PRRSV interaction with the adaptive immune system of host: an update review

Porcine reproductive and respiratory syndrome virus (PRRSV), a highly variable RNA virus, causes a significant threat to the global swine industry. PRRSV suppresses both innate and adaptive immune responses in the host. While only the regulation of innate immunity by PRRSV has been summarized. This article systematically reviews the regulatory roles of PRRSV on the host's adaptive immune system, and summarizes its impact on the behavior of T cells, B cells, macrophages, monocytes, dendritic cells, and natural killer cells (NK cells). PRRSV evades antiviral immunity through multiple mechanisms, including down-regulating antigen-presenting molecules such as major histocompatibility complex class (MHC) -I/II, inducing immunosuppressive microenvironments such as up-regulating interleukin-10 (IL-10) and Programmed Death-Ligand 1 (PD-L1), and interfering with the generation of neutralizing antibodies, thereby weakening the host's antiviral immune response and leading to persistent viral infection. Furthermore, this article explores novel immunology-based control strategies, such as the screening of broadly neutralizing antibodies, multi-epitope vaccine design, chimeric antigen receptor T (CAR-T) cells therapy, and vaccines aimed at enhancing T-cell immunity. By targeting conserved antigenic epitopes or engineering immune cells, these approaches seek to overcome the limitations of conventional vaccines, offering new directions for PRRSV prevention and control.