Related Experiment Video

Updated: Sep 25, 2026

Rescue of Recombinant Newcastle Disease Virus from cDNA
10:55

Rescue of Recombinant Newcastle Disease Virus from cDNA

Published on: October 11, 2013

Classical swine fever virus interferes with cellular antiviral defense: evidence for a novel function of N(pro)

Nicolas Ruggli1, Jon-Duri Tratschin, Matthias Schweizer

  • 1Institute of Virology and Immunoprophylaxis, Mittelhäusern, Switzerland. nicolas.ruggli@ivi.admin.ch

Journal of Virology
|June 14, 2003
PubMed

Insights

Classical swine fever virus uses its N(pro) gene to suppress the host

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Classical swine fever virus (CSFV) efficiently replicates in cells without causing visible damage or interferon secretion.
  • CSFV's interaction with host antiviral mechanisms remains incompletely understood.

Purpose of the Study:

  • To investigate how CSFV interferes with cellular antiviral activities.
  • To determine the role of the CSFV N(pro) gene in modulating host immune responses.

Main Methods:

  • Infection of porcine cell lines (SK-6, PK-15) and macrophages (MPhi) with wild-type CSFV and N(pro)-deleted mutants (DeltaN(pro) CSFV).
  • Assessment of apoptosis resistance induced by polyinosinic-polycytidylic acid [poly(IC)].
  • Measurement of type I interferon (IFN) production.
  • Analysis of viral replication and interference with heterologous virus replication.

Main Results:

  • CSFV infection enhanced resistance to poly(IC)-induced apoptosis in SK-6 cells.
  • CSFV inhibited poly(IC)-induced type I IFN synthesis in MPhi.
  • The N(pro) gene was essential for these immune evasion mechanisms; DeltaN(pro) CSFV mutants failed to confer apoptosis resistance and did not inhibit type I IFN production.
  • DeltaN(pro) CSFV induced type I IFN in MPhi and PK-15 cells and showed impaired replication in these cells.
  • DeltaN(pro) CSFV interfered with vesicular stomatitis virus replication, unlike wild-type CSFV.

Conclusions:

  • The CSFV N(pro) gene plays a crucial role in inhibiting the host's innate immune system.
  • N(pro) function involves suppressing apoptosis and type I IFN responses, contributing to viral persistence.
  • N(pro) is a key determinant of CSFV's virulence and immune evasion strategies.

More Related Videos

Analysis of Group IV Viral SSHHPS Using In Vitro and In Silico Methods10:40

Analysis of Group IV Viral SSHHPS Using In Vitro and In Silico Methods

Published on: December 21, 2019

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors06:02

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors

Published on: September 13, 2018

Related Concept Videos

Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Leaky Scanning02:28

Leaky Scanning

During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R stands for...
Antiviral Nucleoside Inhibitors01:22

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...