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Inserting a nuclear targeting signal into a replication- competent Moloney murine leukemia virus affects viral export and is not sufficient for cell cycle-independent infection

  1. Author:
    Seamon, J. A.
    Jones, K. S.
    Miller, C.
    Roth, M. J.

  2. Author Address

    Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Biochem, 975 Hoes Ln, Piscataway, NJ 08854 USA Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Biochem, Piscataway, NJ 08854 USA SAIC Frederick, Intramural Res Support Program, Frederick, MD 21702 USA Roth MJ Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Biochem, 975 Hoes Ln, Piscataway, NJ 08854 USA
    1. Year: 2002
  2. Journal: Journal of Virology
    1. 76
    2. 16
    3. Pages: 8475-8484
  4. Type of Article: Article
  1. Abstract:

    The effects of inserting reported nuclear localization signals (NLSs) into the Moloney marine leukemia virus (Mo-MuLV) integrase (IN) protein, within a replication-competent viral construct, were studied. In contrast to the virus harboring IN fused to the simian virus 40 (SV40) large T antigen NLS (SV40 NLS) (J. A. Seamon, M. Adams, S. Sengupta, and M. J. Roth, Virology 274:412-419, 2000), a codon-modified SV40 NILS was stably expressed during viral propagation. Incorporation of the codon-modified SV40 NLS into IN, however, altered the packaging of the Gag-Pol precursor in the virus; viral particles contained decreased levels of reverse transcriptase (RT) and IN. In addition, the virus showed delayed kinetics of viral DNA synthesis upon infection. A panel of infectious MuLVs containing alternative IN-NLS fusions was generated and assayed for cell cycle-independent infection. Viral infection with the NLS-tagged proteins, however, remained dependent on passage of the cells through mitosis. This finding has direct implications for engineering murine-based retroviral vectors for gene therapy.

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