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Journal of Virology, June 2003, p. 7101-7105, Vol. 77, No. 12
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.12.7101-7105.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Promyelocytic Leukemia Protein Mediates Interferon-Based Anti-Herpes Simplex Virus 1 Effects

Ana V. Chee,1 Pascal Lopez,1 Pier Paolo Pandolfi,2 and Bernard Roizman1*

The Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, Chicago, Illinois 60637,1 Molecular Biology Program and Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York 100212

Received 8 January 2003/ Accepted 19 March 2003

Herpes simplex virus (HSV) 1 disaggregates the nuclear domain 10 (ND10) nuclear structures and disperses its organizing promyelocytic leukemia protein (PML). An earlier report showed that ectopic overexpression of PML precludes the disaggregation of ND10 but has no effect on viral replication. PML has been reported to mediate the effects of interferon (IFN) and viral mutants lacking ICP0 ({Delta}{alpha}0 mutants). To test the hypothesis that HSV disaggregates ND10 structures and disperses PML to preclude IFN-mediated antiviral effects, we tested the accumulation of viral proteins and virus yields from murine PML+/+ and PML-/- cells mock treated or exposed to IFN-{alpha}, IFN-{gamma}, or both and infected with the wild-type or {Delta}{alpha}0 mutant virus. We report the following results. (i) The levels of growth of wild-type and mutant viruses and of accumulation of viral proteins were not significantly different in untreated PML+/+ and PML-/- cells. (ii) Major effects of IFN-{alpha} and -{gamma} were observed in PML+/+ cells infected with the {Delta}{alpha}0 mutant virus, and more minor effects were observed in cells infected with the wild-type virus. The effects of the IFNs on either wild-type or the mutant virus in PML-/- cells were minimal. (iii) The mixture of IFN-{alpha} and -{gamma} was more effective than either IFN alone, but again, the effect was more drastic in PML+/+ cells than in PML-/- cells. We concluded that the anti-HSV state induced by exogenous IFN is mediated by PML and that the virus targets the ND10 structures and disseminates PML in order to preclude the establishment of the antiviral state induced by IFNs.

* Corresponding author. Mailing address: The Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, 910 E. 58th St., Chicago, IL 60637. Phone: (773) 702-1898. Fax: (773) 702-1631. E-mail: bernard{at}delphi.bsd.uchicago.edu.

Journal of Virology, June 2003, p. 7101-7105, Vol. 77, No. 12
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.12.7101-7105.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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