Antibody repertoire development in fetal and neonatal piglets. XXIII: Fetal piglets infected with a vaccine strain of PRRS Virus display the same immune dysregulation seen in isolator piglets
X.-Z. Suna,
N. Wertza,
K.L. Lagerb,
G. Tobinc,
J.E. Butlera, Corresponding author contact information, E-mail the corresponding author
a Department of Microbiology and Interdisciplinary Immunology Program, University of Iowa, Carver College of Medicine, Iowa City, IA, United States
b National Animal Disease Center (NADC), USDA-ARS, Ames, IA, United States
c Biological Mimetics, Frederick, MD, United States
http://dx.doi.org/10.1016/j.vaccine.2012.03.038
Abstract
The Ig levels and antibody repertoire diversification in fetal piglets infected with an attenuated Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) were measured. Serum Ig levels were greatly elevated in PRRSV-infected fetuses; IgG was elevated >50-fold, IgM > 5?15-fold and IgA > 2-fold compared to control fetuses. Their IgM to IgG to IgA profile was the same as that in isolator piglets infected for the same period with wild-type PRRSV. Fetal animals showed less repertoire diversification than even isolator piglets that were maintained germfree (GF) while the repertoire diversification index (RDI) for PRRSV-infected isolator piglets was 10-fold higher and comparable to littermates infected with swine influenza (S-FLU). However, when expressed as the RDI:Ig ratio, infected fetuses appeared 10-fold less capable of repertoire diversification than uninfected littermates and GF isolator piglets. Compared to S-FLU isolator piglets that resolve the infection, the RDI:Ig of PRRSV-infected isolator piglets was 100-fold lower. Overall, infection of fetuses with an attenuated virus shows the same immune dysregulation seen postnatally in wild type infected isolator piglets, indicating that: (a)
attenuation did not alter the ability of the virus to cause dysregulation and (b) the isolator infectious model reflects the fetal disease.
