Monma Y, Kawana T, Shimizu F
Department of Pediatric Dentistry, Tohoku University School of Dentistry, Sendai, Japan.
Antiviral Res. 1997 Aug;35(3):131-8. doi: 10.1016/s0166-3542(97)00021-1.
Herpes simplex virus (HSV) causes herpes genitalis, primary gingivostomatitis and recurrent herpes labialis. In order to elucidate in vivo mechanisms by which PSK, a biological response modifier, exerts a protective effect against HSV infection, we used an in vitro system to study whether PSK inactivated infectivity of HSV-type 1 (HSV-1) and HSV-type 2 (HSV-2) isolated from patients with herpes genitalis in addition to a laboratory-cultured strain of HSV type 1 (HSV-1-GC+). It was found that HSV-1-GC+ was inactivated by PSK in a dose dependent fashion of concentrations of PSK and virus titers. Concentrations of PSK as low as 0.31 mg/ml was shown to inactivate the infectivity of HSV-1-GC+. Inactivation required at least 30 min of incubation at 37 degrees C with maximal inactivation observed at 60 min incubation time. Similar to HSV-1-GC+, clinically isolated strains of HSV-2 were inactivated by PSK although clinically isolated strains of HSV-1 were resistant to PSK, compared with HSV-2. It was also shown that PSK-treated HSV retained the ability to adsorb to the cell membrane, but did not synthesize viral protein(s). These data illustrate that there is a biological difference in the sensitivity to PSK between HSV type 1 and type 2, and also suggest that PSK could inactivate HSV in lesions at peripheral sites of recurrent herpes.
单纯疱疹病毒（HSV）可引起生殖器疱疹、原发性龈口炎和复发性唇疱疹。为了阐明生物反应调节剂PSK对HSV感染发挥保护作用的体内机制，我们使用体外系统研究PSK是否能使从生殖器疱疹患者分离出的1型单纯疱疹病毒（HSV-1）和2型单纯疱疹病毒（HSV-2）以及实验室培养的1型单纯疱疹病毒株（HSV-1-GC+）的感染性失活。结果发现，HSV-1-GC+被PSK以PSK浓度和病毒滴度的剂量依赖性方式失活。低至0.31mg/ml的PSK浓度就能使HSV-1-GC+的感染性失活。失活需要在37℃孵育至少30分钟，在孵育60分钟时观察到最大失活。与HSV-1-GC+类似，临床分离的HSV-2毒株被PSK失活，尽管与HSV-2相比，临床分离的HSV-1毒株对PSK有抗性。还表明，经PSK处理的HSV保留了吸附到细胞膜的能力，但不能合成病毒蛋白。这些数据表明，HSV-1和HSV-2对PSK的敏感性存在生物学差异，也提示PSK可能使复发性疱疹外周部位病损中的HSV失活。
