Submitted to: American Association for Immunology
Publication Type: Abstract Only
Publication Acceptance Date: 4/1/2003
Publication Date: 5/1/2003
Citation: BOHLKEN, C.D., HAYNES, J.S., SPAETE, R.J., ADOLPHSON, D., VORWALD, A.C., LAGER, K.M., BUTLER, J.E. LYMPHOID HYPERPLASIA IN NEONATAL PIGLETS IS A RESULT OF PRRSV INFECTION. AMERICAN ASSOCIATION FOR IMMUNOLOGY. 2003. ABSTRACT NO. 31.21. p. C20.
Technical Abstract: Porcine reproductive and respiratory syndrome virus (PRRSV) is a prominent pathogen, causing increases in reproductive failure in sows and fatal respiratory illnesses, especially in young piglets. In an effort to study the immunopathological and immunomodulatory effects of PRRSV, isolator piglets were colonized with a benign E. coli on day 3 of life, or kept germ-free, and then inoculated with PRRSV or sham media on day 7. To determine whether PRRSV modulates the humoral immune response, piglets were immunized both with a T-dependent and a T-independent type 2 antigen on day 7. On average, 30-50 fold increases in IgM, 20-80 fold increases in IgG, and 10-20 fold increases in IgA were first observed in plasma 14 days after PRRSV infection, compared to sham-inoculated piglets. In addition, antigen-specific activity (SpAct) peaked 7 days after immunization in PRRSV-infected piglets, whereas in sham animals it peaked 14 days after. Size exclusion HPLC analysis revealed that PRRSV-infected sera contained high molecular weight fractions that contained IgG, suggesting the presence of immune complexes. Kidney lesions were observed and were restricted to PRRSV-infected piglets. These piglets also had bronchial tree-associated lymph nodes and submandibular lymph nodes that were 5-10 times larger than colonized, sham-inoculated animals. Taken together these data indicate that PRRSV-infection is inducing B-cell hyperplasia.