Arginine inactivates human herpesvirus 2 and inhibits genital herpesvirus infection
- Authors:
- Keiko Ikeda
- Hisashi Yamasaki
- Sawako Minami
- Yukiko Suzuki
- Kazuko Tsujimoto
- Yoshihisa Sekino
- Hiroshi Irie
- Tsutomu Arakawa
- A. Hajime Koyama
View Affiliations
Affiliations: Department of Cellular and Molecular Medicine, Division of Virology, Wakayama Medical University Graduate School of Medicine, Wakayama 641-8509, Japan, Department of Reproductive and Developmental Medicine, Division of Reproductive Medicine, Wakayama Medical University Graduate School of Medicine, Wakayama 641-8509, Japan, School of Health and Nursing Science, Wakayama Medical University, Wakayama 641-8509, Japan, Wakayama Shin-ai Women's Junior College, Wakayama 640-0341, Japan, Department of Anatomy, School of Medicine, Teikyo University, Itabashi 173-8605, Japan, Department of Sport and Medical Science, School of Medical Technology, Teikyo University, Itabashi 173-8605, Japan, Alliance Protein Laboratories, Thousand Oaks, CA 91360, USA
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Published online on: October 4, 2012
https://doi.org/10.3892/ijmm.2012.1149
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Pages: 1307-1312
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Abstract
Arginine, among the amino acids, has demonstrated unique properties, including suppression of protein-protein interactions and virus inactivation. We investigated the effects of arginine on the infectivity of human herpesvirus 2 (HHV-2) and the potential application of arginine as a chemotherapeutic agent against genital herpes. Arginine directly inactivated HHV-2 and characterization of the inactivation demonstrated that 1 M arginine at pH 4.3 inactivated the virus more efficiently compared to 0.1 M citrate or 1 M sodium chloride, indicating that neither acidic pH nor ionic strength alone is sufficient for virus inactivation. The effect of arginine was rapid and concentration-dependent. Although virus inactivation was efficient at an acidic pH, arginine inactivated the virus even at a neutral pH, provided that a higher arginine concentration and prolonged incubation time were used. In addition, arginine suppressed the multiplication of HHV-2 under the conditions at which its effect on cell viability was insignificant. Pilot mouse model studies revealed a marked suppression of death by arginine when the mice were infected with HHV-2 through the vaginal route, followed by an intermittent application of acidic arginine by vaginal instillation.
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