Porcine reproductive and respiratory syndrome virus-induced immunosuppression exacerbates the inflammatory response to porcine respiratory coronavirus


Article by:
Renukaradhya GJ, Alekseev K, Jung K, Fang Y, Saif LJ. Viral Immunol. 2010; 23(5):457–466

This study was designed to understand how infections with PRRS and PRCV modulate immune responses, and to see if they correlate with a clinical picture in pigs.
178 seronegative to PRRSV, PRCV, TGEV, and PCV2 16–20 day old piglets were used. After 1 week to acclimate they were assigned to one of four groups: Control, PRRSV-infected, PRCV-infected or PRCV/PRRSV-infected. PRCV infection came 10 days after PRRS infection.

Clinical signs (body temperature, sneezing, coughing, polypnea, and anorexia) and ADG were recorded during 30 days. Samples (nasal swabs and blood) were taken throughout the experimental period. Representative pro-inflammatory (IL-6), Th-1 (IL-12), and anti-inflammatory (IL-10 and TGF-b) cytokine levels in serum and lung were measured.

Clinical signs were more severe in coinfected pigs. A higher incidence of fever (p< 0.05) was found in more than 70% of dual virus–infected pigs, 52% in PRRS-only and no fever detected in PRCV alone group. The PRRS+PRCV had a lower ADG than PRRS-only and the other groups. Growth in PRRS-only pigs was reduced compared with PRCV and control.

In comparison with the control (Mock) group, PRRSV reduced NK cell cytotoxicity by 50-80% whereas in coinfected pigs it was reduced by 80–100%, confirming a synergistic immunosuppression effect. Also, co-infection caused a higher pro-inflammatory cytokines (IL-12 and IL-6).
However, dual-infection piglets had higher frequency of T-regulatory cytokines in lungs than in serum. It could indicate that the immunomodulation occurs at the infection site.

The higher T-cell and myeloid cells concentrations in the groups infected with both virus enhance the increase of Th-1 and pro-inflammatory cytokines, and could explain a higher pneumonia.

The infection with PRRSV affects innate and adaptive immune responses, which contributes to more severe consequences of a trivial (or milder) infection by PRCV.