Epidemiology of Lymphocytic Choriomeningitis in a Mouse Stock Observed for Four Years

Abstract

A small mouse stock in which lymphocytic choriomeningitis is endemic has been observed over a period of 4 years. The disease has persisted during that time, but it has become so mild that it can no longer be recognized by clinical observation. In spite of this fact, all of the stock mice tested, both young and old, carried considerable amounts of virus in their organs and blood. The females readily transmit the infection to their offspring. Intrauterine infection has become the only mode of transmission of the disease in contrast to the situation in 1935 when a certain number of mice were born virus-free and became infected by contact shortly after birth. The present mildness of the disease appears to be due to two factors, namely, the change in its mode of transmission just mentioned, and a shift in the severity of the disease with regard to the age of the host at the time of infection. This shift has occurred gradually since 1935 when the mice infected in utero were the only ones to become sick. Since 1937, however, the virus is quite harmless for such animals and produces symptoms only in suckling mice from the virus-free stock exposed to contact infection. Evidence is presented which suggests that the shift in the severity of the disease was caused by a decrease of the pathogenicity of the virus for embryonic mouse tissue and a concurrent increase of the resistance to intrauterine infection of the mice from the infected stock. Another change noted concerned the communicability of the experimental disease. In contrast to observations made in 1935 the experimental infection of mature mice from the virus-free colony is now very rarely transmitted by contact to healthy mice, young or old. Suckling mice from the same stock infected by intranasal instillation of virus, however, readily transmit the disease and continue to do so as they grow up. The same is true for mice infected naturally. The reason for this discrepancy has not been ascertained, but it has been shown that naturally infected mice capable of transmitting the disease in general discharge large amounts of virus through the nose for a longer period of time than mature mice infected experimentally which fail to transmit their infection. It may likewise be of significance in this connection that the virus can lose its communicability by animal passage. A marked change (chiefly climatic and dietary) in the environmental conditions of the infected stock failed to influence the course and character of the epidemic.

Multiplication of Lymphocytic Choriomeningitis Virus in Thymocytes During its Persistence in Mice

“…In contrast, mice infected with LCM virus in utero or shortly after birth do not generate such cells (Marker & Volkert, 1973;Cihak & Lehmann-Grube, 1974) and in these mice the virus persists indefinitely (Traub, 1939). All other immune functions, including the production of anti-LCM virus antibodies (for review, see Oldstone, 1979) and the rise of cytotoxic T-cells against the related Pichinde virus (Buchmeier et al, 1980) are present in virus-carrier mice.…”

The In Vitro and In Vivo Analysis of Mammalian Tumour Viruses

“…Cells of these two organs may thus be considered as among the main sites of virus multiplication in the animal. With the use of the plaque assay for the polyoma (Sachs, Fogel and Winocour, 1959;Winocour and Sachs, 1959) (Traub, 1939). Such a reversion may perhaps also be found with the polyoma, and this could then explain the absence of multiple tumours in the mice from which the virus was originally isolated.…”

Tolerance as Shown by the Simonsen Reaction on the Chorioallantoic Membrane

“…This has to date been demonstrated in lymphocytic choriomeningitis virus infections in mice by Traub (1939) and by a virus of tlie avian neurolymphomatosis group (RIF) by Rubin et al (1961).…”