Porcine reproductive and respiratory syndrome virus (PRRSV) employs multiple receptor-mediated pathways and effector proteins to enter host cells, replicate, and evade cellular immune responses.
This review summarizes the mechanisms of PRRSV infection and host cell responses, providing insights for identifying antiviral targets in swine breeding.
Porcine reproductive and respiratory syndrome virus (PRRSV) is a far-reaching economic class of pathogen of swine breeding, causing substantial financial losses to the swine industry. Due to the lack of effective control measures and effective vaccines, the virus continues to persist and spread. PRRSV uses complex and tightly regulated processes to enter the host cells. In brief, the process can be divided into three phases: endocytosis, intracellular replication, and release. The virus employs host cell proteins and related pathways to achieve intracellular replication, evading the host's immune response. In response to exogenous intracellular pathogen infection, host cells utilize various strategies to antagonize the viral replication process. This review examines the multiple mechanisms by which PRRSV infects host cells and elucidates the pivotal roles of viral effectors during intracellular replication. In addition, it delves into the host cell response to PRRSV infection. These findings are essential for in-depth understanding and research on PRRSV infection strategies and identifying antiviral targets.
Gao et al. (Wed,) conducted a review in Porcine reproductive and respiratory syndrome virus (PRRSV) infection. PRRSV infection mechanisms was evaluated. Porcine reproductive and respiratory syndrome virus (PRRSV) employs multiple receptor-mediated pathways and effector proteins to enter host cells, replicate, and evade cellular immune responses.