The LEM Domain Proteins Emerin and LAP2a Are Dispensable for Human Immunodeficiency Virus Type 1 and Murine Leukemia Virus Infections

• Published in: Journal of virology 2008-06, Vol.82 (12), p.5860-5868
• Main Authors: MULKY, Alok, COHEN, Tatiana V, KOZLOV, Serguei V, KORBEI, Barbara, FOISNER, Roland, STEWART, Colin L, KEWALRAMANI, Vineet N
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Human immunodeficiency virus 1; Microbiology; Miscellaneous; Murine leukemia virus; Virology
• ISSN: 0022-538X; 1098-5514

The human nuclear envelope proteins emerin and lamina-associated polypeptide 2a (LAP2a) 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, LAP2a, or both emerin and LAP2a. We observed HIV-1 and MLV infectivity in mouse embryonic fibroblasts (MEFs) from emerin knockout, LAP2a knockout, or emerin and LAP2a double knockout mice to be comparable in infectivity to wild-type littermate-derived MEFs, indicating that both emerin and LAP2a 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 LAP2a are not required for the early replication of HIV-1 and MLV in mouse or human cells.