PMID- 14734777
OWN - NLM
STAT- MEDLINE
DCOM- 20040507
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 172
IP  - 3
DP  - 2004 Feb 1
TI  - Lymphoid hyperplasia resulting in immune dysregulation is caused by porcine 
      reproductive and respiratory syndrome virus infection in neonatal pigs.
PG  - 1916-25
AB  - Amid growing evidence that numerous viral infections can produce immunopathology, 
      including nonspecific polyclonal lymphocyte activation, the need to test the 
      direct impact of an infecting virus on the immune system of the host is crucial. 
      This can best be tested in the isolator piglet model in which maternal and other 
      extrinsic influences can be excluded. Therefore, neonatal isolator piglets were 
      colonized with a benign Escherichia coli, or kept germfree, and then inoculated 
      with wild-type porcine reproductive and respiratory syndrome virus (PRRSV) or 
      sham medium. Two weeks after inoculation, serum IgM, IgG, and IgA levels were 30- 
      to 50-, 20- to 80-, and 10- to 20-fold higher, respectively, in animals receiving 
      virus vs sham controls, although <1% was virus specific. PRRSV-infected piglets 
      also had bronchial tree-associated lymph nodes and submandibular lymph nodes that 
      were 5-10 times larger than colonized, sham-inoculated animals. Size-exclusion 
      fast performance liquid chromatography revealed that PRRSV-infected sera 
      contained high-molecular-mass fractions that contained IgG, suggesting the 
      presence of immune complexes. Lesions, inflammatory cell infiltration, glomerular 
      deposits of IgG, IgM, and IgA, and Abs of all three isotypes to basement membrane 
      and vascular endothelium were observed in the kidneys of PRRSV-infected piglets. 
      Furthermore, autoantibodies specific for Golgi Ags and dsDNA could be detected 
      3-4 wk after viral inoculation. These data demonstrate that PRRSV induces B cell 
      hyperplasia in isolator piglets that leads to immunologic injury and suggests 
      that the isolator piglet model could serve as a useful model to determine the 
      mechanisms of virus-induced immunopathology in this species.
FAU - Lemke, Caitlin D
AU  - Lemke CD
AD  - Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, 
      IA 52242, USA. caitlin.lemke@uiowa.edu
FAU - Haynes, Joseph S
AU  - Haynes JS
FAU - Spaete, Rodger
AU  - Spaete R
FAU - Adolphson, Deb
AU  - Adolphson D
FAU - Vorwald, Ann
AU  - Vorwald A
FAU - Lager, Kelly
AU  - Lager K
FAU - Butler, John E
AU  - Butler JE
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Antibodies, Viral)
RN  - 0 (Antigens, Viral)
RN  - 0 (Autoantibodies)
RN  - 0 (Autoantigens)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Immunoglobulins)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Antibodies, Viral/biosynthesis/blood
MH  - Antigens, Viral/analysis
MH  - Autoantibodies/biosynthesis
MH  - Autoantigens/immunology
MH  - Autoimmune Diseases/immunology/pathology/virology
MH  - B-Lymphocyte Subsets/pathology
MH  - Female
MH  - Hyperplasia
MH  - Immunoglobulin G/biosynthesis/blood
MH  - Immunoglobulins/biosynthesis/blood
MH  - Kidney Glomerulus/immunology/pathology/virology
MH  - Lymphoid Tissue/*immunology/*pathology/virology
MH  - Molecular Weight
MH  - Porcine Reproductive and Respiratory Syndrome/*immunology/*pathology/virology
MH  - Porcine respiratory and reproductive syndrome virus/growth & 
      development/*immunology/isolation & purification
MH  - Pregnancy
MH  - Specific Pathogen-Free Organisms
MH  - Swine
EDAT- 2004/01/22 05:00
MHDA- 2004/05/08 05:00
CRDT- 2004/01/22 05:00
PHST- 2004/01/22 05:00 [pubmed]
PHST- 2004/05/08 05:00 [medline]
PHST- 2004/01/22 05:00 [entrez]
AID - 10.4049/jimmunol.172.3.1916 [doi]
PST - ppublish
SO  - J Immunol. 2004 Feb 1;172(3):1916-25. doi: 10.4049/jimmunol.172.3.1916.