Related Experiment Video

Updated: Jul 17, 2026

Feeding of Ticks on Animals for Transmission and Xenodiagnosis in Lyme Disease Research
08:23

Feeding of Ticks on Animals for Transmission and Xenodiagnosis in Lyme Disease Research

Published on: August 31, 2013

Microevolution of tick-borne encephalitis virus in course of host alternation

Lidiya Iu Romanova1, Anatoly P Gmyl, Tatiana I Dzhivanian

  • 1M.P. Chumakov Institute of Poliomyelitis and Viral Encephalitides, Russian Academy of Medical Sciences, Moscow Region 142782, Russia.

Virology
|January 30, 2007
PubMed

Insights

Tick-borne encephalitis (TBE) virus adapts to different hosts, showing distinct variants. Genetic changes, particularly in the E protein, drive these adaptations, influencing virus behavior in ticks and mammals.

Area of Science:

  • Virology
  • Molecular Biology
  • Arthropod-borne Viruses

Background:

  • Tick-borne encephalitis (TBE) virus causes significant neurological disease.
  • Understanding virus adaptation to different hosts is crucial for disease control.
  • Previous studies have shown TBE virus can adapt to different hosts, but the genetic basis is not fully understood.

Purpose of the Study:

  • To investigate the genetic and phenotypic differences between a mouse brain-adapted TBE virus strain and its tick-adapted derivative.
  • To identify the specific genetic mutations responsible for altered virus phenotypes.
  • To explore the concept of TBE virus heterogeneity and host switching.

Main Methods:

  • Comparative genomics of mouse-adapted (EK-328) and tick-adapted TBE virus strains.
  • Phenotypic analysis including plaque size, cell culture replication, tick yield, and neuroinvasiveness in mice.
  • Biochemical assays such as heparin-sepharose binding.
  • Reverse passaging experiments in vivo and in vitro.
  • Plaque purification of tick-adapted virus.

Main Results:

  • The tick-adapted TBE virus exhibited a small-plaque phenotype, slower replication in cell culture, higher yield in ticks, decreased neuroinvasiveness in mice, and increased heparin-sepharose binding.
  • Fifteen nucleotide substitutions distinguished the two variants, with six leading to protein sequence alterations.
  • Two specific amino acid substitutions in the E protein were identified as responsible for the observed phenotypic differences.
  • TBE virus exists as a heterogeneous population with variants adapted to either ticks or mammals, with host switching altering variant ratios.

Conclusions:

  • TBE virus exhibits significant genetic and phenotypic heterogeneity, with distinct variants adapted to tick or mammalian hosts.
  • Specific mutations in the viral E protein are key drivers of host adaptation and associated phenotypic changes.
  • The dynamic interplay between virus variants and host environments shapes TBE virus evolution and virulence.

More Related Videos

Tick Microbiome Characterization by Next-Generation 16S rRNA Amplicon Sequencing07:21

Tick Microbiome Characterization by Next-Generation 16S rRNA Amplicon Sequencing

Published on: August 25, 2018

A Capsule-Based Model for Immature Hard Tick Stages Infestation on Laboratory Mice07:05

A Capsule-Based Model for Immature Hard Tick Stages Infestation on Laboratory Mice

Published on: July 9, 2020

Related Concept Videos

Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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...
Evolution of New Traits in Microbes01:24

Evolution of New Traits in Microbes

Microorganisms evolve rapidly due to their large population sizes and short generation times, often exhibiting measurable changes within days under laboratory conditions. Natural selection acts on standing genetic variation, enabling the retention and amplification of beneficial traits that confer fitness advantages in changing environments.Adaptive Pigment Regulation in RhodobacterIn Rhodobacter, a genus of purple non-sulfur bacteria, light-harvesting pigments such as bacteriochlorophyll and...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Rocky Mountain Spotted Fever01:26

Rocky Mountain Spotted Fever

Rocky Mountain Spotted Fever (RMSF) is a severe tick-borne illness caused by Rickettsia rickettsii, a Gram-negative, coccobacillary bacterium. This pathogen is an obligate intracellular parasite, requiring a host cell for replication. Transmission occurs through the bite of an infected tick. In the United States, the most important vectors are Dermacentor variabilis (American dog tick) and Dermacentor andersoni (Rocky Mountain wood tick), though other tick species may also serve as vectors.