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

Abstract

Porcine reproductive and respiratory syndrome (PRRS) is a contagious disease caused by the porcine reproductive and respiratory syndrome virus (PRRSV). PRRS is also called “blue ear disease” because of the characteristic blue ear in infected sows and piglets. Its main clinical features are reproductive disorders of sows, breathing difficulties in piglets, and fattening in pigs, which cause considerable losses to the swine industry. NSP9, a non-structural protein of PRRSV, plays a vital role in PRRSV replication and virulence because of its RNA-dependent RNA polymerase (RdRp) structure. The NSP9 sequence is highly conserved and contains T cell epitopes, which are beneficial for the development of future vaccines. NSP9 acts as the protein interaction hub between virus and host during PRRSV infection, especially in RNA replication and transcription. Herein, we comprehensively review the application of NSP9 in terms of genetic evolution analysis, interaction with host proteins that affect virus replication, interaction with other viral proteins, pathogenicity, regulation of cellular immune response, antiviral drugs, vaccines, and detection methods. This review can therefore provide innovative ideas and strategies for PRRSV prevention and control.

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

“…Porcine reproductive and respiratory syndrome virus (PRRSV) can cause fever and anorexia in infected pigs, late abortion, premature delivery, stillbirth, weak and mummified fetuses in pregnant sows, and death of pigs of all ages (mainly piglets) because of respiratory diseases [ 1 ]. Infection with highly pathogenic strains can cause fever, skin cyanosis, dyspnea, and acute death in adult pigs.…”

Zinc Oxide–Selenium Nanoparticles for Inhibiting the Proliferation of Porcine Reproductive and Respiratory Syndrome Virus

“…An alternative explanation is that ZnO–Se NPs could impact the process of PRRSV replication by interfering with the proteins involved in PRRSV replication within host cells. Nonstructural protein 9 (Nsp9), functioning as a RNA-dependent RNA polymerase (RdRp), is crucial for genome replication and subgenomic (sg mRNA) synthesis and plays a pivotal role in viral replication . It has been previously reported that some host proteins such as Annexin A2 (ANXA2), DEAD-box RNA helicase 5 (DDX5), retinoblastoma protein (pRb), and nucleotide-binding oligomerization domain-like receptor X1 (NLRX1) can bind Nsp9 to regulate replication of PRRSV.…”

“…Nonstructural protein 9 (Nsp9), functioning as a RNA-dependent RNA polymerase (RdRp), is crucial for genome replication and subgenomic (sg mRNA) synthesis and plays a pivotal role in viral replication. 44 It has been previously reported that some host proteins such as Annexin A2 (ANXA2), 45 DEAD-box RNA helicase 5 (DDX5), 46 retinoblastoma protein (pRb), 47 and nucleotidebinding oligomerization domain-like receptor X1 (NLRX1) 48 can bind Nsp9 to regulate replication of PRRSV. Therefore, the expression of some host proteins that can interact with Nsp9 was examined by RT-qPCR.…”

“…PRRSV Nsp9 has RNA-dependent RNA polymerase activity and is the major replication enzyme of the virus. 44 ZnO−Se NPs have the potential to affect PRRSV replication by altering the expression of proteins that interact with Nsp9 in the host cell. In our work, both RT-qPCR and Western blot results demonstrated a significant increase in mRNA and protein expression of NLRX1 in the ZnO−Se NPs treated group compared to the control group at 48 h. NLRX1, a member of the NLR family proteins, was initially identified as a key mediator of immune defense and inflammation.…”

“…To date, targeting the host cell factors required for viral replication is another therapeutic approach. PRRSV Nsp9 has RNA-dependent RNA polymerase activity and is the major replication enzyme of the virus . ZnO–Se NPs have the potential to affect PRRSV replication by altering the expression of proteins that interact with Nsp9 in the host cell.…”