| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Microbiology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455, U.S.A.
Neonatal infection of FVB mice with lactate dehydrogenase-elevating virus (LDV) prevented the normal formation of anti-LDV antibodies observed in mice infected at 5 days of age or older. Even 22 weeks post-infection, the concentration of circulating anti-LDV antibodies in neonatally infected mice was insignificant. However, the time course and level of persistent viraemia were the same in neonatally infected mice lacking anti-LDV antibodies as in mice infected at 5 or 15 days of age which developed normal antiviral immune responses. The results support the view that LDV replication in mice is unaffected by antiviral immune responses and instead is primarily dependent on the rate of regeneration of LDV-permissive macrophages. This view is further supported by the following findings. Treatment of mice with cyclophosphamide or dexamethasone, which are known to increase plasma LDV levels, increased the proportion of LDV-permissive macrophages in the peritoneum. Injection of mice with interleukin-3, which is known to stimulate macrophage development, increased plasma LDV levels in persistently infected mice 10- to 100-fold. During the first month of age when mice possess a higher proportion of LDV-permissive macrophages than older mice and peritoneal macrophages exhibit self-sustained growth, the persistent plasma LDV titres were also 10- to 100-fold higher than in older mice. The polyclonal activation of B cells induced by LDV that results in a permanent elevation of IgG2a or IgG2b in the circulation, and the formation of 180K to 300K immune complexes containing IgG2a or IgG2b were also the same in neonatally infected mice and mice infected 5 or 15 days after birth. Thus, the polyclonal activation of B cells occurs in the absence of an antiviral humoral immune response and the immune complexes do not contain anti-LDV antibodies. The immune complexes probably consist of autoantibodies formed in the course of the polyclonal activation of B cells and their cellular antigens.
Received 13 September 1993;
accepted 26 November 1993.
This article has been cited by other articles:
|
|
 |
|
  R. Marques, I. Antunes, U. Eksmond, J. Stoye, K. Hasenkrug, and G. Kassiotis B Lymphocyte Activation by Coinfection Prevents Immune Control of Friend Virus Infection J. Immunol., September 1, 2008; 181(5): 3432 - 3440. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
J. E. Butler, C. D. Lemke, P. Weber, M. Sinkora, and K. M. Lager Antibody Repertoire Development in Fetal and Neonatal Piglets: XIX. Undiversified B Cells with Hydrophobic HCDR3s Preferentially Proliferate in the Porcine Reproductive and Respiratory Syndrome J. Immunol., May 15, 2007; 178(10): 6320 - 6331. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. D. Lemke, J. S. Haynes, R. Spaete, D. Adolphson, A. Vorwald, K. Lager, and J. E. Butler Lymphoid Hyperplasia Resulting in Immune Dysregulation Is Caused by Porcine Reproductive and Respiratory Syndrome Virus Infection in Neonatal Pigs J. Immunol., February 1, 2004; 172(3): 1916 - 1925. [Abstract] [Full Text]
|
|
|
|
 |
|
 P. G. W. Plagemann, Q. A. Jones, and W. A. Cafruny N-Glycans on the short ectodomain of the primary envelope glycoprotein play a major role in the polyclonal activation of B cells by lactate dehydrogenase-elevating virus J. Gen. Virol., September 1, 2000; 81(9): 2167 - 2175. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| INT J SYST EVOL MICROBIOL | MICROBIOLOGY | J GEN VIROL |
| J MED MICROBIOL | ALL SGM JOURNALS | |
