Efficient replication of pneumonia virus of mice (PVM) in a mouse macrophage cell line
Kimberly D Dyer1, Ingrid Mm Schellens, Cynthia A Bonville
1Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. kdyer@niaid.nih.gov
Abstract:
Pneumonia virus of mice (PVM; family Paramyxoviridae, subfamily Pneumovirinae) is a natural respiratory pathogen of rodent species and an important new model for the study of severe viral bronchiolitis and pneumonia. However, despite high virus titers typically detected in infected mouse lung tissue in vivo, cell lines used routinely for virus propagation in vitro are not highly susceptible to PVM infection. We have evaluated several rodent and primate cell lines for susceptibility to PVM infection, and detected highest virus titers from infection of the mouse monocyte-macrophage RAW 264.7 cell line. Additionally, virus replication in RAW 264.7 cells induces the synthesis and secretion of proinflammatory cytokines relevant to respiratory virus disease, including tumor necrosis factor-alpha (TNF-alpha), interferon-beta (IFN-beta), macrophage inflammatory proteins 1alpha and 1beta (MIP-1alpha and MIP-1beta) and the functional homolog of human IL-8, mouse macrophage inflammatory peptide-2 (MIP-2). Identification and characterization of a rodent cell line that supports the replication of PVM and induces the synthesis of disease-related proinflammatory mediators will facilitate studies of molecular mechanisms of viral pathogenesis that will complement and expand on findings from mouse model systems.
Insights
Pneumonia virus of mice (PVM) replicates efficiently in RAW 264.7 cells, a mouse macrophage cell line. This model aids research into PVM-induced respiratory disease by enabling study of viral pathogenesis and cytokine responses.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Pneumonia virus of mice (PVM) is a rodent respiratory pathogen.
- PVM is a valuable model for studying viral bronchiolitis and pneumonia.
- Current in vitro models poorly support PVM replication.
Purpose of the Study:
- To identify a rodent cell line supporting PVM replication.
- To characterize PVM-induced cytokine production in vitro.
- To facilitate studies of PVM pathogenesis.
Main Methods:
- Screened rodent and primate cell lines for PVM susceptibility.
- Quantified PVM titers in infected cell lines.
- Measured cytokine and chemokine secretion (TNF-α, IFN-β, MIP-1α/β, MIP-2) from infected cells.
Main Results:
- RAW 264.7 cells showed the highest PVM titers.
- PVM infection induced secretion of key proinflammatory cytokines (TNF-α, IFN-β, MIP-1α/β, MIP-2).
- These cytokines are relevant to respiratory virus disease.
Conclusions:
- RAW 264.7 cells are a suitable model for PVM replication in vitro.
- This model supports studying PVM-induced inflammation and pathogenesis.
- Findings complement existing PVM mouse models.
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