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JAC Advance Access originally published online on May 29, 2003
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Journal of Antimicrobial Chemotherapy (2003) 52, 8-10
© 2003 The British Society for Antimicrobial Chemotherapy

Leading Article

Antiviral function of pyrrolidine dithiocarbamate against influenza virus: the inhibition of viral gene replication and transcription

Noboru Uchide* and Kunio Ohyama

Department of Biochemistry, School of Pharmacy, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan

Keywords: influenza virus, apoptosis, antiviral

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   Inhibition of influenza virus-induced apoptosis by pyrrolidine dithiocarbamate through antiviral activity: role of reactive oxygen species in apoptosis
 
The pathogenesis of influenza virus infection involves virus replication in epithelial cells of the respiratory tract and the degeneration of infected cells resulting from subsequent events.1 Influenza virus induces cellular degeneration following infection of cultured cells in vitro, and the cytopathic effect (CPE) occurs principally through apoptotic cell death.1–10 Influenza virus replication is an essential process for the induction of apoptosis;3–6 however, the precise mechanism of influenza virus-induced apoptosis is unclear. Recently, several reports have described the effect of antioxidants such as pyrrolidine dithiocarbamate (PDTC), N-acetyl-L-cysteine (NAC) and 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox) on influenza virus-induced apoptosis in terms of the involvement of reactive oxygen species (ROS) in a possible mechanism of apoptosis induction (Table 1).3,7–9,11,12


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  		Table 1..  Effects of several chemical agents on influenza virus-induced CPE and their antioxidant properties and antiviral activities
 
Early studies revealed that the effect of antioxidants on CPE has been . . . [Full Text of this Article]


   Inhibition of influenza virus gene replication and transcription by PDTC: potential antiviral drugs for therapy of influenza
 

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