|LU, ZHENGCHUN - University Of Kentucky|
|ZHANG, JIANQIANG - University Of Kentucky|
|HUANG, CHENGJIN - Fort Dodge Animal Health|
|GO, YUN YOUNG - Fort Dodge Animal Health|
|ROWLAND, RAYMOND - Kansas State University|
|TIMONEY, PETER - University Of Kentucky|
|BALASURIYA, UDENI - University Of Kentucky|
Submitted to: Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/27/2012
Publication Date: 6/26/2012
Citation: Lu, Z., Zhang, J., Huang, C.M., Go, Y.Y., Faaberg, K.S., Rowland, R.R., Timoney, P.J., Balasuriya, U.B. 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.
Interpretive Summary: Porcine reproductive and respiratory syndrom virus (PRRSV) is the foremost disease of swine in the United States. In this report, infectious viruses were made of family co-member equine arteritis virus with proteins containing PRRSV amino acids (ectodomains of GP5 and M) that are thought to influence cell tropism. It was discovered that three chimeric viruses were able to infect EAV susceptible cells but not PRRSV susceptible cells. The basic knowledge concerning the molecular interaction requirements of the virus in order to infect host cells and the development of infectious engineered chimeras may be utilized to produce second generation vaccines to aid in the control of PRRS.
Technical Abstract: Equine arteritis virus (EAV) and porcine reproductive and respiratory syndrome virus (PRRSV) are members of family Arteriviridae; they share many biological properties but differ significantly in cellular tropism. Using an infectious cDNA clone of EAV, we engineered a panel of six chimeric viruses by exchanging the N-terminal ectodomains and/or full-lengths of the two major envelope proteins (GP5 and M) from PRRSV. The recombinant viruses expressing the N-terminal ectodomain of PRRSV GP5 alone or M alone or together (GP5ecto, Mecto and GP5&Mecto, respectively) in the EAV backbone were viable and genetically stable. Compared to the parental virus, these three chimeric viruses produced lower titers and smaller plaque sizes indicating that they have a compromised phenotype. The three chimeric viruses could only infect EAV susceptible cell lines but not PRRSV susceptible cells. Therefore, the two major envelope proteins may not be determining factors in the cellular tropism of EAV and other arteriviruses.