Host Defense Mechanisms against Infection with Influenza Virus. I. Effect of Sensitized Spleen Cells on Infection in Vitro

Sensitized murine spleen cells decrease the spread of influenza infection in cell cultures derived from human and syngeneic murine tissues. This control of infection is immune-specific and can be induced by immunization with identical hemagglutinin or neuraminidase antigens. The antiviral effect is...

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Bibliographic Details
Published in:The Journal of infectious diseases 1974-09, Vol.130 (3), p.248-256
Main Authors: Ennis, Francis A., Ruth, William A., Wells, Martha A.
Format: Article
Language:English
Subjects:
Adsorption
Animals
Antibodies
Antibody Formation
Antiserum
Antivirals
Cells, Cultured - immunology
Hemagglutinins
Immunity, Cellular
Immunoglobulin G
In Vitro Techniques
Infections
Lymphocytes
Lymphocytes - immunology
Macrophages - immunology
Major Articles
Male
Mice
Mice, Inbred Strains
Neuraminidase - immunology
Orthomyxoviridae
Orthomyxoviridae - immunology
Simplexvirus - immunology
Spleen - immunology
Spleen cells
Time Factors
Viral infections
Viruses
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Summary:Sensitized murine spleen cells decrease the spread of influenza infection in cell cultures derived from human and syngeneic murine tissues. This control of infection is immune-specific and can be induced by immunization with identical hemagglutinin or neuraminidase antigens. The antiviral effect is evident in the absence of added immune serum and can be blocked by adsorption of sensitized spleen cells with antiserum to murine IgG. The antiviral effect persists despite separation by agar of the sensitized spleen cells from the virus-infected monolayer. Spleen cells that do not adhere to glass are quantitatively more capable of limiting the spread of influenza virus in cell culture than are glass-adhering cells. These results suggest that mice immunized with influenza virus have sensitized spleen cells that elaborate antibody to influenza virus, which can act locally to control the spread of infection.
ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/130.3.248