Research Progress in Porcine Reproductive and Respiratory Syndrome Virus–Host Protein Interactions

Abstract

Porcine reproductive and respiratory syndrome (PRRS) is a highly contagious disease caused by porcine reproductive and respiratory syndrome virus (PRRSV), which has been regarded as a persistent challenge for the pig industry in many countries. PRRSV is internalized into host cells by the interaction between PRRSV proteins and cellular receptors. When the virus invades the cells, the host antiviral immune system is quickly activated to suppress the replication of the viruses. To retain fitness and host adaptation, various viruses have evolved multiple elegant strategies to manipulate the host machine and circumvent against the host antiviral responses. Therefore, identification of virus–host interactions is critical for understanding the host defense against viral infections and the pathogenesis of the viral infectious diseases. Most viruses, including PRRSV, interact with host proteins during infection. On the one hand, such interaction promotes the virus from escaping the host immune system to complete its replication. On the other hand, the interactions regulate the host cell immune response to inhibit viral infections. As common antiviral drugs become increasingly inefficient under the pressure of viral selectivity, therapeutic agents targeting the intrinsic immune factors of the host protein are more promising because the host protein has a lower probability of mutation under drug-mediated selective pressure. This review elaborates on the virus–host interactions during PRRSV infection to summarize the pathogenic mechanisms of PRRSV, and we hope this can provide insights for designing effective vaccines or drugs to prevent and control the spread of PRRS.

Variations in the NSP4 gene of the type 2 porcine reproductive and respiratory syndrome virus isolated in China from 1996 to 2021

“…Shi et al [ 37 ] screened targeted NSP4 antiviral drugs and obtained two antiviral candidate drugs with remarkable inhibitory activities. Analyzing the spatial structure of NSP4 protein and studying the genetic evolution of NSP4 can help screen key amino acid sites, thereby identifying important antiviral targets for the design of new drug molecules [ 38 ], as well as providing a theoretical basis for vaccine development or NSP4 gene detection methods in future.…”

Optimized protocol for double vaccine immunization against classical swine fever and porcine reproductive and respiratory syndrome

“…The potential role of PRRSV in regulating the host immune system is supported by the fact that the virus preferentially replicates and persists in macrophages, which implies that PRRSV has the ability to escape from or modulate the host immune system [ 13 ]. Once it invades the pig body, PRRSV first attacks macrophages in the lungs and can severely damage the phagocytic, bactericidal, and secretory functions of macrophages, resulting in decreased immune function [ 33 ].…”

“…Porcine reproductive and respiratory syndrome (PRRS) is a swine disease that is characterized by reproductive disorders and respiratory diseases and has a significant economic impact on the swine industry [ 8 , 9 ]. The etiological pathogenic agent of PRRS is the PRRS virus (PRRSV) [ 10 , 11 ], a positive-stranded RNA virus that is classified within the family Arteriviridae of the order Nidovirales [ 12 , 13 ]. PRRS emerged almost simultaneously in North America and Europe in the late 1980s and then spread quickly to other parts of the world within a few years [ 14 – 16 ].…”

Research Progress on the NSP9 Protein of Porcine Reproductive and Respiratory Syndrome Virus

“…Some cellular proteins can interact with PRRSV NSP9, and their interactions can regulate viral replication. In MARC-145 cells and porcine alveolar macrophages (PAMs) infected with PRRSV, some cellular proteins, including interleukin-2 enhancer-binding factor 2 (ILF2), can be translocated from the nucleus to the cytoplasm and co-localize with NSP9 and NSP2 of PRRSV ( 31 ). In contrast, ILF2 is only located in the nucleus in non-infected cells.…”