Pseudorabies virus infection induces lymphocyte depletion associated with cellular apoptosis and endoplasmic reticulum stress in the mouse spleen.

BACKGROUND

The spleen is a highly organized lymphoid organ with a critical role in antimicrobial immune responses. Pseudorabies virus (PRV) is widely recognized for its ability to induce immunosuppression, with the spleen being one of the primary parenchymal organs of target. Viral infections often disrupt endoplasmic reticulum (ER) homeostasis, leading to ER stress and subsequent apoptosis. This study aimed to investigate the relationship between PRV-induced spleen damage and ER stress.

RESULTS

Both classical (Min-A) and variant (SX-2018) PRV strains caused significant histopathological damage in the mouse spleen, including marked reductions in CD8+ T cell populations and increased lymphocyte apoptosis. Further analyses revealed that PRV infection triggered ER stress and activated the PERK-eIF2α-ATF4-CHOP signaling pathway in the spleen. Notably, treatment with the ER stress inhibitor 4-phenylbutyric acid(4-PBA) mitigated lymphocyte depletion and improved survival rates in PRV-infected mice.

CONCLUSIONS

PRV infection leads to lymphocyte depletion in mouse spleens, closely associated with ER stress and apoptosis.