Related Experiment Video
Updated: Jun 19, 2026

Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery
Published on: November 5, 2019
EPIDEMIOLOGY OF LYMPHOCYTIC CHORIOMENINGITIS IN A MOUSE STOCK OBSERVED FOR FOUR YEARS
1Department of Animal and Plant Pathology of The Rockefeller Institute for Medical Research, Princeton, New Jersey, and the Veterinärhygienisches und Tierseucheninstut of the University of Giessen, Giessen, Germany.
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.
Insights
Lymphocytic choriomeningitis virus (LCMV) infection in mice has become milder due to changes in transmission and host-pathogen interactions. Intrauterine transmission now predominates, with reduced viral pathogenicity and increased host resistance contributing to the observed mildness.
Area of Science:
- Virology
- Immunology
- Epidemiology
Background:
- Lymphocytic choriomeningitis (LCM) is endemic in a specific mouse stock.
- LCMV infection dynamics have been observed over a 4-year period.
- The disease has become clinically inapparent despite persistent viral presence.
Purpose of the Study:
- To investigate the changes in LCMV transmission and pathogenicity in a mouse stock.
- To understand the factors contributing to the observed mildness of LCMV infection.
- To analyze shifts in host-pathogen interactions and disease communicability.
Main Methods:
- Longitudinal observation of an LCMV-endemic mouse stock over 4 years.
- Monitoring viral load in organs and blood of infected mice.
- Assessing transmission routes (intrauterine, contact) and host age-specific susceptibility.
- Investigating viral pathogenicity and host resistance to infection.
Main Results:
- LCMV infection persists but is clinically mild and undetectable by observation.
- Intrauterine transmission is now the sole route, unlike in 1935.
- Viral pathogenicity has decreased for embryonic tissues, and host resistance to intrauterine infection has increased.
- Suckling mice infected via intranasal instillation or naturally transmit LCMV readily, while experimentally infected mature mice do not.
Conclusions:
- The mildness of LCMV is attributed to a shift towards intrauterine transmission and changes in host-pathogen interactions.
- Reduced viral pathogenicity and increased host resistance contribute to the attenuated disease.
- Distinct transmission patterns exist between naturally/neonatally infected and experimentally infected adult mice.

