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Updated: Aug 11, 2026

Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
[Immune response of (C57BL/6xA/Sn)F1 mice in mycoplasm-virus infection]
Abstract:
Mixed Rauscher leukemia virus (RLV) and M. arthritidis infection of (C57BL/6xA/Sn)f1 mice-hybrids, highly resistant to RLV, was accompanied by a progressive inhibition of rosette-forming cells (RFC) and plaque-forming cells (PFC), resulting in the induction of malignant erythroblastosis identical by cytology to Rauscher leukemia. The mice-hybrids infected with A. laidlawii and RLV developed significant splenomegaly on the 21st day of the infection, and their immune response was almost entirely suppressed, but both RFC and PFC populations as well as the spleen weight returned to the initial level by the 62d day the infection. A possible role of mycoplasm in the induction and development of Rauscher leukemia is discussed.
Insights
Mixed Rauscher leukemia virus (RLV) and Mycoplasma arthritidis infection in mice induced malignant erythroblastosis. Despite initial immune suppression and splenomegaly, immune cell populations and spleen weight recovered by day 62.
Area of Science:
- Virology
- Immunology
- Microbiology
Context:
- Investigates the interaction between Rauscher leukemia virus (RLV) and Mycoplasma arthritidis in a resistant mouse model.
- Examines the impact of co-infection on immune cell populations and spleen development.
Purpose:
- To determine the effect of M. arthritidis co-infection on RLV-induced leukemia.
- To evaluate the immune response and pathological changes in infected mice.
Summary:
- Co-infection with RLV and M. arthritidis in (C57BL/6xA/Sn)f1 mice led to malignant erythroblastosis, mimicking Rauscher leukemia.
- Significant splenomegaly and suppression of rosette-forming cells (RFC) and plaque-forming cells (PFC) were observed.
- Immune parameters and spleen weight normalized by day 62, suggesting a transient but significant effect of mycoplasma.
Impact:
- Suggests a potential role for Mycoplasma in the pathogenesis of Rauscher leukemia.
- Highlights the complex interplay between viral and bacterial infections in immune modulation.
- Provides insights into host-pathogen interactions and disease development.

