Characterizing the thymic lesions in piglets infected with attenuated strains of highly pathogenic porcine reproductive and respiratory syndrome virus

• The ability of HP-PRRSV inducing thymus atrophy reduced following the virus pathogenicity attenuated.
• HP-PRRSV HuN4-F23 strain could still cause the thymus atrophy, accompanied by thymocytes apoptosis.
• HP-PRRSV HuN4-F30 strain had already lost the ability to induce the thymus atrophy.
• HP-PRRSV HuN4-F23 and HuN4-F30 could be chosen for studying the molecular mechanism of the thymus lesions induced by HP-PRRSV HuN4 infection.

Piglets infected with the highly pathogenic PRRSV (HP-PRRSV) HuN4 strain develop severe thymus atrophy. However, the attenuated strain HuN4-F112 does not lead to lesions in organs. Here, we have characterized the thymic lesions in piglets infected with attenuated strains of HP-PRRSV HuN4 isolated at different passages in the attenuation process to produce HuN4-F112 from the parent HuN4 strain (HuN4-F5, HuN4-F15, HuN4-F23, HuN4-F30, and HuN4-F112). The thymic effects of infection were evaluated in terms of the thymus/body weight ratio, pathological changes, and thymocytes apoptosis. The ability of HP-PRRSV to induce thymus atrophy was reduced following attenuation after 23 passages; the HuN4-F23, but not HuN4-F30, caused thymus atrophy. The ability of the virus to induce thymocyte apoptosis decreased as it became attenuated. In addition, the viral load in the thymus was reduced as the virus was attenuated. The HuN4-F23 and HuN4-F30 strains might provide insight into the molecular mechanisms of HP-PRRSV pathogenesis. Taken together, our results indicate that the ability of HP-PRRSV to induce thymic atrophy is related to its pathogenicity.