Herpes Simplex Virus Type 1 Infection in Mice with Severe Combined Immunodeficiency (SCID)

Abstract

For many years, the role of acquired immunity—that is, T lymphocytes and antibodies—in the protection against herpes simplex virus (HSV) has been our major interest. We have used neonatally thymectomized mice (1) and athymic nude mice (2) to study this, and others have used newborn mice (3), mice treated with antithymocyte sera (4), or mice treated with cyclophosphamide (5). In 1983 Bosma et al. (6) reported that they had observed a CB-17 inbred strain, BALB/c· C57BL/Ka-Igh-1^b/ICR (N17F34), that had no detectable serum immunoglobulins, which has been found to be an inheritable defect under the control of a recessive gene (scid). These mice were also deficient in both Band T-lymphocyte functions, and were named severe combined immunodeficiency (SCID) mice. The newly developed immunologically deficient mouse strain attracted our attention as a good experimental model for systemic HSV infection in immunocompromised hosts.