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Role of NK cells in immunomodulator-mediated resistance to herpesvirus infection
Journal article   Peer reviewed

Role of NK cells in immunomodulator-mediated resistance to herpesvirus infection

Steven C. Kunder, Linxian Wu and Page S. Morahan
Antiviral research, v 21(2), pp 103-118
1993
DOI: https://doi.org/10.1016/0166-3542(93)90047-M
PMID: 8393316
Featured in Collection :   UN Sustainable Development Goals @ Drexel

Abstract

Biological response modifier HSV-2 MCMV NK cells
Seven chemically diverse biological response modifiers (BRM) were compared for antiviral activity in intact and NK cell-depleted CD-1 mice. Both spontaneous and BRM-induced splenic NK cell cytotoxicity were depleted for at least 5 days following treatment with the monoclonal antibody NK1.1. Antiviral protection of standard doses of MVE-2, pIC, pICLC, rmIFN-τ and CL246, 738 against lethal MCMV or HSV-2 infections was not abrogated by NK cell depletion, demonstrating that NK cells are not required for BRM-induced antiviral activity against these herpesviruses. When mice were treated with 100000 U of rHuIFN-α B/D, NK cells were not required for activity against MCMV, while at a dose of 25000 U, NK cells appeared to be partially required against MCMV. At lower doses, the activity of rHuIFN-α B/D against MCMV appeared dependent upon the presence of NK cells. A similar dose-related requirement for NK cells was observed for activity of OK-432. Thus, at higher doses of rHuIFN-α B/D and OK-432, elements of the natural immune system in addition to or other than NK cells are apparently involved, while at lower doses NK cells appear to play a more important role in antiviral protection against MCMV infection.

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Web of Science research areas
Pharmacology & Pharmacy
Virology
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