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Primary host defense mechanism of mice against intraperitoneal infection with herpes simplex virus type 1 (HSV-1) was studied using heat-killed Lactobacillus casei YIT 9018 (LC 9018), a bacterial immunostimulant, in combination with inactivated HSV-1 antigen. Peritoneal exudate cells (PECs) in the early period of mice pretreated intraperitoneally (ip) with LC 9018 showed the cytotoxic activity against BALB/3T3 cells infected with HSV-1, in vitro, whereas PECs induced by thioglycollate broth did not. The limitation of HSV-1 replication in monolayers of HSV-1-infected PECs induced by LC 9018 was greater than that in PECs induced by thioglycollate broth. Both activities of PECs induced by LC 9018 were markedly enhanced by the administration of inactivated HSV-1 antigen which showed an interferon-producing activity in the early period after the treatment. These results suggest that the host defense mechanism of mice against intraperitoneal infection with HSV-1 may be mainly related to peritoneal macrophages activated by and interferon produced by the administration of LC 9018 and inactivate HSV-1 antigen.

Primary Resistance Induced in Mice by Lactobacillus casei Following Infection with Herpes Simplex Virus