The symptoms and histopathology of many virus diseases depend not so much on damage to the cells by virus but on the immunological reaction to the infection. The earliest (Traub, 1935) and still extensively studied (Oldstone & Dixon, 1970) infection of this type is murine lymphocytic choriomeningitis. From the in vivo work it has been commonly accepted that lymphocytic choriomengitis virus (LCMV) is intrinsically temperate, but there are numerous examples of LCMV-induced cytopathic effects (c.p.e.) in tissue culture (Pfau & Camyre, 1968). We have recently shown that c.p.e. in LCMV-infected L cells is largely regulated by an interference phenomenon (Welsh & Pfau, 1972). Cell culture-grown stocks of LCMV contain a transmissible component that specifically interferes with LCMV infective centre formation, synthesis and cytolytic activity; this interfering component sediments with the infectious virus particle, fails to pass through a Millipore filter of 25 nm pore size, and is inactivated by heat (60 °C), neutral red and LCMV-immune serum (Welsh & Pfau, 1970, 1972).