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Journal of Virology, November 2008, p. 11140-11151, Vol. 82, No. 22
0022-538X/08/$08.00+0     doi:10.1128/JVI.00269-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Identification of Postentry Restrictions to Mason-Pfizer Monkey Virus Infection in New World Monkey Cells{triangledown}

William E. Diehl,1,2 Elizabeth Stansell,1,2,{dagger} Shari M. Kaiser,3,{ddagger} Michael Emerman,3 and Eric Hunter1,2*

Emory Vaccine Center, Yerkes National Primate Research Center, Emory University, Atlanta, Georgia 30329,1 Department of Pathology, Emory University, 1364 Clifton Road N.E., Atlanta, Georgia 30322,2 Department of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 981093

Received 6 February 2008/ Accepted 8 September 2008

TRIM5{alpha} has been shown to be a major postentry determinant of the host range for gammaretroviruses and lentiviruses and, more recently, spumaviruses. However, the restrictive potential of TRIM5{alpha} against other retroviruses has been largely unexplored. We sought to determine whether or not Mason-Pfizer monkey virus (M-PMV), a prototype betaretrovirus isolated from rhesus macaques, was sensitive to restriction by TRIM5{alpha}. Cell lines from both Old World and New World primate species were screened for their susceptibility to infection by vesicular stomatitis virus G protein pseudotyped M-PMV. All of the cell lines tested that were established from Old World primates were found to be susceptible to M-PMV infection. However, fibroblasts established from three New World monkey species specifically resisted infection by this virus. Exogenously expressing TRIM5{alpha} from either tamarin or squirrel monkeys in permissive cell lines resulted in a block to M-PMV infection. Restriction in the resistant cell line of spider monkey origin was determined to occur at a postentry stage. However, spider monkey TRIM5{alpha} expression in permissive cells failed to restrict M-PMV infection, and interference with endogenous TRIM5{alpha} in the spider monkey fibroblasts failed to relieve the block to infectivity. Our results demonstrate that TRIM5{alpha} specificity extends to betaretroviruses and suggest that New World monkeys have evolved additional mechanisms to restrict the infection of at least one primate betaretrovirus.

* Corresponding author. Mailing address: 954 Gatewood Rd. N.E., Atlanta, GA 30329. Phone: (404) 727-8487. Fax: (404) 727-9316. E-mail: eric.hunter2{at}emory.edu

{triangledown} Published ahead of print on 17 September 2008.

{dagger} Present address: New England Primate Research Center, Harvard University, One Pine Hill Drive, P.O. Box 9102, Southborough, MA 01772.

{ddagger} Present address: Institute for Systems Biology, Seattle, WA 98103.

Journal of Virology, November 2008, p. 11140-11151, Vol. 82, No. 22
0022-538X/08/$08.00+0     doi:10.1128/JVI.00269-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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