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Updated: Aug 5, 2026

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Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
[Strain-dependent disruption of the functional activity of bone marrow stromal cells from mice infected with
Voprosy Virusologii
|June 8, 1999
Abstract:
Infection of mice with influenza A virus disturbs the proliferative activity of bone marrow stromal fibroblasts involved in regulation of bone marrow hemopoiesis. Myelosuppression induced by influenza A virus can be a result of dysfunction of bone marrow stromal tissue. Disorders in multiplication of bone marrow fibroblasts induced by influenza virus are strain-dependent.
Insights
Influenza A virus infection impairs bone marrow fibroblast proliferation, potentially causing myelosuppression. The impact on fibroblast multiplication is dependent on the specific influenza virus strain.
Area of Science:
- Hematology
- Virology
- Immunology
Context:
- Bone marrow stromal fibroblasts are crucial for regulating hematopoiesis.
- Influenza A virus infection is known to affect various host systems.
Purpose:
- To investigate the effect of influenza A virus infection on the proliferative activity of bone marrow stromal fibroblasts.
- To determine if influenza A virus-induced myelosuppression is linked to bone marrow stromal tissue dysfunction.
- To assess the strain-dependency of influenza virus effects on bone marrow fibroblast multiplication.
Summary:
- Influenza A virus infection disrupts the proliferative capacity of bone marrow stromal fibroblasts.
- This disruption suggests that bone marrow stromal tissue dysfunction may underlie influenza A virus-induced myelosuppression.
- The observed disorders in fibroblast multiplication are contingent upon the specific strain of influenza virus.
Impact:
- This research highlights a novel mechanism by which influenza A virus can induce myelosuppression.
- Understanding the strain-specific effects is critical for predicting and managing influenza-related complications.
- Findings may inform therapeutic strategies targeting bone marrow recovery during viral infections.

