This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jung, Y. T. Articles by Kozak, C. A. Search for Related Content PubMed PubMed Citation Articles by Jung, Y. T. Articles by Kozak, C. A.

 Previous Article  |  Next Article 

Journal of Virology, November 2004, p. 12189-12197, Vol. 78, No. 22
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.22.12189-12197.2004

Novel Host Range and Cytopathic Variant of Ecotropic Friend Murine Leukemia Virus

Yong Tae Jung, Tiyun Wu, and Christine A. Kozak^*

Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland

Received 23 March 2004/ Accepted 1 July 2004

A variant ecotropic Friend murine leukemia virus, F-S MLV, is capable of inducing the formation of large multinucleated syncytia in Mus dunni cells. This cytopathicity resembles that of Spl574 MLV, a novel variant recently isolated from the spleen of a Mus spicilegus mouse neonatally inoculated with Moloney MLV. F-S MLV is an N-tropic Friend MLV that also has the unusual ability to infect hamster cells, which are normally resistant to mouse ecotropic MLVs. Syncytium induction by both F-S MLV and Spl574 is accompanied by the accumulation of large amounts of unintegrated viral DNA, a hallmark of pathogenic retroviruses, but not previously reported for mouse ecotropic gammaretroviruses. Sequencing and site-specific mutagenesis determined that the syncytium-inducing phenotype of F-S MLV can be attributed to a single amino acid substitution (S84A) in the VRA region of the viral env gene. This site corresponds to that of the single substitution previously shown to be responsible for the cytopathicity of Spl574, S82F. The S84A substitution in F-S MLV also contributes to the ability of this virus to infect hamster cells, but Spl574 MLV is unable to infect hamster cells. Because this serine residue is one of the critical amino acids that form the CAT-1 receptor binding site, and because M. dunni and hamster cells have variant CAT-1 receptors, these results suggest that syncytium formation as well as altered host range may be a consequence of altered interaction between virus and receptor.

Present address: Department of Microbiology, Dankook University, Cheonan, Korea 330-714.

This article has been cited by other articles:

• Yan, Y., Kozak, C. A. (2008). Novel Postentry Resistance to AKV Ecotropic Mouse Gammaretroviruses in the African Pygmy Mouse, Mus minutoides. J. Virol. 82: 6120-6129 [Abstract] [Full Text]  
• Yoshii, H., Kamiyama, H., Amanuma, H., Oishi, K., Yamamoto, N., Kubo, Y. (2008). Mechanisms underlying glycosylation-mediated loss of ecotropic receptor function in murine MDTF cells and implications for receptor evolution. J. Gen. Virol. 89: 297-305 [Abstract] [Full Text]  
• Rainey, G. J. A., Coffin, J. M. (2006). Evolution of Broad Host Range in Retroviruses Leads to Cell Death Mediated by Highly Cytopathic Variants. J. Virol. 80: 562-570 [Abstract] [Full Text]