Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Viruses with RNA Genomes

Viruses with RNA Genomes

RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...

Immune Response Against Viral Pathogens

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 Synthesis

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...

Inhibitors Of Virion Release

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...

Size and Structure of Viral Genomes

Size and Structure of Viral Genomes

Viral genomes exhibit remarkable diversity in size, structure, and composition, influencing their replication strategies and interactions with host cells. These genomes consist of either DNA or RNA and may be linear or circular. Additionally, they can be single-stranded or double-stranded, with each configuration affecting how the virus propagates within a host. RNA viruses, for instance, generally have smaller genomes than DNA viruses, a factor that contributes to their high mutation rates and...

Microbial Interactions: Parasitism

Microbial Interactions: Parasitism

Parasitism is a form of microbial interaction in which parasitic microbes exploit a host organism for nutrients and shelter, often at the host's expense. Unlike mutualistic relationships, where both organisms benefit, parasitism benefits only the parasite and harms the host.Classification of ParasitesMicrobial parasites are broadly classified based on their location relative to the host.Ectoparasites remain on the host’s surface, such as the skin or outer tissues, drawing nutrients...

You might also read

Related Articles

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

Sort by

Same author

microRNA-203a-3p sensitizes cisplatin through disruption of RAN-dependent RRM2 nuclear localization and mitochondrial stress readouts.

Biochimica et biophysica acta. Gene regulatory mechanisms·2026

Same author

Integrated omics and virtual screening predict Tabularin as a dual inhibitor of the prognostic microRNAs mir-19a and mir-32 in colorectal cancer.

Computational biology and chemistry·2026

Same author

E-InfertilityTest: Implementing an explainable AI framework for male infertility assessment.

Biochemical and biophysical research communications·2026

Same author

AI in multi-omics analysis in stem cell research.

Progress in molecular biology and translational science·2026

Same author

KLF5-mediated transcriptional activation of miR-203a inhibits EMT and increases cisplatin sensitivity by targeting SNAI2 in tongue cancer.

Archives of biochemistry and biophysics·2026

Same author

An intronic bidirectional promoter-driven lncRNA (LjPLR) putatively modulates a late nodulin gene during nodulation in Lotus japonicus.

Molecular biology reports·2026

Search research articles

Related Experiment Video

Updated: Jun 27, 2026

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

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

Published on: September 13, 2018

Cellular versus viral microRNAs in host-virus interaction.

Zhumur Ghosh¹, Bibekanand Mallick, Jayprokas Chakrabarti

¹Computational Biology Group, Indian Association for the Cultivation of Science, Jadavpur, Calcutta 700 032, India. ghosh.jhumur@gmail.com

Nucleic Acids Research

|December 20, 2008

Summary

MicroRNAs (miRNAs) regulate gene expression and impact host-pathogen interactions during viral infections. Understanding these interactions can lead to novel antiviral therapies.

More Related Videos

MicroRNA-based Regulation of Picornavirus Tropism

MicroRNA-based Regulation of Picornavirus Tropism

Published on: February 6, 2017

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Published on: October 7, 2011

Related Experiment Videos

Last Updated: Jun 27, 2026

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

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

Published on: September 13, 2018

MicroRNA-based Regulation of Picornavirus Tropism

MicroRNA-based Regulation of Picornavirus Tropism

Published on: February 6, 2017

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Published on: October 7, 2011

Area of Science:

Molecular Biology
Virology
Genetics

Background:

MicroRNAs (miRNAs) are small non-coding RNAs regulating gene expression.
miRNAs play a crucial role in host-pathogen interactions, particularly during viral infections.
Both hosts and viruses utilize miRNAs to modulate cellular responses.

Purpose of the Study:

To summarize recent updates on miRNA-induced gene silencing in host-virus interactions.
To explore how viruses exploit cellular miRNA pathways and encode their own miRNAs.
To discuss the potential of miRNA-based therapies against viral infections.

Main Methods:

Literature review of recent studies on miRNAs and viral infections.
Analysis of molecular mechanisms of miRNA-mediated gene silencing.
Discussion of viral strategies involving miRNAs.

Main Results:

Host miRNAs can modulate viral gene expression, influencing infection outcomes.
Viruses encode miRNAs to evade host antiviral responses and exploit cellular pathways.
The complex interplay between host and viral miRNAs affects viral tropism, latency, and oncogenesis.

Conclusions:

Understanding miRNA-mediated host-virus interactions is key to explaining viral pathogenesis.
miRNA research offers promising avenues for developing effective, non-toxic antiviral therapies.