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Related Concept Videos

Predator-Prey Interactions02:39

Predator-Prey Interactions

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Predators consume prey for energy. Predators that acquire prey and prey that avoid predation both increase their chances of survival and reproduction (i.e., fitness). Routine predator-prey interactions elicit mutual adaptations that improve predator offenses, such as claws, teeth, and speed, as well as prey defenses, including crypsis, aposematism, and mimicry. Thus, predator-prey interactions resemble an evolutionary arms race.
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Defenses Against Pathogens and Herbivores02:26

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Defense Against Bacterial Pathogens01:31

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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
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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.
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Van der Waals Interactions01:24

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Atoms and molecules interact with each other through intermolecular forces. These electrostatic forces arise from attractive or repulsive interactions between particles with permanent, partial, or temporary charges. The intermolecular forces between neutral atoms and molecules are ion–dipole, dipole–dipole, and dispersion forces, collectively known as van der Waals forces.
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piRNA - Piwi-interacting RNAs02:57

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PIWI-interacting RNAs, or piRNAs, are the most abundant short non-coding RNAs. More than 20,000 genes have been found in humans that code for piRNAs while only 2000 genes have been found for miRNAs. piRNAs can act at the transcriptional and post-transcriptional levels and have a vital role in silencing transposable elements present in germ cells. They are also involved in epigenetic silencing and activation. Previously, they were thought to function only in germ cells but new evidence suggests...
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Updated: Jan 23, 2026

Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
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Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions

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Human Coronavirus: Host-Pathogen Interaction.

To Sing Fung1, Ding Xiang Liu1

  • 1Guangdong Province Key Laboratory of Microbial Signals and Disease Control and Integrative Microbiology Research Centre, South China Agricultural University, Guangzhou 510642, Guangdong, People's Republic of China;

Annual Review of Microbiology
|June 22, 2019
PubMed
Summary
This summary is machine-generated.

Human coronaviruses (HCoV) cause respiratory illnesses, with recent zoonotic strains like SARS-CoV and MERS-CoV posing significant threats. This review details how HCoV manipulates host factors and signaling pathways, including stress responses and immunity, for replication.

Keywords:
ER stressMAPKapoptosiscoronavirushost-virus interactioninnate immunity

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Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Human coronaviruses (HCoV) cause a spectrum of respiratory diseases, ranging from mild to severe.
  • The emergence of zoonotic HCoVs, such as SARS-CoV and MERS-CoV, highlights their pandemic potential.
  • HCoV replication involves intricate interactions with host cellular machinery and signaling pathways.

Purpose of the Study:

  • To review host factors and signaling pathways exploited by HCoV during infection.
  • To elucidate the mechanisms underlying HCoV pathogenesis and host-pathogen interactions.
  • To discuss the interplay between HCoV infection and cellular processes like stress response, autophagy, apoptosis, and innate immunity.

Main Methods:

  • Literature review of recent studies on HCoV-host interactions.
  • Analysis of signaling pathways activated during HCoV infection.
  • Examination of cellular responses including stress, autophagy, apoptosis, and innate immunity.

Main Results:

  • HCoV infection hijacks diverse host factors to facilitate viral replication.
  • Activated signaling pathways modulate antiviral immunity and contribute to disease severity.
  • HCoV employs specific strategies to crosstalk with and modulate host cellular pathways.

Conclusions:

  • Understanding HCoV-host interactions is crucial for developing effective antiviral strategies.
  • The intricate interplay between HCoV and host pathways offers potential therapeutic targets.
  • Further research into these mechanisms can illuminate HCoV pathogenesis and host defense.