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Journal of General Virology (2000), 81, 1763-1771.
© 2000 Society for General Microbiology

Animal: DNA Viruses

The role of the UL41 gene of herpes simplex virus type 1 in evasion of non-specific host defence mechanisms during primary infection

Tatsuo Suzutani1, Masayoshi Nagamine1, Taiichiro Shibaki1, Masahiro Ogasawara1, Itsuro Yoshida1, Toru Daikoku2, Yukihiro Nishiyama2 and Masanobu Azuma1

Department of Microbiology, Asahikawa Medical College, Asahikawa 078-8510, Japan1
Laboratory of Virology, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya 466-8550, Japan2

Author for correspondence: Tatsuo Suzutani. Fax +81 166 68 2399. e-mail suzutani{at}asahikawa-med.ac.jp

The UL41 gene product (vhs) of herpes simplex virus (HSV) is packaged in the virion, and mediates host protein synthesis shutoff at the early stage of the virus replication cycle. In order to clarify the role of vhs in virus replication and virulence, we isolated a completely UL41-deficient mutant (the VR{Delta}41 strain) and its revertant (the VR{Delta}41R strain). In the mouse encephalitis model, the replication of strain VR{Delta}41 was inhibited after 2 days post-infection, resulting in low virulence, by {gamma}-ray-sensitive cells such as lymphocytes and/or neutrophils. The result suggested that some cytokines, produced in VR{Delta}41-inoculated brains, activate and induce the migration of {gamma}-ray-sensitive cells to the infection site. Therefore, cytokines produced by HSV-1-infected human cells were screened, and potent inductions of interleukin (IL)-1{beta}, IL-8 and macrophage inflammatory protein-1{alpha} by VR{Delta}41 infection were observed. Moreover, the VR{Delta}41 strain showed 20- and 5-fold higher sensitivity to interferon-{alpha} and -{beta} compared to the wild-type strain, respectively. These results indicate that one important role of vhs in vivo is evasion from non-specific host defence mechanisms during primary infection through suppression of cytokine production in HSV-infected cells and reduction of the anti-HSV activity of interferon-{alpha} and -{beta}.




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