Kunder S C, Kelly K M, Morahan P S
Department of Microbiology and Immunology, Medical College of Pennsylvania, Philadelphia 19129.
Antiviral Res. 1993 Jun;21(2):129-39. doi: 10.1016/0166-3542(93)90049-o.
The role of interferon alpha/beta (IFN) induction by the immunomodulators pICLC and CL246,738 was investigated in CD-1 mice infected with murine cytomegalovirus (MCMV) or herpes simplex virus type 2 (HSV-2). Mice were treated with either normal sheep serum or anti-alpha/beta IFN antiserum, inoculated with the immunomodulators, and infected with virus. Because anti-IFN treatment also decreased natural resistance to HSV-2 and MCMV, two viral challenge doses were used to ensure that the mice with control serum or anti-IFN antiserum received biologically equivalent infections. Antiviral protection of pICLC and CL246,738 against HSV-2 infection was completely abrogated by treatment with anti-alpha/beta interferon antiserum. Mice treated with pICLC also lost antiviral protection against MCMV when interferon alpha/beta was depleted. These results indicate that induction of interferon alpha/beta appears to be a major mechanism for both natural resistance and pICLC-induced antiviral protection against MCMV and HSV-2 herpesvirus infections.
研究了免疫调节剂聚肌胞苷酸-聚左旋赖氨酸-羧甲基纤维素（pICLC）和CL246,738在感染鼠巨细胞病毒（MCMV）或2型单纯疱疹病毒（HSV-2）的CD-1小鼠中诱导α/β干扰素（IFN）的作用。用正常绵羊血清或抗α/β干扰素抗血清处理小鼠，接种免疫调节剂，然后感染病毒。由于抗干扰素治疗也会降低对HSV-2和MCMV的天然抵抗力，因此使用了两种病毒攻击剂量，以确保接受对照血清或抗干扰素抗血清的小鼠受到生物学等效的感染。用抗α/β干扰素抗血清处理完全消除了pICLC和CL246,738对HSV-2感染的抗病毒保护作用。当α/β干扰素被耗尽时，用pICLC处理的小鼠对MCMV的抗病毒保护作用也丧失。这些结果表明，α/β干扰素的诱导似乎是对MCMV和HSV-2疱疹病毒感染的天然抵抗力以及pICLC诱导的抗病毒保护的主要机制。
