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Related Concept Videos

In vitro Mutagenesis01:16

In vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
In-vitro Mutagenesis01:16

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Mutations in Microorganisms01:18

Mutations in Microorganisms

Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).

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Related Experiment Video

Updated: Jun 27, 2026

A Protocol for Functional Assessment of Whole-Protein Saturation Mutagenesis Libraries Utilizing High-Throughput Sequencing
11:36

A Protocol for Functional Assessment of Whole-Protein Saturation Mutagenesis Libraries Utilizing High-Throughput Sequencing

Published on: July 3, 2016

In Silico Saturation-Mutagenesis-Based Genomic Mutation Risk Assessment for Enterovirus B.

Linglin Wang1, Jiajie Tang1, Yongtao Jia1,2

  • 1School of Public Health, Health Science Center, Ningbo University, Ningbo 315211, China.

Viruses
|June 26, 2026
PubMed
Summary

Enterovirus B (EVB) genomic variations pose risks for diseases like hand, foot, and mouth disease. This study developed a risk assessment framework using computational methods and machine learning to identify high-risk mutations, aiding future antiviral drug and vaccine development.

Keywords:
bioinformaticscoxsackievirus Bdeep mutational scanning (DMS)echovirusenterovirus Bfitnessmachine learningreceptor-binding affinitysaturation mutagenesisstructural stability

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Last Updated: Jun 27, 2026

A Protocol for Functional Assessment of Whole-Protein Saturation Mutagenesis Libraries Utilizing High-Throughput Sequencing
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Published on: July 3, 2016

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12:31

In Vivo Modeling of the Morbid Human Genome using Danio rerio

Published on: August 24, 2013

Area of Science:

  • Virology
  • Genomics
  • Computational Biology

Background:

  • Enterovirus B (EVB) is a prevalent human enterovirus species causing significant childhood diseases.
  • Current lack of antiviral drugs or vaccines necessitates enhanced monitoring and risk assessment of EVB genomic variations.
  • Key EVB serotypes include Coxsackievirus B (CVB) and echoviruses (E).

Purpose of the Study:

  • To evaluate the impact of structural protein mutations on EVB structural stability and receptor-binding affinity.
  • To develop a machine learning-based risk prediction model for EVB fitness.
  • To integrate multiple phenotypes for comprehensive EVB genomic variation risk assessment.

Main Methods:

  • Computational saturation mutagenesis using FoldX on representative EVB serotypes (CVB1, CVB3, E6, E30).
  • Machine learning model construction based on deep mutational scanning data for CVB3, applied to other EVB serotypes.
  • Integration of structural stability, receptor-binding affinity, and fitness data for risk evaluation.
  • Molecular evolution analysis and mutation profiling to track high-risk mutants in natural viral sequences.

Main Results:

  • Identified N-terminus and C-terminus of VP1, and EF loop of VP2 as high-risk regions for EVB genomic variation.
  • High-risk mutations were found to significantly influence viral evolutionary history.
  • The developed framework successfully assessed genomic variation risk across EVB serotypes.

Conclusions:

  • The study provides a novel multi-phenotypic, multi-data framework for assessing EVB genomic variation risk.
  • Findings offer crucial insights for the development of targeted antiviral drugs and vaccines against EVB.
  • Identifying high-risk mutation sites can guide future surveillance and intervention strategies for EVB outbreaks.