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Related Concept Videos

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...
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...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
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...
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
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...

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Related Experiment Video

Updated: Jun 23, 2026

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

NPC1 promotes HTNV replication by controlling innate immune response.

Hansong Qi1, Yuechun Wu1,2, Rong Wei1,2

  • 1Key Laboratory of Genetic Evolution and Animal Models, Yunnan International Joint Laboratory of Zoonotic Viruses, Yunnan Key Laboratory of Biodiversity Information, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China.

Frontiers in Immunology
|June 22, 2026
PubMed
Summary

Hantaan virus (HTNV) infection is linked to Niemann-Pick C1 (NPC1), a cholesterol transporter. NPC1 promotes HTNV replication by suppressing the host

Keywords:
HTNVNPC1glycoproteininnate immunityprotein interaction

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Electroporation-Based CRISPR-Cas9-Mediated Gene Knockout in THP-1 Cells and Single-Cell Clone Isolation
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Electroporation-Based CRISPR-Cas9-Mediated Gene Knockout in THP-1 Cells and Single-Cell Clone Isolation

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Last Updated: Jun 23, 2026

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

Electroporation-Based CRISPR-Cas9-Mediated Gene Knockout in THP-1 Cells and Single-Cell Clone Isolation
09:29

Electroporation-Based CRISPR-Cas9-Mediated Gene Knockout in THP-1 Cells and Single-Cell Clone Isolation

Published on: February 28, 2025

Area of Science:

  • Virology
  • Immunology
  • Computational Biology

Background:

  • Hantaan virus (HTNV) is a significant pathogen causing hemorrhagic fever with renal syndrome (HFRS) in Asia.
  • Understanding virus-host interactions, especially protein-protein interactions, is crucial for HFRS pathogenesis and patient outcomes.
  • The specific interactions between HTNV and host proteins remain largely uncharacterized.

Purpose of the Study:

  • To identify host proteins that interact with the HTNV glycoprotein (GP).
  • To elucidate the role of identified host factors in HTNV replication and pathogenesis.
  • To explore potential antiviral targets based on virus-host interactions.

Main Methods:

  • Utilized deep-learning-based virtual screening (MaSIF) to predict potential host-virus interactions.
  • Employed immunoprecipitation coupled with mass spectrometry (IP-MS) to experimentally validate protein-protein interactions.
  • Investigated the functional role of identified host factors in HTNV replication and innate immune response.

Main Results:

  • Identified Niemann-Pick C1 (NPC1), a host cholesterol transporter, as a binding partner of HTNV GP.
  • Demonstrated that NPC1 significantly promotes HTNV replication.
  • Found that NPC1 mitigates the anti-viral innate immune response following HTNV infection, a novel function.

Conclusions:

  • NPC1 interacts with HTNV GP and facilitates viral replication.
  • NPC1 plays a previously unrecognized role in suppressing antiviral immunity during HTNV infection.
  • NPC1 represents a potential therapeutic target for antiviral strategies against HTNV.