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) A correction has been published 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 Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kim, I.-J. Articles by Blackman, M. A. Search for Related Content PubMed PubMed Citation Articles by Kim, I.-J. Articles by Blackman, M. A.

Perturbation of B Cell Activation in SLAM-Associated Protein-Deficient Mice Is Associated with Changes in Gammaherpesvirus Latency Reservoirs¹

In-Jeong Kim^*, Claire E. Burkum^*, Tres Cookenham^*, Pamela L. Schwartzberg, David L. Woodland^* and Marcia A. Blackman^2,*

^* Trudeau Institute, Saranac Lake, NY 12983; and Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

Signaling lymphocyte activation molecule (SLAM)-associated protein (SAP)) interactions with SLAM family proteins play important roles in immune function. SAP-deficient mice have defective B cell function, including impairment of germinal center formation, production of class-switched Ig, and development of memory B cells. B cells are the major reservoir of latency for both EBV and the homologous murine gammaherpesvirus, gammaherpesvirus 68. There is a strong association between the B cell life cycle and viral latency in that the virus preferentially establishes latency in activated germinal center B cells, which provides access to memory B cells, a major reservoir of long-term latency. In the current studies, we have analyzed the establishment and maintenance of HV68 latency in wild-type and SAP-deficient mice. The results show that, despite SAP-associated defects in germinal center and memory B cell formation, latency was established and maintained in memory B cells at comparable frequencies to wild-type mice, although the paucity of memory B cells translated into a 10-fold reduction in latent load. Furthermore, there were defects in normal latency reservoirs within the germinal center cells and IgD⁺"naive" B cells in SAP-deficient mice, showing a profound effect of the SAP mutation on latency reservoirs.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants AI51602 and AI42927 (to M.A.B.), intramural funds from National Human Genome Research Institute, National Institutes of Health Grant (to P.L.S.), and by the Trudeau Institute.

² Address correspondence and reprint requests to Dr. Marcia A. Blackman, Trudeau Institute, 154 Algonquin Avenue, Saranac Lake, NY 12983. E-mail address: mblackman{at}trudeauinstitute.org

³ Abbreviations used in this paper: KSHV, Kaposi’s sarcoma-associated herpesvirus; dpi, days postinfection; HV68, gammaherpesvirus 68; LDA/PCR, limiting dilution-nested PCR assay; PNA, peanut lectin (agglutinin); SAP, SLAM-associated protein; SLAM, signaling lymphocyte activation molecule; NP, nucleoprotein.

This article has been cited by other articles:

				T. Oliphant, G. E. Nybakken, S. K. Austin, Q. Xu, J. Bramson, M. Loeb, M. Throsby, D. H. Fremont, T. C. Pierson, and M. S. Diamond Induction of Epitope-Specific Neutralizing Antibodies against West Nile Virus J. Virol., November 1, 2007; 81(21): 11828 - 11839. [Abstract] [Full Text] [PDF]

				S. S. Cush, K. M. Anderson, D. H. Ravneberg, J. L. Weslow-Schmidt, and E. Flano Memory Generation and Maintenance of CD8+ T Cell Function during Viral Persistence J. Immunol., July 1, 2007; 179(1): 141 - 153. [Abstract] [Full Text] [PDF]