@article{mbs:/content/journal/jgv/10.1099/0022-1317-53-1-31, author = "Zawatzky, R. and Hilfenhaus, J. and Marcucci, F. and Kirchner, H.", title = "Experimental Infection of Inbred Mice with Herpes Simplex Virus Type 1. I. Investigation of Humoral and Cellular Immunity and of Interferon Induction", journal= "Journal of General Virology", year = "1981", volume = "53", number = "1", pages = "31-38", doi = "https://doi.org/10.1099/0022-1317-53-1-31", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-53-1-31", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "Summary Considerable differences exist in the lethality of herpes simplex virus type 1 (HSV-1) after intraperitoneal (i.p.) infection in different inbred strains of mice. In this study humoral and cellular immunity and interferon production were compared in resistant and susceptible mice. The serum IgG response, as determined by an enzyme-linked immunosorbent assay (ELISA), was the same in different strains of mice. There was also no difference in neutralizing antibodies between resistant C57BL/6 and susceptible DBA/2 mice. The production of macrophage migration inhibitory factor, obtained from spleen cells of mice 7 days after infection with different doses of HSV-1, was the same in resistant and susceptible mice. Serum interferon could be detected 8 h after i.p. injection of 107 p.f.u. of HSV-1, but not at lower virus doses. At 8 h, high interferon titres [>1000 reference research units (iu)/ml] were observed in the serum of C57BL/6 mice but low titres (about 100 iu/ml) were found in the serum of DBA/2 mice. At 24 h, the titres were low in both strains of mice. Interferon production was also measured in vitro in spleen cell cultures exposed to inactivated HSV-1. These studies also showed high interferon production in spleen cell cultures of resistant mice, whereas low titres were produced by spleen cells of susceptible mice. Thus, our study has failed to reveal any differences in humoral or cellular immunity in mice resistant or susceptible to HSV but a difference in HSV-induced interferon production.", }