Tick-borne encephalitis pathophysiology: Difference between revisions
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*Translation of the virus yields a 3414 amino acid long polyprotein. | *Translation of the virus yields a 3414 amino acid long polyprotein. | ||
*The polyprotein is cleaved by both cellular and viral proteases. | *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 cleaving process results in three structural proteins called C, prM, and E as well as seven non-structural proteins.<ref name= "Enceph Prime"> Tick-borne Encephalitis Virus: A General Overview. http://cdn.intechopen.com/pdfs-wm/20866.pdf. Accessed February 4, 2016. </ref> | ||
*The C protein forms a virion nucleocapsid through binding to viral DNA. | *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 E protein is necessary as a ligand to cell receptors and as a fusion protein. | ||
| Line 38: | Line 38: | ||
*Finally the processes concludes as the positive-stranded genome is translated while the negative-strand of RNA provides grounds for the RNA 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. | *Assembly of the virus occurs within the endoplasmic reticulum. | ||
*Post-assembly immature virions are released within the cell. | *Post-assembly immature virions are released within the cell.<ref name= "Enceph Prime"> Tick-borne Encephalitis Virus: A General Overview. http://cdn.intechopen.com/pdfs-wm/20866.pdf. Accessed February 4, 2016. </ref> | ||
[[Image:Tick-borne encephalitis pathogenisis.jpg|400px|left|thumb| ''Schematic drawing of the steps during TBE virus infection. (1) TBE virus transmission | |||
from an infected tick, (2) TBE virus replication in regional lymph node, (3) primary viremia, | |||
(4) replication of the virus in other organs and tissues, (5) secondary viremia, (6) TBE virus | |||
crossing of the blood-brain barrier, and (7) virus infection of the brain''<ref name= "Enceph Prime"> Tick-borne Encephalitis Virus: A General Overview. http://cdn.intechopen.com/pdfs-wm/20866.pdf. Accessed February 4, 2016. </ref>]] | |||
===Viral pathway within a mammalian host=== | ===Viral pathway within a mammalian host=== | ||
*Virus replication commonly occurs within subcutaneous tissue. | *Virus replication commonly occurs within subcutaneous tissue. | ||
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*The later phase results in the infection of the CNS. | *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. | *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. | *Other immune responses such as the upregulation of proinflammatory cytokines increase the permeability of the blood-brain barrier.<ref name= "Enceph Prime"> Tick-borne Encephalitis Virus: A General Overview. http://cdn.intechopen.com/pdfs-wm/20866.pdf. Accessed February 4, 2016. </ref> | ||
==References== | ==References== | ||
Revision as of 15:32, 5 February 2016
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ilan Dock, B.S.
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Tick-borne encephalitis Microchapters |
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Tick-borne encephalitis pathophysiology On the Web |
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Risk calculators and risk factors for Tick-borne encephalitis pathophysiology |
Overview
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.[1]
- 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.[1]
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.[1]
References
- ↑ 1.0 1.1 1.2 1.3 Tick-borne Encephalitis Virus: A General Overview. http://cdn.intechopen.com/pdfs-wm/20866.pdf. Accessed February 4, 2016.