The role of natural killer cells and interferon in resistance to acute infection of mice with herpes simplex virus type 1
Biochemistry & Molecular Pharmacology
Graduate School of Biomedical Sciences; Department of Pathology; Department of Molecular Genetics and Microbiology
Medical Subject Headings
Acute Disease; Aging; Animals; Cell Line; Female; Herpes Simplex; Immunity, Natural; Immunization, Passive; Interferons; Killer Cells, Natural; Lymphocyte Depletion; Lymphoma; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Simplexvirus
Life Sciences | Medicine and Health Sciences
The relative roles of interferon (IFN) and natural killer (NK) cells in herpes simplex virus type 1 (HSV-1) infection of mice were examined. Adoptive transfer of adult mouse leukocytes into 4- to 6-day-old suckling mice protected the recipients from HSV-1 infection, as judged by viral titers in the spleen 2 days postinfection. Protection was mediated by several classes of leukocytes, including those depleted of NK cell activity by antibody to asialo GM1 and those depleted of macrophages by size separation. Mice receiving these leukocytes produced significantly higher levels of IFN 6 hr postinfection (early IFN) than did HSV-1-infected mice not receiving donor leukocytes. Antibody to IFN, under conditions that blocked early but not late IFN synthesis, greatly enhanced HSV-1 synthesis in mice receiving leukocytes and completely removed the protective effect mediated by leukocytes. High doses of anti-asialo GM1 blocked both NK cell activity and early IFN production and resulted in high titers of HSV-1. This effect on virus synthesis was not seen if mice were given antibody 1 day postinfection. Lower doses of anti-asialo GM1, which still depleted NK cell activity but had no effect on early IFN production, did not enhance HSV-1 synthesis. Depletion of NK cell activity with a low dose of antibody had no effect on the reduced HSV-1 synthesis resulting from prophylactic IFN treatment or on the enhanced HSV-1 synthesis resulting from antibody to IFN treatment. Thus, resistance to acute HSV-1 infection in mice correlates with early IFN production but not with NK cell activity, suggesting that NK cells are not major mediators of natural resistance in this model and that the antiviral effect of IFN is not mediated by NK cells.
Rights and Permissions
Citation: J Immunol. 1986 May 1;136(9):3481-5.
Journal of immunology (Baltimore, Md. : 1950)
Bukowski, Jack F. and Welsh, Raymond M., "The role of natural killer cells and interferon in resistance to acute infection of mice with herpes simplex virus type 1" (1986). GSBS Student Publications. 147.