Antiviral effect of octyl gallate against DNA and RNA viruses

• Published in: Antiviral research 2007-02, Vol.73 (2), p.85-91
• Main Authors: Uozaki, Misao, Yamasaki, Hisashi, Katsuyama, Yukiko, Higuchi, Masanori, Higuti, Tomihiko, Koyama, A. Hajime
• Format: Article
• Language: English
• Subjects: Animals; Antibiotics. Antiinfectious agents. Antiparasitic agents; Antiviral agents; Antiviral Agents - pharmacology; Biological and medical sciences; Cell death; Cercopithecus aethiops; DNA Viruses - drug effects; DNA Viruses - physiology; Gallic acid; Gallic Acid - analogs & derivatives; Gallic Acid - pharmacology; Herpes simplex virus; Herpes simplex virus 1; Herpesvirus 1, Human - drug effects; Herpesvirus 1, Human - physiology; Medical sciences; Octyl gallate; Pharmacology. Drug treatments; Poliovirus; RNA Viruses - drug effects; RNA Viruses - physiology; Vero Cells; Vesicular stomatitis virus; Virus Replication - drug effects
• ISSN: 0166-3542; 1872-9096
• DOI: 10.1016/j.antiviral.2006.07.010

The effects of gallic acid (3,4,5-trihydroxybenzoic acid) and its alkyl esters on virus growth and virion infectivity were examined. All the compounds tested showed an inhibitory effect on the growth of herpes simplex virus type 1 (HSV-1) in HEp-2 or Vero cells. The antiviral activity of gallic acid alkyl esters was enhanced by increasing the number of carbon in the alkyl moieties of the compounds, reaching maximum at a carbon number of 12 (lauryl gallate), but both cytocidal activity and cytopathic effect of the compounds were also significantly increased simultaneously. Among these compounds, octyl gallate showed a marked antiviral effect with a relatively moderate cytotoxity. In addition, octyl gallate suppressed the multiplication of RNA viruses, such as vesicular stomatitis virus and poliovirus. Quantitative characterization of the HSV-1 infection in the presence of octyl gallate revealed that: (1) this reagent can directly inactivate HSV-1 (virucidal activity), (2) it suppresses both the intracellar multiplication and the release of the virus, (3) it selectively accelerates death of the virus-infected cells and (4) the addition of the reagent even at 6-h post infection completely abolishes the formation of progeny virus in the infected cells.