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Related Experiment Video

Updated: Jun 2, 2026

Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells

Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells

Published on: November 12, 2015

Nuclear remodelling during viral infections.

H Zakaryan¹, T Stamminger

¹Laboratory of Cell Biology, Institute of Molecular Biology of NAS, Yerevan, Armenia. hovakim@yba.am

Cellular Microbiology

|April 20, 2011

Summary

Viruses hijack the host cell nucleus for replication due to limited coding capacity. Viral infections cause significant nuclear remodelling and interfere with antiviral defense mechanisms within the nucleus.

Area of Science:

Cell Biology
Virology
Molecular Biology

Background:

Viruses possess limited coding capacity and rely on host cell machinery for replication.
The host cell nucleus is a critical site exploited by both DNA and RNA viruses.
Viral infection leads to substantial alterations in nuclear structure and function.

Purpose of the Study:

To review the significant changes occurring within the host cell nucleus during viral infections.
To highlight the interplay between viruses and nuclear structures, including antiviral defense mechanisms.

Main Methods:

Literature review of studies on viral-nuclear interactions.
Analysis of documented nuclear remodelling events during viral pathogenesis.
Examination of viral strategies to overcome nuclear-based antiviral defenses.

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Last Updated: Jun 2, 2026

Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells

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Published on: November 12, 2015

Functional Imaging of Viral Transcription Factories Using 3D Fluorescence Microscopy

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Published on: January 18, 2018

Identification of Nucleolar Factors During HIV-1 Replication Through Rev Immunoprecipitation and Mass Spectrometry

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Published on: June 26, 2019

Main Results:

Viruses extensively remodel the nucleus to facilitate viral replication.
Subnuclear structures like promyelocytic leukaemia nuclear bodies function as antiviral defenses.
Viruses actively antagonize these nuclear defense mechanisms by altering subnuclear structures.

Conclusions:

The host cell nucleus is a dynamic battleground during viral infections.
Understanding nuclear alterations provides insights into viral replication strategies and host-pathogen interactions.
Targeting nuclear modifications could offer novel antiviral therapeutic strategies.