Japanese encephalitis pathophysiology: Difference between revisions

Jump to navigation Jump to search
mNo edit summary
No edit summary
Line 53: Line 53:
|}
|}


Japanese encephalitis is contracted by the [[bite]] of an infected [[mosquito]], primarily ''Culex tritaeniorhynchus''. Japanese encephalitis virus circulates between a mosquito vector and either pigs or water birds (such as herons) in Southeast Asia.<ref name=NHSUKJapEnceph> Japanese encephalitis. National Health Service United Kingdom (2016). http://www.nhs.uk/Conditions/Japanese-encephalitis/Pages/Introduction.aspx Accessed on April 12, 2016. </ref> Transmission to humans requires mosquito species capable of creating a "bridge" between infected animals and uninfected humans; this occurs when humans become part of the enzootic cycle. The [[incubation period]] is 5-15 day(s).<ref name=CDCJaEnceph2> Japanese Encephalitis Symptoms and Treatment. Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Division of Vector-Borne Diseases. (2015) http://www.cdc.gov/japaneseencephalitis/symptoms/ Accessed on April 12, 2016. </ref>  Humans are dead-end hosts for the virus, meaning there is an insufficient amount of Japanese encephalitis virus in the blood stream to infect a mosquito; there is also no evidence of person to person spread.


Japanese encephalitis virus is transmitted in the following pattern:<ref name=ViralZoneFlavi> Flavivirus. SIB Swiss Institute of Bioinformatics. (2015) http://viralzone.expasy.org/viralzone/all_by_species/24.html Accessed on April 12, 2016</ref>
#Attachment of the [[viral envelope]] protein E to host receptors mediates internalization into the host cell by [[clathrin|clathrin-mediated]] [[endocytosis]], or by [[apoptotic]] mimicry.
#Fusion of [[biological membrane|virus membrane]] with host [[endosome|endosomal]] membrane. RNA genome is released into the cytoplasm.
#The [[positive-sense ssRNA virus]] is [[translate]]d into a [[polyprotein]], which is cleaved into all structural and non-structural proteins necessary for RNA synthesis ([[replication]] and [[transcription]]).
#[[Replication]] takes place at the surface of [[endoplasmic reticulum]] in [[cytoplasm]]ic viral factories. A [[dsRNA]] [[genome]] is synthesized from the genomic ssRNA(+).
#The [[dsRNA]] [[genome]] is [[transcribed]]/[[replicated]], thereby providing viral mRNAs/new ssRNA(+) genomes.
#Virus assembly occurs at the [[endoplasmic reticulum]]. The virion buds via the host endosomal sorting complexes required for transport (ESCRT), and is sent to the [[Golgi apparatus]].
#The prM protein is cleaved in the Golgi, thereby maturing the [[virion]] which is fusion competent.
#New virions are released by [[exocytosis]].
On microscopic histopathological analysis, the enveloped, spherical, and [[icosahedral]]-like virion shape are characteristic findings of Japanese encephalitis.





Revision as of 14:48, 12 April 2016

Japanese encephalitis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Japanese encephalitis from Other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications, and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT

MRI

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Japanese encephalitis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Japanese 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 Japanese encephalitis pathophysiology

CDC on Japanese encephalitis pathophysiology

Japanese encephalitis pathophysiology in the news

Blogs on Japanese encephalitis pathophysiology

Directions to Hospitals Treating Japanese encephalitis

Risk calculators and risk factors for Japanese encephalitis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Anthony Gallo, B.S. [2]

Overview

Pathophysiology

Japanese encephalitis virus is usually transmitted via mosquitos to the human host. Japanese encephalitis virus contains positive-sense viral RNA; this RNA has its genome directly utilized as if it were mRNA, producing a single protein which is modified by host and viral proteins to form the various proteins needed for replication. The following table is a summary of the Japanese encephalitis virus:[1][2]

Characteristic Data
Nucleic acid RNA
Sense ssRNA(+)
Virion Enveloped
Capsid Spherical
Symmetry Yes; T=3-like organization; icosahedral-like
Capsid monomers Unknown
Envelope length (diameter) 50 nm
Additional envelope information Mature virons contain 2 virus-encoded membrane proteins (M and E); immature virons contain a protein precursor
Genome shape Linear
Genome length 10-11 kb
Nucleotide cap Yes
Polyadenylated tail No; a loop structure is formed instead
Incubation period 5-15

Japanese encephalitis is contracted by the bite of an infected mosquito, primarily Culex tritaeniorhynchus. Japanese encephalitis virus circulates between a mosquito vector and either pigs or water birds (such as herons) in Southeast Asia.[3] Transmission to humans requires mosquito species capable of creating a "bridge" between infected animals and uninfected humans; this occurs when humans become part of the enzootic cycle. The incubation period is 5-15 day(s).[4] Humans are dead-end hosts for the virus, meaning there is an insufficient amount of Japanese encephalitis virus in the blood stream to infect a mosquito; there is also no evidence of person to person spread.

Japanese encephalitis virus is transmitted in the following pattern:[1]

  1. Attachment of the viral envelope protein E to host receptors mediates internalization into the host cell by clathrin-mediated endocytosis, or by apoptotic mimicry.
  2. Fusion of virus membrane with host endosomal membrane. RNA genome is released into the cytoplasm.
  3. The positive-sense ssRNA virus is translated into a polyprotein, which is cleaved into all structural and non-structural proteins necessary for RNA synthesis (replication and transcription).
  4. Replication takes place at the surface of endoplasmic reticulum in cytoplasmic viral factories. A dsRNA genome is synthesized from the genomic ssRNA(+).
  5. The dsRNA genome is transcribed/replicated, thereby providing viral mRNAs/new ssRNA(+) genomes.
  6. Virus assembly occurs at the endoplasmic reticulum. The virion buds via the host endosomal sorting complexes required for transport (ESCRT), and is sent to the Golgi apparatus.
  7. The prM protein is cleaved in the Golgi, thereby maturing the virion which is fusion competent.
  8. New virions are released by exocytosis.

On microscopic histopathological analysis, the enveloped, spherical, and icosahedral-like virion shape are characteristic findings of Japanese encephalitis.


Japanese encephalitis (JE) virus is a flavivirus which is antigenically related to St. Louis encephalitis virus.

Culex mosquito laying eggs. (Photograph by Richard G. Weber)
  • In rice fields, breeding mosquitoes (primarily Mosquito-borne Culex tritaeniorhynchus group) become infected with Japanese encephalitis virus.
  • Mosquitoes become infected by feeding on domestic pigs and wild birds infected with the Japanese encephalitis virus. Infected mosquitoes then transmit the Japanese encephalitis virus to humans and animals during the feeding process.
  • The Japanese encephalitis virus is amplified in the blood systems of domestic pigs and wild birds.
  • Japanese encephalitis virus is NOT transmitted from person-to-person. For example, one cannot get the virus from touching or kissing a person who has the disease, or from a health care worker who has treated someone with the disease.
  • Only domestic pigs and wild birds are carriers of the Japanese encephalitis virus.
  • Japanese encephalitis outbreaks are usually circumscribed and do not cover large areas. They usually do not last more than a couple of months, dying out after the majority of the pig amplifying hosts have become infected.


Gallery


References

  1. 1.0 1.1 Flavivirus. SIB Swiss Institute of Bioinformatics. (2015) http://viralzone.expasy.org/viralzone/all_by_species/24.html Accessed on April 12, 2016
  2. Japanese encephalitis - Frequently Asked Questions. CDC Centers for Disease Control and Prevention. (2015) http://www.cdc.gov/japaneseencephalitis/qa/index.html Accessed on April 12, 2016
  3. Japanese encephalitis. National Health Service United Kingdom (2016). http://www.nhs.uk/Conditions/Japanese-encephalitis/Pages/Introduction.aspx Accessed on April 12, 2016.
  4. Japanese Encephalitis Symptoms and Treatment. Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Division of Vector-Borne Diseases. (2015) http://www.cdc.gov/japaneseencephalitis/symptoms/ Accessed on April 12, 2016.
  5. "Public Health Image Library (PHIL)".