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Journal of Virology, August 2007, p. 8149-8156, Vol. 81, No. 15
0022-538X/07/$08.00+0     doi:10.1128/JVI.00407-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Simian Varicella Virus Expresses a Latency-Associated Transcript That Is Antisense to Open Reading Frame 61 (ICP0) mRNA in Neural Ganglia of Latently Infected Monkeys{triangledown}

Yang Ou,1 Kara A. Davis,1 Vicki Traina-Dorge,2 and Wayne L. Gray1*

Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205,1 Tulane National Primate Research Center, Covington, Louisiana 704332

Received 26 February 2007/ Accepted 3 May 2007

Simian varicella virus (SVV) and varicella-zoster virus (VZV) are closely related alphaherpesviruses that cause varicella (chickenpox) in nonhuman primates and humans, respectively. After resolution of the primary disease, SVV and VZV establish latent infection of neural ganglia and may later reactivate to cause a secondary disease (herpes zoster). This study investigated SVV gene expression in neural ganglia derived from latently infected vervet monkeys. SVV transcripts were detected in neural ganglia, but not in liver or lung tissues, of latently infected animals. A transcript mapping to open reading frame (ORF) 61 (herpes simplex virus type 1 [HSV-1] ICP0 homolog) was consistently detected in latently infected trigeminal, cervical, and lumbar ganglia by reverse transcriptase PCR. Further analysis confirmed that this SVV latency-associated transcript (LAT) was oriented antisense to the gene 61 mRNA. SVV ORF 21 transcripts were also detected in 42% of neural ganglia during latency. In contrast, SVV ORF 28, 29, 31, 62, and 63 transcripts were not detected in ganglia, liver, or lung tissues of latently infected animals. The results demonstrate that viral gene expression is limited during SVV latency and that a LAT antisense to an ICP0 homolog is expressed. In this regard, SVV gene expression during latency is similar to that of HSV-1 and other neurotropic animal alphaherpesviruses but differs from that reported for VZV.

* Corresponding author. Mailing address: Dept. of Microbiology and Immunology, Slot 511, University of Arkansas for Medical Sciences, 4301 W. Markham St., Little Rock, AR 72205. Phone: (501) 686-5187. Fax: (501) 686-5359. E-mail: graywaynel{at}uams.edu

{triangledown} Published ahead of print on 16 May 2007.

Journal of Virology, August 2007, p. 8149-8156, Vol. 81, No. 15
0022-538X/07/$08.00+0     doi:10.1128/JVI.00407-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Wang, L., Sommer, M., Rajamani, J., Arvin, A. M. (2009). Regulation of the ORF61 Promoter and ORF61 Functions in Varicella-Zoster Virus Replication and Pathogenesis. J. Virol. 83: 7560-7572 [Abstract] [Full Text]  


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