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Journal of Virology, June 2003, p. 6167-6177, Vol. 77, No. 11
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.11.6167-6177.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Complete Sequence and Comparative Analysis of the Genome of Herpes B Virus (Cercopithecine Herpesvirus 1) from a Rhesus Monkey

Ludmila Perelygina,1* Li Zhu,1 Holley Zurkuhlen,1 Ryan Mills,2 Mark Borodovsky,2 and Julia K. Hilliard1

Viral Immunology Center, Department of Biology, Georgia State University, Atlanta, Georgia 30303,1 School of Biology and School of Biomedical Engineering, Georgia Institute of Technology, Atlanta, Georgia 30332-023022

Received 19 November 2002/ Accepted 3 March 2003

The complete DNA sequence of herpes B virus (Cercopithecine herpesvirus 1) strain E2490, isolated from a rhesus macaque, was determined. The total genome length is 156,789 bp, with 74.5% G+C composition and overall genome organization characteristic of alphaherpesviruses. The first and last residues of the genome were defined by sequencing the cloned genomic termini. There were six origins of DNA replication in the genome due to tandem duplication of both oriL and oriS regions. Seventy-four genes were identified, and sequence homology to proteins known in herpes simplex viruses (HSVs) was observed in all cases but one. The degree of amino acid identity between B virus and HSV proteins ranged from 26.6% (US5) to 87.7% (US15). Unexpectedly, B virus lacked a homolog of the HSV {gamma}134.5 gene, which encodes a neurovirulence factor. Absence of this gene was verified in two low-passage clinical isolates derived from a rhesus macaque and a zoonotically infected human. This finding suggests that B virus most likely utilizes mechanisms distinct from those of HSV to sustain efficient replication in neuronal cells. Despite the considerable differences in G+C content of the macaque and B virus genes (51% and 74.2%, respectively), codons used by B virus are optimal for the tRNA population of macaque cells. Complete sequence of the B virus genome will certainly facilitate identification of the genetic basis and possible molecular mechanisms of enhanced B virus neurovirulence in humans, which results in an 80% mortality rate following zoonotic infection.

* Corresponding author. Mailing address: Viral Immunology Center, Department of Biology, Georgia State University, MSC 8L0389, 33 Gilmer St. SE, Unit 8, Atlanta, GA 30303-3088. Phone: (404) 651-0002. Fax: (404) 651-0812. E-mail: biolmp{at}panther.gsu.edu.

Journal of Virology, June 2003, p. 6167-6177, Vol. 77, No. 11
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.11.6167-6177.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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