Effects of tumor necrosis factor on viral replication and pulmonary inflammation during acute mouse adenovirus type 1 respiratory infection.
CD8 T cells contribute to effective clearance of mouse adenovirus type 1 (MAV-1) and to virus-induced pulmonary inflammation. We characterized effects of a CD8 T cell effector, TNF, on MAV-1 pathogenesis. TNF inhibited MAV-1 replication in vitro. TNF deficiency or immunoneutralization had no effect on lung viral loads or viral gene expression in mice infected intranasally with MAV-1. Absence of TNF delayed virus-induced weight loss and reduced histological evidence of pulmonary inflammation, although concentrations of proinflammatory cytokines and chemokines in bronchoalveolar lavage fluid (BALF) were not significantly affected. BALF concentrations of IL-10 were greater in TNF-deficient mice compared to controls. Our data indicate that TNF is not essential for control of viral replication in vivo, but virus-induced TNF contributes to some aspects of immunopathology and disease. Redundant CD8 T cell effectors and other aspects of immune function are sufficient for antiviral and pro-inflammatory responses to acute MAV-1 respiratory infection.
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Related Subject Headings
- Virus Replication
- Virology
- Tumor Necrosis Factor-alpha
- Pneumonia
- Mice, Inbred C57BL
- Mice
- Mastadenovirus
- Male
- Lung
- Interleukin-10
Citation
Published In
DOI
EISSN
Publication Date
Volume
Start / End Page
Location
Related Subject Headings
- Virus Replication
- Virology
- Tumor Necrosis Factor-alpha
- Pneumonia
- Mice, Inbred C57BL
- Mice
- Mastadenovirus
- Male
- Lung
- Interleukin-10