Classical swine fever virus (CSFV) protects cells from double-stranded (ds) RNA-mediated apoptosis and IFN-alpha/beta induction. This phenotype is lost when CSFV lacks N(pro) (DeltaN(pro) CSFV). In the present study, we demonstrate that N(pro) counteracts dsRNA-mediated apoptosis and IFN-alpha/beta induction independently of other CSFV elements. For this purpose, we generated porcine SK-6 and PK-15 cell lines constitutively expressing N(pro) fused to the enhanced green fluorescent protein (EGFP). The survival of the SK6-EGFP-N(pro) cell line after polyinosinic polycytidylic acid [poly(IC)] treatment was comparable to that of CSFV-infected SK-6 cells and was significantly higher than the survival of the parent cell line. In PK-15 cells, the presence of EGFP-N(pro) prevented the DeltaN(pro) CSFV- and poly(IC)-mediated IFN-alpha/beta production. Importantly, N(pro) also inhibited IFN-alpha and IFN-beta promoter-driven luciferase expression in human cells and blocked IFN-alpha/beta induction mediated by Newcastle disease virus. This establishes a novel function for N(pro) in counteraction of the IFN-alpha/beta induction pathway.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.virol.2005.06.033 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Immune Escape Strategy of Rabies Virus and Its Pathogenicity Mechanisms.
Viruses
November 2024
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, Guangxi University, Nanning 530004, China.
In contrast to most other rhabdoviruses, which spread by insect vectors, the rabies virus (RABV) is a very unusual member of the Rhabdoviridae family, since it has evolved to be fully adapted to warm-blooded hosts and spread directly between them. There are differences in the immune responses to laboratory-attenuated RABV and wild-type rabies virus infections. Various investigations showed that whilst laboratory-attenuated RABV elicits an innate immune response, wild-type RABV evades detection.
View Article and Find Full Text PDFA sensitive assay for measuring whole-blood responses to type I IFNs.
Proc Natl Acad Sci U S A
October 2024
Laboratory of Human Genetics of Infectious Diseases, Necker Branch, Institut National de la Santé et de la Recherche Médicale U1163, Necker Hospital for Sick Children, Paris 75015, France.
Article Synopsis
- Inborn errors or autoantibodies (auto-Abs) against type I interferons (IFNs) can lead to severe viral infections.
- Researchers developed a straightforward blood test that can identify these conditions by stimulating blood with glycosylated IFN-α2, -β, or -ω and measuring IP-10 levels.
- The study found that IP-10 levels in patients with inherited deficiencies only increase with type II IFN (IFN-γ), while those with auto-Abs can still respond to non-neutralized type I IFNs.
Dual nature of type I interferon responses and feedback regulations by SOCS1 dictate malaria mortality.
J Adv Res
August 2024
Department of Joint Surgery, the Fifth Affiliated Hospital of Southern Medical University, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China; Guangdong Provincial Key Lab of Single Cell Technology and Application, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Clinical Laboratory Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong 510000, China. Electronic address:
Introduction: Type I interferon (IFN-I, IFN-α/β), precisely controlled by multiple regulators, including suppressor of cytokine signaling 1 (SOCS1), is critical for host defense against pathogens. However, the impact of IFN-α/β on malaria parasite infections, beneficial or detrimental, remains controversial.
Objectives: The contradictory results are suspected to arise from differences in parasite species and host genetic backgrounds.
Non-infectious immune complexes downregulate the production of interferons and tumor necrosis factor-α in primary porcine alveolar macrophages .
Front Vet Sci
June 2024
College of Animal Science, Anhui Science and Technology University, Chuzhou, China.
Porcine reproductive and respiratory syndrome (PRRS) caused by the PRRS virus (PRRSV) has been harming the pig industry worldwide for nearly 40 years. Although scientific researchers have made substantial efforts to explore PRRSV pathogenesis, the immune factors influencing PRRSV infection still need to be better understood. Infectious virus-antibody immune complexes (ICs) formed by PRRSV and sub-or non-neutralizing antibodies specific for PRRSV may significantly promote the development of PRRS by enhancing PRRSV replication through antibody-dependent enhancement.
View Article and Find Full Text PDFInflammatory & Apoptotic Factor Fluctuations Associated with Japanese Encephalitis Virus Infection in Transgenic IFNAR1 Mice.
Curr Microbiol
June 2024
Laboratory of Influenza Research, College of Veterinary Medicine, Institute of Influenza Virus, Chungnam National University, 99 Dae-Hak Ro, Yuseong Gu, Daejeon, 34134, Republic of Korea.
Japanese encephalitis virus (JEV) is an orthoflavivirus that causes Japanese encephalitis, a mosquito-borne viral infection that primarily affects humans and animals. JEV is a major cause of encephalitis in many parts of Asia, particularly in rural and agricultural areas. In this study, we used the IFNAR1 mice model to investigate alterations in cytokine and apoptotic factor levels in IFNAR1 mice upon JEV infection.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!