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Journal of Virology, June 2008, p. 5860-5868, Vol. 82, No. 12
0022-538X/08/$08.00+0 doi:10.1128/JVI.00076-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
Are Dispensable for Human Immunodeficiency Virus Type 1 and Murine Leukemia Virus Infections
,
HIV Drug Resistance Program,1 Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, Maryland 21702,2 Max F. Perutz Laboratories, Department of Medical Biochemistry, Medical University of Vienna, A-1030 Vienna, Austria3
Received 11 January 2008/ Accepted 31 March 2008
The human nuclear envelope proteins emerin and lamina-associated polypeptide 2
(LAP2
) have been proposed to aid in the early replication steps of human immunodeficiency virus type 1 (HIV-1) and murine leukemia virus (MLV). However, whether these factors are essential for HIV-1 or MLV infection has been questioned. Prior studies in which conflicting results were obtained were highly dependent on RNA interference-mediated gene silencing. To shed light on these contradictory results, we examined whether HIV-1 or MLV could infect primary cells from mice deficient for emerin, LAP2
, or both emerin and LAP2
. We observed HIV-1 and MLV infectivity in mouse embryonic fibroblasts (MEFs) from emerin knockout, LAP2
knockout, or emerin and LAP2
double knockout mice to be comparable in infectivity to wild-type littermate-derived MEFs, indicating that both emerin and LAP2
were dispensable for HIV-1 and MLV infection of dividing, primary mouse cells. Because emerin has been suggested to be important for infection of human macrophages by HIV-1, we also examined HIV-1 transduction of macrophages from wild-type mice or knockout mice, but again we did not observe a difference in susceptibility. These findings prompted us to reexamine the role of human emerin in supporting HIV-1 and MLV infection. Notably, both viruses efficiently infected human cells expressing high levels of dominant-negative emerin. We thus conclude that emerin and LAP2
are not required for the early replication of HIV-1 and MLV in mouse or human cells.
Published ahead of print on 9 April 2008.
Supplemental material for this article may be found at http://jvi.asm.org/.
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