Ito M, Barron A L
J Virol. 1974 Jun;13(6):1312-8. doi: 10.1128/JVI.13.6.1312-1318.1974.
The infectivity of herpes simplex virus type 1 (HSV-1) was inactivated after treatment with either concanavalin A (ConA) or periodate. Phytohemagglutinin, wheat germ agglutinin, pokeweed mitogen, and neuraminidase failed to inactivate the virus. The effect of ConA could be specifically inhibited or reversed by the addition of alpha-methyl-d-glucoside or alpha-methyl-d-mannoside. Evidence was obtained that HSV-1 inactivated by ConA could adsorb to host cells. Viral aggregation was not a major mechanism in the inactivation of HSV-1 by ConA. Under the experimental conditions employed, inactivation of HSV-1 was faster by ConA than by antiserum and less temperature dependent. A ConA-resistant fraction was detected which appeared to adsorb less quickly than untreated virus, and penetration of ConA-resistant fraction was strikingly slow. The presence of aggregates in the virus preparation did not appear to account for the ConA-resistant fraction. Inactivation of viral infectivity by ConA was obtained only with enveloped viruses, since HSV-1, HSV-2, pseudorabies, and vesicular stomatitis virus were inactivated and vaccinia and echovirus type 6 were not.
用伴刀豆球蛋白A(ConA)或高碘酸盐处理后,单纯疱疹病毒1型(HSV-1)的感染性被灭活。植物血凝素、麦胚凝集素、商陆有丝分裂原和神经氨酸酶未能使该病毒灭活。ConA的作用可通过添加α-甲基-D-葡萄糖苷或α-甲基-D-甘露糖苷而被特异性抑制或逆转。有证据表明,被ConA灭活的HSV-1可吸附到宿主细胞上。病毒聚集不是ConA灭活HSV-1的主要机制。在所采用的实验条件下,ConA使HSV-1灭活的速度比抗血清更快,且对温度的依赖性更小。检测到一个ConA抗性组分,其吸附速度似乎比未处理的病毒慢,并且ConA抗性组分的穿透非常缓慢。病毒制剂中聚集体的存在似乎不能解释ConA抗性组分。仅对有包膜病毒,ConA可使病毒感染性灭活,因为HSV-1、HSV-2、伪狂犬病病毒和水疱性口炎病毒被灭活,而痘苗病毒和6型艾柯病毒未被灭活。