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Viral Structure

Viral Structure

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.

Retroviruses

Retroviruses

Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...

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Retrovirus Life Cycles

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Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the...

Viral Mutations

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A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material...

Mechanisms of Retrovirus-induced Cancers

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Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...

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Related Experiment Video

Updated: May 12, 2025

Prediction of HIV-1 Coreceptor Usage Tropism by Sequence Analysis using a Genotypic Approach

Prediction of HIV-1 Coreceptor Usage Tropism by Sequence Analysis using a Genotypic Approach

Published on: December 1, 2011

Predicting Motif-Mediated Interactions Based on Viral Genomic Composition.

Sobia Idrees^1,2, Keshav Raj Paudel², Mithila Banik³

¹School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2033, Australia.

International Journal of Molecular Sciences

|May 7, 2025

Summary

This summary is machine-generated.

Viruses mimic host proteins using short linear motifs (SLiMs) to infect cells. This study reveals that viral genomic composition, particularly dsDNA viruses, influences this mimicry, impacting virus-host interactions and antiviral therapy development.

Keywords:

bioinformatics short linear motifs viral mimicry virus–host interactions

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Last Updated: May 12, 2025

Prediction of HIV-1 Coreceptor Usage Tropism by Sequence Analysis using a Genotypic Approach

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Published on: December 1, 2011

Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins

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Published on: August 31, 2017

A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions

A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions

Published on: July 18, 2013

Area of Science:

Virology and Molecular Biology
Bioinformatics and Computational Biology

Background:

Viruses hijack host cellular machinery for replication, often by mimicking host protein short linear motifs (SLiMs).
Predicting viral mimicry is difficult due to the inherent degeneracy of SLiMs, despite growing virus-host protein-protein interaction (vhPPI) data.

Purpose of the Study:

To investigate the influence of viral genomic composition on SLiM mimicry.
To elucidate the mechanisms by which viruses utilize SLiMs to hijack host cellular functions.
To identify novel virus-host interactions mediated by SLiMs.

Main Methods:

Assessed domain-motif interaction (DMI) enrichment differences across various viral groups.
Utilized SLiMEnrich v.1.5.1 to predict novel DMIs based on known viral motifs at varying stringency levels.
Analyzed viral genomic composition's role in SLiM mimicry and vhPPIs.

Main Results:

Double-stranded DNA (dsDNA) viruses showed significantly higher capture of known DMIs compared to other viral types.
Double-stranded RNA (dsRNA) viruses exhibited greater DMI enrichment than single-stranded RNA (ssRNA) viruses.
Identified novel vhPPIs mediated by SLiMs, with specific patterns observed across different viral genomic contexts.

Conclusions:

Viral genomic composition plays a crucial role in the extent and nature of SLiM mimicry.
Understanding these virus-host SLiM interactions is key to deciphering viral hijacking strategies.
Findings may inform the development of targeted antiviral therapies by exploiting viral mimicry mechanisms.