Tick-borne encephalitis pathophysiology: Difference between revisions
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Created page with "__NOTOC__ {{CMG}} {{AE}} {{IMD}} {{Tick-borne encephalitis}} ==Overview== ==Human pathogenesis== ===Genomics=== *The responsible virus, '''''Tick-Borne Encephalitis Virus'..." |
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==Overview== | ==Overview== | ||
== | __NOTOC__ | ||
{{CMG}} {{AE}} {{IMD}} | |||
{{Tick-borne encephalitis}} | |||
===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=== | ===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. | ||
*The ' | *A host cell will internalize the virus using endocytosis. | ||
*Other | *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== | |||
{{Reflist|2}} | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 21:53, 4 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 |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Tick-borne encephalitis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Tick-borne encephalitis pathophysiology |
|
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 |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Tick-borne encephalitis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Tick-borne encephalitis pathophysiology |
|
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.