Related Experiment Video

Updated: Aug 20, 2026

Fluorescence-based Neuraminidase Inhibition Assay to Assess the Susceptibility of Influenza Viruses to The Neuraminidase Inhibitor Class of Antivirals
09:31

Fluorescence-based Neuraminidase Inhibition Assay to Assess the Susceptibility of Influenza Viruses to The Neuraminidase Inhibitor Class of Antivirals

Published on: April 15, 2017

Attenuating mutations of the matrix gene of influenza A/WSN/33 virus

Teresa Liu1, Zhiping Ye

  • 1Laboratory of Pediatric and Respiratory Viral Diseases, Division of Viral Products, Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland, USA.

Journal of Virology
|January 15, 2005
PubMed

Insights

Mutating basic amino acids 101RKLKR105 in influenza virus M1 protein created a double mutant (R101S-R105S) that was attenuated in mice. This M1 mutant shows potential for developing live influenza virus vaccines.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • The influenza virus matrix protein (M1) is crucial for viral replication.
  • Specific basic amino acids (101RKLKR105) in M1 are implicated in RNP binding and nuclear localization.

Purpose of the Study:

  • To investigate the function of the 101RKLKR105 region in influenza A virus M1 protein.
  • To assess the impact of mutations in this region on viral replication and pathogenicity in vivo.

Main Methods:

  • Reverse genetics was used to introduce single (R101S, R105S) and double (R101S-R105S) mutations into the M gene of influenza A/WSN/33.
  • Viral replication was assessed at different temperatures.
  • BALB/c mice were infected to evaluate viral attenuation, replication in lungs, and survival rates.
  • Immunized mice were challenged with wild-type virus.

Main Results:

  • Individual mutations (R101S, R105S) had minimal effects on viral replication.
  • The double mutation (R101S-R105S) resulted in temperature sensitivity and reduced viral replication at restrictive temperatures.
  • The R101S-R105S double mutant virus was significantly attenuated in mice compared to wild-type.
  • Mice infected with the R101S-R105S mutant were fully protected against lethal challenge with wild-type virus.

Conclusions:

  • The 101RKLKR105 region of influenza M1 protein is important for viral replication and virulence.
  • The attenuated R101S-R105S double mutant exhibits promising properties for live influenza virus vaccine development.

More Related Videos

Monitoring Influenza Virus Survival Outside the Host Using Real-Time Cell Analysis09:02

Monitoring Influenza Virus Survival Outside the Host Using Real-Time Cell Analysis

Published on: February 20, 2021

Generation of Escape Variants of Neutralizing Influenza Virus Monoclonal Antibodies07:55

Generation of Escape Variants of Neutralizing Influenza Virus Monoclonal Antibodies

Published on: August 29, 2017

Related Concept Videos

Leaky Scanning02:28

Leaky Scanning

During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R stands for...
Influenza01:27

Influenza

Influenza is an acute, highly communicable viral disease that affects the respiratory tract and is responsible for seasonal epidemics worldwide. Influenza A is the most prevalent type associated with widespread outbreaks and is subtyped based on two surface glycoproteins: hemagglutinin (H) and neuraminidase (N), as in H1N1. These glycoproteins are essential for viral infectivity, transmission, and immune recognition. Transmission occurs primarily through respiratory droplets and contaminated...
Inhibitors Of Virion Release01:25

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...
Viral Mutations00:36

Viral Mutations

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 for adaptive...
Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...