Key result
Intraperitoneal LD50s for the L, M, and S variants of Mengo encephalomyelitis virus in mice were 1, 1-5 x 10^4, and 2-10 x 10^4 p.f.u.'s respectively, while intracerebral LD50s were all 1-5 p.f.u.'s.
The three variants of Mengo encephalomyelitis virus show markedly different lethalities when administered intraperitoneally but similar lethalities when administered intracerebrally in mice.
No immediate implications for human care; leaves open mechanistic insights into Mengo virus variant attenuation for further animal studies.
The distribution of infectious virus particles in various tissues of the mouse was determined following the intraperitoneal injection of three plaque variants of Mengo encephalomyelitis virus. When lethal doses were administered, virus appeared first in the spleen and lymph nodes (suggesting that these are the primary target organs for the agents), followed by its appearance in spinal cord and brain, in which tissues the infectious titers increased progressively until the death of the animals. Low levels of virus were sometimes found in lung, heart and kidney at 24–48 hours post‐challenge, but disappeared from these tissues at later times. Virus was never detected in blood or liver, suggesting that the virus moves throughout the animal by way of the lymphatic system. When sub‐lethal doses of virus were injected, it was detectable only in spleen and lymph nodes, and disappeared from these tissues by 8–9 days post‐challenge. The LD50's for the three variants when injected by both the intraperitoneal and intracerebral routes were determined. The I.P.‐LD50's for the L (large plaque former), M (medium plaque former) and S (minute plaque former) variants in 14–16 gm mice were found to be 1, 1–5 × 104 and 2–10 × 104 p.f.u.'s, respectively. The I.C.‐LD50's were essentially the same (1–5 p.f.u.'s) for all three variants. The possibility that the differences in the I.P.‐LD50's may be due to differences in the abilities of the variants to stimulate interferon production or in their sensitivities to its antiviral action is discussed.
No takes yet. Share an insight, caveat, or question.
Colter et al. (1965) studied Mengo encephalomyelitis virus infection. Three plaque variants of Mengo encephalomyelitis virus (L, M, S) was evaluated on LD50 (lethal dose 50%). Intraperitoneal LD50s for the L, M, and S variants of Mengo encephalomyelitis virus in mice were 1, 1-5 x 10^4, and 2-10 x 10^4 p.f.u.'s respectively, while intracerebral LD50s were all 1-5 p.f.u.'s.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: