Abstract
Effector mechanisms responsible for resistance against ectromelia virus including antiviral activity of non-immune macrophages, antiviral antibody, delayed footpad reaction to viral antigen, and interferon induction after viral infection were depressed in BALB/c mice bearing syngeneic Meth A tumor. The degree of viral growth correlated well with the depression of delayed footpad reaction, antibody production, and interferon induction. Therefore, modification of macrophage functions by a tumor-bearing state and treatment with PSK may contribute to this modification of antiviral resistance, at an early phase of infection. Cytotoxic activity may not be the principal effector, since the cytotoxicity was induced in normal and tumor-bearing mice to almost the same extent yet an extensive viral growth occurred only in the latter.
MeSH Terms
Animals
Antibodies, Viral/biosynthesis
Antiviral Agents/therapeutic use
Ectromelia virus/growth & development
Ectromelia, Infectious/drug therapy,immunology
Hypersensitivity, Delayed/immunology
Immune Tolerance/drug effects
Immunity, Innate/drug effects
Interferons/analysis
Kinetics
Liver/analysis
Male
Mice
Mice, Inbred BALB C
Poxviridae Infections/immunology
Proteoglycans/therapeutic use
Spleen
T-Lymphocytes, Cytotoxic/immunology
Chemicals
Antibodies, Viral
Antiviral Agents
Proteoglycans
polysaccharide-K
Interferons
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Tsuru S
Nomoto K
Taniguchi M
Fujisawa H
Zinnaka Y
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22 references, click to expand
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