ArticleJournal of virology2018
Host Factor SPCS1 Regulates the Replication of Japanese Encephalitis Virus through Interactions with Transmembrane Domains of NS2B.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Development of JEV NS1 Specific Capture-ELISA Based on a Single Monoclonal Antibody.Animals : an open access journal from MDPI · 2026Article
- Zika virus recruits karyopherin α6 for efficient replication via NS2B.Journal of virology · 2026Article
- Virus-host interactome reveals host cellular pathways perturbed by tick-borne encephalitis virus infection.iScience · 2026Article
- SPCS2 serves as a critical host factor for JEV replication by regulating viral protein stability and virion assembly.Microbiology spectrum · 2026Article
- Signal peptidase complex mediates rotavirus VP7 processing and virion assembly.PLoS pathogens · 2026Article
- Signal peptidase complex mediates rotavirus VP7 processing and virion assembly.bioRxiv : the preprint server for biology · 2025Article
- Decoding Alzheimer's Disease With Depression: Molecular Insights and Therapeutic Target.Journal of cellular and molecular medicine · 2025Article
- Functional Roles and Host Interactions ofPathogens (Basel, Switzerland) · 2025Review
- Host Factor Rab4b PromotesMicroorganisms · 2024Article
- The Signal Peptidase FoSpc2 Is Required for Normal Growth, Conidiation, Virulence, Stress Response, and Regulation of Light Sensitivity in Fusarium odoratissimum.Microbiology spectrum · 2023Article
- Simultaneous membrane and RNA binding by tick-borne encephalitis virus capsid protein.PLoS pathogens · 2023Article
- Japanese Encephalitis Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Whole-Blood 3-Gene Signature as a Decision Aid for Rifapentine-based Tuberculosis Preventive Therapy.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022Article
- Transmembrane transport process and endoplasmic reticulum function facilitate the role of gene cel1b in cellulase production of Trichoderma reesei.Microbial cell factories · 2022Article
- SPCS1-Dependent E2-p7 processing determines HCV Assembly efficiency.PLoS pathogens · 2022Article
- Spc1 regulates the signal peptidase-mediated processing of membrane proteins.Journal of cell science · 2021Article
- Article
- Iminosugars: A host-targeted approach to combat Flaviviridae infections.Antiviral research · 2020Review
- The G Protein-Coupled Receptor FFAR2 Promotes Internalization during Influenza A Virus Entry.Journal of virology · 2020Article
- Hsp40 Protein DNAJB6 Interacts with Viral NS3 and Inhibits the Replication of the Japanese Encephalitis Virus.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal peptidase complex subunit 1 (SPCS1) is a newly identified host factor that regulates flavivirus replication, but the molecular mechanism is not fully understood. Here, using Japanese encephalitis virus (JEV) as a model, we investigated the mechanism through which the host factor SPCS1 regulates the replication of flaviviruses. We first validated the regulatory function of SPCS1 in JEV propagation by knocking down and knocking out endogenous SPCS1. The loss of SPCS1 function markedly reduced intracellular virion assembly and the production of infectious JEV particles but did not affect cell entry, RNA replication, or translation of the virus. SPCS1 was found to interact with nonstructural protein 2B (NS2B), which is involved in posttranslational protein processing and virus assembly. Serial deletion mutation of the JEV NS2B protein revealed that two transmembrane domains, NS2B(1-49) and NS2B(84-131), interact with SPCS1. Further mutagenesis analysis of conserved flavivirus residues in two SPCS1 interaction domains of NS2B demonstrated that G12A, G37A, and G47A in NS2B(1-49) and P112A in NS2B(84-131) weakened the interaction with SPCS1. Deletion mutation of SPCS1 revealed that SPCS1(91-169), which contains two transmembrane domains, was involved in interactions with both NS2B(1-49) and NS2B(84-131). Taken together, these results demonstrate that SPCS1 affects viral replication by interacting with NS2B, thereby influencing the posttranslational processing of JEV proteins and the assembly of virions.
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