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Journal of Virology, February 2006, p. 1214-1221, Vol. 80, No. 3
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.3.1214-1221.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The Complete Genome Sequence of Herpesvirus Papio 2 (Cercopithecine Herpesvirus 16) Shows Evidence of Recombination Events among Various Progenitor Herpesviruses{dagger}

Shaun D. Tyler1 and Alberto Severini1,2*

National Microbiology Laboratory, Public Health Agency of Canada,1 Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada2

Received 2 August 2005/ Accepted 5 November 2005

We have sequenced the entire genome of herpesvirus papio 2 (HVP-2; Cercopithecine herpesvirus 16) strain X313, a baboon herpesvirus with close homology to other primate alphaherpesviruses, such as SA8, monkey B virus, and herpes simplex virus (HSV) type 1 and type 2. The genome of HVP-2 is 156,487 bp in length, with an overall GC content of 76.5%. The genome organization is identical to that of the other members of the genus Simplexvirus, with a long and a short unique region, each bordered by inverted repeats which end with an "a" sequence. All of the open reading frames detected in this genome were homologous and colinear with those of SA8 and B virus. The HSV gene RL1 ({gamma}134.5; neurovirulence factor) is not present in HVP-2, as is the case for SA8 and B virus. The HVP-2 genome is 85% homologous to its closest relative, SA8. However, segment-by-segment bootstrap analysis of the genome revealed at least two regions that display closer homology to the corresponding sequences of B virus. The first region comprises the UL41 to UL44 genes, and the second region is located within the UL36 gene. We hypothesize that this localized and defined shift in homology is due to recombination events between an SA8-like progenitor of HVP-2 and a herpesvirus species more closely related to the B virus. Since some of the genes involved in these putative recombination events are determinants of virulence, a comparative analysis of their function may provide insight into the pathogenic mechanism of simplexviruses.

* Corresponding author. Mailing address: National Microbiology Laboratory, Canadian Science Centre for Human and Animal Health, 1015 Arlington Street, Winnipeg, Manitoba R3E 3R2, Canada. Phone: (204) 789-6022. Fax: (204) 789-2140. E-mail: Alberto_Severini{at}phac-aspc.gc.ca.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, February 2006, p. 1214-1221, Vol. 80, No. 3
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.3.1214-1221.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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