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* Department of Microbiology and Interdisciplinary Immunology Program, University of Iowa, Iowa City, IA 52242;
Robarts Research Institute, London, Ontario, Canada;
Czech Academy of Science, Novi Hradek, Czech Republic; and
Virus and Prion Diseases of Livestock Research Unit, National Animal Disease Center, U.S. Department of Agriculture-Agricultural Research Service, Ames, IA 50010
Porcine respiratory and reproductive syndrome virus (PRRSV) causes an extraordinary increase in the proportion of B cells resulting in lymphoid hyperplasia, hypergammaglobulinemia, and autoimmunity in neonatal piglets. Spectratypic analysis of B cells from neonatal isolator piglets show a non-Gaussian pattern with preferential expansion of clones bearing certain H chain third complementary region (HCDR3) lengths. However, only in PRRSV-infected isolator piglets was nearly the identical spectratype observed for all lymphoid tissues. This result suggests dissemination of the same dominant B cell clones throughout the body. B cell expansion in PRRS was not associated with preferential VH gene usage or repertoire diversification and these cells appeared to bear a naive phenotype. The B cell population observed during infection comprised those with hydrophobic HCDR3s, especially sequences encoded by reading frame 3 of DHA that generates the AMVLV motif. Thus, the hydropathicity profile of B cells after infection was skewed to favor those with hydrophobic binding sites, whereas the normally dominant region of the hydropathicity profile containing neutral HCDR3s was absent. We believe that the hypergammaglobulinemia results from the products of these cells. We speculate that PRRSV infection generates a product that engages the BCR of naive B cells, displaying the AMVLV and similar motifs in HCDR3 and resulting in their T-independent proliferation without repertoire diversification.
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 Porkboard Grant 05-174, U.S. Department of Agriculture-Agricultural Research Service Cooperative Agreement 58-3625-4-155, and Grant 523/07/0088 from the Grant Agency of the Czech Republic.
2 Address correspondence and reprint requests to Dr. John E. Butler, University of Iowa, Department of Microbiology, 51 Newton Road, Iowa City, IA 52242. E-mail address: john-butler{at}uiowa.edu
3 Abbreviations used in this paper: SAg, superantigen; PRRS, porcine reproductive and respiratory syndrome; PRRSV, PRRS virus; HCDR3, H chain third complementary region; dpi, days postinfection; BAL, bronchoalveolar lavage; VN, virus neutralizing; ORF, open reading frame; RF, reading frame; MLN, mesenteric lymph node; FCM, flow cytometric analysis; TON, tonsil; BLN, tracheal-bronchial lymph node; Spl, spleen; IPP, ileal Peyer’s patch; pnt, polynucleotide; BM, bone marrow; PIC, parasite-infected young pig; H.I., hydropathicity index.
This article has been cited by other articles:
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  J. E. Butler, N. Wertz, P. Weber, and K. M. Lager Porcine Reproductive and Respiratory Syndrome Virus Subverts Repertoire Development by Proliferation of Germline-Encoded B Cells of All Isotypes Bearing Hydrophobic Heavy Chain CDR3 J. Immunol., February 15, 2008; 180(4): 2347 - 2356. [Abstract] [Full Text] [PDF]
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