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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Avian Disease and Oncology Research » Research » Publications at this Location » Publication #324611

Research Project: EMPLOYING GENOMICS, EPIGENETICS, AND IMMUNOGENETICS TO CONTROL DISEASES INDUCED BY AVIAN TUMOR VIRUSES

Location: Avian Disease and Oncology Research

Title: In vitro characterization of felid herpesvirus 1 (FHV-1) mutants generated by recombineering in a recombinant BAC vector

Author
item TAI, SHELDON S-H - Michigan State University
item HOLZ, CARINE - Michigan State University
item ENGSTROM, MICHAEL - Michigan State University
item Cheng, Hans
item MAES, ROGER - Michigan State University

Submitted to: Virus Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/4/2016
Publication Date: 5/6/2016
Publication URL: http://handle.nal.usda.gov/10113/62755
Citation: Tai, S., Holz, C., Engstrom, M.D., Cheng, H.H., Maes, R.K. 2016. In vitro characterization of felid herpesvirus 1 (FHV-1) mutants generated by recombineering in a recombinant BAC vector. Virus Research. 221(2016):15-22. doi: 10.1016/j.virusres.2016.05.001.

Interpretive Summary: Felid herpesvirus 1 (FHV1) accounts for ~50% of all diagnosed viral upper respiratory disease in domestic cats, and is also a significant cause of ocular diseases in cats worldwide. Thus, it is of both scientific and veterinary interest to control this virus. Using a molecular clone, specific genes were deleted from the viral genome and tested for virulence. The results yield specific recombinant viruses that provide critical information on viral gene function and may serve as novel vaccines. Furthermore, this information provides a useful model for other herpesvirus-induced diseases such as Marek’s disease in poultry.

Technical Abstract: Felid herpesvirus 1 (FHV-1) mutants were constructed using two-step Red-mediated recombination techniques based on a virulent full-length FHV-1 BAC clone. The individual mutant viruses generated were deficient in glycoprotein C (gC), glycoprotein E (gE),US3 serine/threonine protein kinase (PK), or both gE and thymidine kinase (TK). The gC- mutant virus produced plaques that were similar in size to those resulting from infection with the C-27 parent strain. In contrast, the gE-, PK-, and gE-PK-deletion mutants produced plaques that were significantly smaller Multistep in vitro growth kinetics of the gE-, PK-, and gE-PK-viruses were slightly delayed compared to those of the C-27 parent strain. Peak progeny titers of these three mutants were approximately 10-foldlower than those generated with the C-27 strain. There was no delay in the growth kinetics of the gC-mutant, but the progeny virus titer obtained with this mutant was at least 3 logs lower compared to the parental strain titer. Based upon their in vitro characteristics, these mutants will be useful for the development of novel immunization strategies against this important feline pathogen.