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{{Tick-borne encephalitis}}
{{Tick-borne encephalitis}}


===Transmission===
==Transmission==
*The ''Ixodidae'' family of hard ticks have been reported as the vector and reservoir of the Tick-borne encephalitis virus.  
*The ''Ixodidae'' family of hard ticks have been reported as the vector and reservoir of the Tick-borne encephalitis virus.  
*Other modes of transmission include the consumption of raw milk as well as vertical transmission from mother to fetus.
*Other modes of transmission include the consumption of raw milk as well as vertical transmission from mother to fetus.

Revision as of 14:43, 5 February 2016

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ilan Dock, B.S.

Tick-borne encephalitis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Tick-borne encephalitis from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

MRI

CT

Other Diagnostic Studies

Treatment

Medical Therapy

Future or Investigational New Therapies

Prevention

Case Studies

Case #1

Tick-borne encephalitis pathophysiology On the Web

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Tick-borne encephalitis pathophysiology in the news

Blogs on Tick-borne encephalitis pathophysiology

Directions to Hospitals Treating Tick-borne encephalitis

Risk calculators and risk factors for Tick-borne encephalitis pathophysiology

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Ilan Dock, B.S.

Tick-borne encephalitis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Tick-borne encephalitis from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

MRI

CT

Other Diagnostic Studies

Treatment

Medical Therapy

Future or Investigational New Therapies

Prevention

Case Studies

Case #1

Tick-borne encephalitis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Tick-borne encephalitis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Tick-borne encephalitis pathophysiology

CDC on Tick-borne encephalitis pathophysiology

Tick-borne encephalitis pathophysiology in the news

Blogs on Tick-borne encephalitis pathophysiology

Directions to Hospitals Treating Tick-borne encephalitis

Risk calculators and risk factors for Tick-borne encephalitis pathophysiology

Transmission

  • The Ixodidae family of hard ticks have been reported as the vector and reservoir of the Tick-borne encephalitis virus.
  • Other modes of transmission include the consumption of raw milk as well as vertical transmission from mother to fetus.

Virology

  • Member of the Falvivirus genus
  • Flaviviridae family
  • Three subtypes: Far East, European, and Siberian
  • Viral strains are mostly homogeneous within infected European tick populations.
  • Diversity exists within viral strains carried by Siberian and Far Eastern tick populations. Thus these populations host antigenic variations and a variety of subtypes.
  • However the antigenic similarity within these populations allows for a generalized protection method among the different subtypes.

Genomics

  • (+)ssRNA genome enclosed in a capsid protein.
  • Genome is protected by a lipid bilayer, provided by the host or target cell.
  • Virus's physical attributes include a spherical particle with an approximate diameter of 50-60nm.
  • The genome lacks a 3'-poly(A) tail, yet provides a 5' cap.
  • In terms of length, the genome spans an average of 11kb.

Pathogenesis

  • The process begins as the virus binds to a host cell receptor.
  • A host cell will internalize the virus using endocytosis.
  • Post-endocytosis, acidification of the viral envelope causes conformation changes of the E protein, resulting in the attachment of the viral envelope to a endosomal vesicle.
  • Once properly mounted on the endosomal vesicle, the viral envelope will release the viral nucleocapsid into the surrounding cytoplasm.
  • Translation of the virus yields a 3414 amino acid long polyprotein.
  • The polyprotein is cleaved by both cellular and viral proteases.
  • The cleaving process results in three structural proteins called C, prM, and E as well as seven non-structural proteins.
  • The C protein forms a virion nucleocapsid through binding to viral DNA.
  • The E protein is necessary as a ligand to cell receptors and as a fusion protein.
  • The other non-structural proteins serve as proteases, polymerases, complement binding antigens, or function within the replication process.
  • Finally the processes concludes as the positive-stranded genome is translated while the negative-strand of RNA provides grounds for the RNA replication process.
  • Assembly of the virus occurs within the endoplasmic reticulum.
  • Post-assembly immature virions are released within the cell.

Viral pathway within a mammalian host

  • Virus replication commonly occurs within subcutaneous tissue.
  • Dendritic cells transport the virus to the lymph nodes.
  • The virus replicates at a high rate within the lymph nodes, further travelling into the bloodstream.
  • Lymphocytes suffer great reductions due to infection with the regional lymph nodes.
  • Further infection of external tissues occur within the viremic phase
  • The later phase results in the infection of the CNS.
  • Furthermore a host's immune system will add to the severity of the infection, as resulting immune response includes inflammation CD8+ T-cells infiltrating the brain.
  • Other immune responses such as the upregulation of proinflammatory cytokines increase the permeability of the blood-brain barrier.


References

References