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. 1997 Nov;71(11):8672–8677. doi: 10.1128/jvi.71.11.8672-8677.1997

Overexpression of interleukin-4 delays virus clearance in mice infected with respiratory syncytial virus.

J E Fischer 1, J E Johnson 1, R K Kuli-Zade 1, T R Johnson 1, S Aung 1, R A Parker 1, B S Graham 1
PMCID: PMC192331  PMID: 9343225

Abstract

Although interleukin-4 (IL-4) expression has been implicated in vaccine-enhanced respiratory syncytial virus (RSV) disease, its role in mediating the immune response to primary RSV infection remains unclear. To assess the effect of IL-4 production on typical RSV infection, transgenic mice which either overexpress or fail to express IL-4 were challenged intranasally with RSV and their responses were compared to those of the parent strains. IL-4-deficient mice eliminated virus from the lung as quickly as did C57BL/6 controls. In contrast, mice which constitutively overexpress IL-4 showed delayed virus clearance compared with mice of the FVB/N control strain, although peak viral titers did not differ. IL-4 overexpression increased the magnitude of the subsequent antibody response. Lung lymphocytes harvested from IL-4-overexpressing mice post-RSV challenge showed diminished RSV-specific cytolytic activity compared with controls. Both IL-4-deficient and IL-4-overexpressing strains resisted rechallenge. These data imply that constitutive IL-4 expression delays or suppresses the development of a virus-specific cytotoxic lymphocyte population important in clearing primary RSV infection.

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Selected References

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