Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

6.0K
Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
6.0K
Viral Replication: Lysogenic Cycle01:16

Viral Replication: Lysogenic Cycle

1.1K
The lysogenic cycle is a crucial viral replication strategy that allows bacteriophages to persist within host cells without immediately destroying them. This process is primarily observed in temperate phages, such as bacteriophage lambda (λ), which infects Escherichia coli. The cycle allows the viral genome to persist across bacterial generations while keeping host cells viable.Integration of the Viral GenomeUpon infection, bacteriophage lambda attaches to the bacterial surface and injects...
1.1K
Viral Mutations00:36

Viral Mutations

39.4K
A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material...
39.4K
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

6.7K
Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
6.7K
Viral Recombination00:57

Viral Recombination

24.8K
Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.
24.8K
Viral Replication: Lytic Cycle01:20

Viral Replication: Lytic Cycle

1.0K
Bacteriophages, or phages, are viruses that specifically infect bacteria. Among them, T-even bacteriophages, such as T4, exhibit a well-characterized lytic replication cycle in Escherichia coli (E. coli). This process ensures the rapid proliferation of the virus while ultimately leading to the destruction of the bacterial host.Attachment and DNA InjectionThe infection process begins with the recognition and binding of the T4 phage to the E. coli cell surface. Tail fibers of the phage...
1.0K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Guidelines for the prevention and management of mother-to-child transmission of tuberculosis.

Quantitative imaging in medicine and surgery·2026
Same author

RNF31 restricts EV-A71 replication through innate immune activation and VP4 degradation, and is antagonized by viral 3C proteases.

PLoS pathogens·2026
Same author

Loss of Drosophila nucleostemin 1 disrupts ribosomal protein homeostasis and rRNA processing to trigger apoptosis via the Xrp1/Irbp18 complex.

Cell death discovery·2026
Same author

Cleavage of TOM1 by the SARS-CoV-2 main protease NSP5 prevents autophagic degradation of viral envelope.

Journal of virology·2026
Same author

RNF138-Mediated Ubiquitination and Degradation of NS5 Restricts Tick-Borne Encephalitis Virus Infection.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Synergistic Remodeling of Tumor Immune Microenvironment via a DNA Nanodevice Integrating STING Activation and Lysosome-Targeted PD-L1 Degradation.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Related Experiment Video

Updated: Dec 26, 2025

Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy
09:13

Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy

Published on: November 1, 2011

17.8K

Induction of SOCS Expression by EV71 Infection Promotes EV71 Replication.

Wenying Gao1, Min Hou1, Xin Liu1

  • 1The First Hospital of Jilin University, Institute of Virology and AIDS Research & Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130021, China.

Biomed Research International
|March 10, 2020
PubMed
Summary

Enterovirus 71 (EV71) infection boosts suppressor of cytokine signaling (SOCS) proteins, which are vital for viral spread. This mechanism helps EV71 evade the host immune system by blocking key signaling pathways.

More Related Videos

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

10.8K
Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
06:02

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

Published on: September 13, 2018

7.3K

Related Experiment Videos

Last Updated: Dec 26, 2025

Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy
09:13

Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy

Published on: November 1, 2011

17.8K
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

10.8K
Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
06:02

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

Published on: September 13, 2018

7.3K

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Enterovirus 71 (EV71) causes hand, foot, and mouth disease (HFMD) with no current antiviral treatments.
  • Viruses can evade host immunity by increasing suppressor of cytokine signaling (SOCS) proteins.
  • The role of SOCS proteins in EV71 immune evasion was previously unknown.

Purpose of the Study:

  • To investigate whether EV71 manipulates SOCS protein expression to evade host immunity.
  • To elucidate the mechanism by which EV71 interacts with SOCS proteins and the JAK/STAT pathway.

Main Methods:

  • EV71 infection was studied in vitro and in vivo.
  • SOCS protein expression was analyzed at mRNA and protein levels.
  • SOCS1 and SOCS3 knockdown experiments were performed.
  • STAT3 phosphorylation and NF-κB signaling were assessed.

Main Results:

  • EV71 infection significantly increased SOCS1 and SOCS3 expression.
  • Knockdown of SOCS1 or SOCS3 reduced EV71 infectivity.
  • SOCS3 was found to inhibit interferon-induced STAT3 phosphorylation, promoting viral infection.
  • SOCS expression was independent of type I interferon but blocked by NF-κB inhibition.

Conclusions:

  • EV71 upregulates SOCS1 and SOCS3 expression in an interferon-independent manner.
  • SOCS proteins, particularly SOCS3, play a critical role in facilitating EV71 infection.
  • EV71 evades host immunity by suppressing the JAK/STAT pathway via SOCS proteins.