HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Case, L. K. Articles by Golovkina, T. V. Search for Related Content PubMed PubMed Citation Articles by Case, L. K. Articles by Golovkina, T. V.

Molecular and Cellular Basis of the Retrovirus Resistance in I/LnJ Mice¹

The Jackson Laboratory, Bar Harbor, ME 04609

Previously, we showed that IFN- elicited by mouse mammary tumor virus (MMTV) infection in I/LnJ mice stimulated production of virus-neutralizing Abs, mostly of the IgG2a isotype. These Abs coated virions secreted by infected I/LnJ cells, and thus completely prevented virus transmission to offspring. However, the mechanism of virus neutralization by isotype-specific Abs remained unknown. Ab coating is capable of blocking virus infection by interfering with receptor-virus binding, by virus opsonization, by complement activation, and via FcR-mediated effector mechanisms. The aim of the studies described in this work was to uncover the cellular basis of anti-virus Ab production, to evaluate the importance of the IgG2a subclass of IgGs in virus neutralization, and to investigate which of the blocking mechanisms plays a role in virus neutralization. We showed that I/LnJ-derived bone marrow cells, specifically IFN--producing CD4⁺ T cells, were key cells conferring resistance to MMTV infection in susceptible mice upon transfer. We also established that a unique bias in the subclass selection toward the IgG2a isotype in infected I/LnJ mice was not due to their potent neutralizing ability, as anti-virus Abs of other isotypes were also able to neutralize the virus, but were a product of virally induced IFN-. Finally, we demonstrated that F(ab')₂ of anti-MMTV IgGs neutralized the virus as efficiently as total IgGs, suggesting that Ab-mediated interference with viral entry is the sole factor inhibiting virus replication in I/LnJ mice. We propose and discuss possible mechanisms by which infected I/LnJ mice eradicate retrovirus.

This article has been cited by other articles:

				C. M. Okeoma, M. Shen, and S. R. Ross A Novel Block to Mouse Mammary Tumor Virus Infection of Lymphocytes in B10.BR Mice J. Virol., February 1, 2008; 82(3): 1314 - 1322. [Abstract] [Full Text] [PDF]

				L. K. Case, L. Petell, L. Yurkovetskiy, A. Purdy, K. J. Savage, and T. V. Golovkina Replication of Beta- and Gammaretroviruses Is Restricted in I/LnJ Mice via the Same Genetic Mechanism J. Virol., February 1, 2008; 82(3): 1438 - 1447. [Abstract] [Full Text] [PDF]

				C. C. MacDearmid, L. K. Case, C. L. Starling, and T. V. Golovkina Gradual Elimination of Retroviruses in YBR/Ei Mice J. Virol., March 1, 2006; 80(5): 2206 - 2215. [Abstract] [Full Text] [PDF]