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Journal of Virology, August 2004, p. 8878-8884, Vol. 78, No. 16
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.16.8878-8884.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Expression in a Recombinant Murid Herpesvirus 4 Reveals the In Vivo Transforming Potential of the K1 Open Reading Frame of Kaposi's Sarcoma-Associated Herpesvirus

Jill Douglas,1 Bernadette Dutia,1 Susan Rhind,2 James P. Stewart,3 and Simon J. Talbot1*

Centre for Infectious Diseases,1 Department of Veterinary Pathology, University of Edinburgh, Edinburgh,2 Department of Medical Microbiology, University of Liverpool, Liverpool, United Kingdom3

Received 19 January 2004/ Accepted 2 April 2004

Murid herpesvirus 4 (commonly called MHV-68) is closely related to Kaposi's sarcoma-associated herpesvirus (KSHV) and provides an excellent model system for investigating gammaherpesvirus-associated pathogenesis. MHV-76 is a naturally occurring deletion mutant of MHV-68 that lacks 9,538 bp of the left end of the unique portion of the genome encoding nonessential pathogenesis-related genes. The KSHV K1 protein has been shown to transform rodent fibroblasts in vitro and common marmoset T lymphocytes in vivo. Using homologous recombination techniques, we successfully generated recombinants of MHV-76 that encode green fluorescent protein (MHV76-GFP) and KSHV K1 (MHV76-K1). The replication of MHV76-GFP and MHV76-K1 in cell culture was identical to that of MHV-76. However, infection of BALB/c mice via the intranasal route revealed that MHV76-K1 replicated to a 10-fold higher titer than MHV76-GFP in the lungs at day 5 postinfection (p.i.). We observed type 2 pneumocyte proliferation in areas of consolidation and interstitial inflammation of mice infected with MHV76-K1 at day 10 p.i. MHV76-K1 established a 2- to 3-fold higher latent viral load than MHV76-GFP in the spleens of infected mice on days 10 and 14 p.i., although this was 10-fold lower than that established by wild-type MHV-76. A salivary gland tumor was present in one of four mice infected with MHV76-K1, as well as an increased inflammatory response in the lungs at day 120 p.i. compared with that of mice infected with MHV-76 and MHV76-GFP.

* Corresponding author. Mailing address: Centre for Infectious Diseases, University of Edinburgh, R(D)SVS, Summerhall, Edinburgh EH9 1QH, United Kingdom. Phone: 44 131 6507938. Fax: 44 131 6506511. E-mail: stalbot{at}ed.ac.uk.

Journal of Virology, August 2004, p. 8878-8884, Vol. 78, No. 16
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.16.8878-8884.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Brinkmann, M. M., Schulz, T. F. (2006). Regulation of intracellular signalling by the terminal membrane proteins of members of the Gammaherpesvirinae.. J. Gen. Virol. 87: 1047-1074 [Abstract] [Full Text]  


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