Murine natural killer cells limit coxsackievirus B3 replication

E. K. Godeny, C. J. Gauntt

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86 Scopus citations


Previous indirect evidence suggested that natural killer (NK) cells play a role in coxsackie virus B3 serotype 3, myocarditic variant (CVB3(m))-induced myocarditis by limiting virus replication. In this study, we present direct evidence that NK cells can limit CVB3(m) replication both in vitro and in vivo. Virus titers are lowered in primary murine neonatal skin fibroblast (MNSF) cultures incubated with activated splenic large granular lymphocytes (LGL) taken from mice 3 days postinoculation of CVB3(m), a time of maximal NK cell activity. The antiviral effect of this cell population is diminished by complement-mediated lysis with the use of anti-asialo GM1 antiserum but not with anti-Lyt-2 monoclonal antibody. Neither interferon nor anti-CVB3(m)-neutralizing antibody was detected in these cultures. Although activated LGL initiate lysis within CVB3(m)-infected MNSF in vitro within 3 hr of addition, they do not lyse uninfected MNSF cultures. CVB3(m) replication is required for expression of surface changes on MNSF that result in lysis by NK cells because cell cultures treated with compounds that prevent CVB3(m) replication are not killed by LGL. LGL also do not lyse MNSF cultures inoculated with UV-inactivated virus. Mice inoculated with activated LGL and subsequently challenged with CVB3(m) had reduced titers of virus in heart tissues in comparison to titers of CVB3(m) in heart tissues of mice not given LGL. The antiviral activity of the LGL preparation was abolished by prior treatment with anti-asialo GM1 antiserum plus complement but not by prior treatment with anti-Lyt-2 monoclonal antibody and complement. These data suggest that NK cells can specifically limit a nonenveloped virus infection by killing virus-infected cells.

Original languageEnglish (US)
Pages (from-to)913-918
Number of pages6
JournalJournal of Immunology
Issue number3
StatePublished - 1987

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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