Oakes J E, Rosemond-Hornbeak H
Infect Immun. 1978 Aug;21(2):489-95. doi: 10.1128/iai.21.2.489-495.1978.
Young adult mice infected with 3 X 10(6) plaque-forming units of herpes simplex virus type 2 (HSV-2) died within 9 to 12 days after spread of the virus from the sites of infection to the spinal cord and brain. Administration of HSV-2-neutralizing antisera prepared in syngenic mice or in rabbits inhibited spread of the virus from the footpad of infected animals and prevented death. A single intraperitoneal inoculum of antiserum (virus-neutralizing titer of 1:128) was effective in protecting mice when the antiserum was given at 8 to 48 h, but not at 72 h, after virus inoculation. Immune sera absorbed with HSV-2-infected cells no longer protected mice from subcutaneous infection, whereas absorption with noninfected cells had no effect. Thus, HSV-2-specific antibodies appeared to be responsible for the protection observed. If the mice were given a sublethal dose of irradiation (390 rads) at 24 h before antibody transfer, protection was no longer obtained. This suggested that the mechanism of protection probably was not solely due to in vivo neutralization of virus, but required the participation of a radiosensitive component which has not yet been defined.
感染3×10⁶个2型单纯疱疹病毒(HSV - 2)蚀斑形成单位的年轻成年小鼠,在病毒从感染部位扩散至脊髓和脑之后的9至12天内死亡。给同基因小鼠或兔子制备的HSV - 2中和抗血清,可抑制病毒从受感染动物的足垫扩散,并防止死亡。当在病毒接种后8至48小时给予抗血清(病毒中和效价为1:128)时,单次腹腔接种抗血清可有效保护小鼠,但在72小时给予则无效。用HSV - 2感染细胞吸收的免疫血清不再能保护小鼠免受皮下感染,而用未感染细胞吸收则无影响。因此,HSV - 2特异性抗体似乎是观察到的保护作用的原因。如果在抗体转移前24小时给小鼠给予亚致死剂量的辐射(390拉德),则不再能获得保护。这表明保护机制可能不仅仅是由于体内病毒中和,还需要一种尚未明确的放射敏感成分的参与。