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Ras controls herpes virus penetration in cells

Tudor Toma

Genome Biology 2001, 2:spotlight-20010723-01  doi:10.1186/gb-spotlight-20010723-01

The electronic version of this article is the complete one and can be found online at:

Published:23 July 2001

© 2001 BioMed Central Ltd

Research news

The molecular basis of host-cell permissiveness to herpes simplex viruses (HSV) is under intense investigation because of HSV prevalence in human disease and its potential use as an anti-cancer therapeutic. In the August issue of Nature Cell Biology, Faris Farassati and colleagues from the University of Calgary, Alberta, Canada show for the first time that oncogenes in Ras signalling pathway are essential in host-cell permissiveness to herpes simplex virus 1.

Farassati et al. exposed to the HSV-1 virus (strain F) parental Swiss mouse embryo fibroblasts (NIH-3T3 cells) and NIH-3T3 cells transformed with the oncogenes v-erbB, sos or ras - all activators of the Ras signaling pathway. Permissiveness to HSV-1 infection (assessed by induction of cytopathic effects, viral protein synthesis and virus output) was significantly increased in NIH-3T3 cells transformed with Ras activators. In addition inhibitors of the Ras signaling pathway, such as farnesyl transferase inhibitor 1 and PD98059, effectively suppressed HSV-1 infection of ras-transformed cells (Nat Cell Biol 2001, 3:745-750).

These results may provide models for treating herpes virus infections, for example by downregulating the Ras pathway in infected cells. The authors also speculate that the association of herpes infections with cancers may be due to enhanced HSV permissiveness of cancer cells with an activated Ras signaling pathway.


  1. [ ] webcite

    Farassati F, Yang A, Lee PWK: Oncogenes in Ras signalling pathway dictate host-cell permissiveness to herpes simplex virus 1. Nat Cell Biol 2001, 3:745-750.

  2. [ ] webcite

    University of Calgary