Enhancement of a secondary antibody response to vesicular stomatitis virus 'G' protein by IFN-γ treatment at primary immunization

K. P. Anderson, E. H. Fennie, Tilahun Yilma

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

IFN-γ is a secreted polypeptide product of stimulated T lymphocytes with immunomodulatory properties as well as antiviral activity. We have investigated the effects of IFN-γ treatment on a neutralizing antibody response to vesicular stomatitis virus (VSV) when administered in conjunction with immunization using purified envelope glycoprotein 'G' of VSV. Administration of rIFN-γ to mice or cattle at the time of primary immunization with VSV G glycoprotein enhanced the magnitude of a secondary virus-neutralizing antibody response after a booster administration of the same Ag without IFN-γ treatment. Enhancement was statistically significant and occurred at relatively low doses of IFN-γ in the absence of any additional adjuvants. Furthermore, cattle treated with IFN-γ at the time of a single primary immunization were more resistant to VSV challenge than those immunized without IFN-γ treatment. IFN-γ treatment in conjunction with a single primary immunization may therefore provide a practical means of enhancing protection from a viral challenge without the use of inflammatory adjuvants or booster immunizations.

Original languageEnglish (US)
Pages (from-to)3599-3604
Number of pages6
JournalJournal of Immunology
Volume140
Issue number10
StatePublished - 1988
Externally publishedYes

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Vesicular Stomatitis
Antibody Formation
Immunization
Viruses
Neutralizing Antibodies
Glycoproteins
Therapeutics
Secondary Immunization
Antiviral Agents
vesicular stomatitis virus G protein
T-Lymphocytes
Peptides

ASJC Scopus subject areas

  • Immunology

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Enhancement of a secondary antibody response to vesicular stomatitis virus 'G' protein by IFN-γ treatment at primary immunization. / Anderson, K. P.; Fennie, E. H.; Yilma, Tilahun.

In: Journal of Immunology, Vol. 140, No. 10, 1988, p. 3599-3604.

Research output: Contribution to journalArticle

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