;167(1-2):93-122.
- Thaa B, Sinhadri BC, Tielesch C, Krause E, Veit M. Signal peptide cleavage from GP5 of PRRSV: a minor fraction of molecules retains the decoy epitope, a presumed molecular cause for viral persistence. PLoS One 2013;8(6):e65548.
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