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Viral Structure

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Viruses are extraordinarily diverse in shape and size, but they all have several structural features in common. All viruses have a core that contains a DNA- or RNA-based genome. The core is surrounded by a protective coat of proteins called the capsid. The capsid is composed of subunits called capsomeres. The capsid and genome-containing core are together known as the nucleocapsid.

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Bacterial Cell Wall

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Related Experiment Video

Updated: Nov 19, 2025

Separating Bacteria by Capsule Amount Using a Discontinuous Density Gradient

Separating Bacteria by Capsule Amount Using a Discontinuous Density Gradient

Published on: January 7, 2019

Capsule carbohydrate structure determines virulence in Acinetobacter baumannii.

Yuli Talyansky¹, Travis B Nielsen^1,2,3, Jun Yan¹

¹Department of Molecular Microbiology & Immunology, University of Southern California, Los Angeles, California, United States of America.

|February 2, 2021

Summary

A specific gene, gtr6, in Acinetobacter baumannii controls its capsule structure. Loss of gtr6 function enhances bacterial virulence by evading immune cell detection.

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Area of Science:

Microbiology
Bacterial Pathogenesis
Immunology

Background:

Acinetobacter baumannii is a challenging antibiotic-resistant pathogen.
Understanding A. baumannii virulence factors is crucial for developing new therapies.

Purpose of the Study:

To investigate the role of capsule assembly gene gtr6 in A. baumannii virulence.
To determine how variations in capsular structure affect host-pathogen interactions.

Main Methods:

Comparative genomics to identify virulence-associated gene variations.
Construction of isogenic gtr6 mutants in A. baumannii.
In vitro phagocytosis assays and in vivo infection models in mice.
Complement deposition assays and CR3 receptor blocking experiments.

Main Results:

A transposon insertion in gtr6 led to loss of a capsular carbohydrate branchpoint and increased virulence.
gtr6-disrupted strains showed resistance to phagocytosis, higher bacterial burden, and increased lethality in vivo.
gtr6+ strains were readily phagocytized in a complement-dependent manner mediated by the CR3 receptor.
Abrogation of CR3 function increased the virulence of hypovirulent gtr6+ strains.

Conclusions:

Loss-of-function mutations in the capsule assembly gene gtr6 significantly enhance A. baumannii virulence.
Capsular structure dictates virulence by modulating complement deposition and opsonophagocytosis.
Targeting capsule assembly or CR3-mediated pathways may offer novel therapeutic strategies against A. baumannii.