Difference between revisions of "Equine Encephalitis Virus"
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====Diseases==== | ====Diseases==== | ||
[[Equine Viral Encephalomyelitides|Equine viral encephalomyelitides]] | [[Equine Viral Encephalomyelitides|Equine viral encephalomyelitides]] | ||
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| + | ====Pathogenesis==== | ||
| + | After inoculation into an equine host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes. Viral replication occurs in macrophages and neutrophils with subsequent shedding and significant clearance of viral particles. No further clinical signs develop if clearance is successful but neutralizing Abs are still produced. Viral immunological avoidance mechanisms include erythrocyte and leukocyte absorption. After incomplete elimination, residual virus infects endothelial cells and concentrates in highly vascular organs such as the liver and spleen. In these organs, viral replication produces circulating virus. The second viraemic period is typically associated with early clinical signs. CNS infection occurs within 3-5 days. | ||
Revision as of 17:48, 6 July 2010
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This article is still under construction. |
Viral Family
Members of the Togaviridae are small, lipid- and protein-enveloped RNA viruses. Within this family are disease-causing arboviruses (insect-borne virsuses) of the Alphavirus genus.
Viral Genus
Alphaviruses are single-stranded, linear, positive-sense RNA viruses, 60-70nm in diameter.
Important Serotypes
During equine and human epidemics of encephalitis in the Western Hemisphere, the most frequently isolated alphaviruses have included:
- Eastern Equine Encephalitis virus (EEV)
- Western EEV
- Venezuelan EEV
Diseases
Equine viral encephalomyelitides
Pathogenesis
After inoculation into an equine host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes. Viral replication occurs in macrophages and neutrophils with subsequent shedding and significant clearance of viral particles. No further clinical signs develop if clearance is successful but neutralizing Abs are still produced. Viral immunological avoidance mechanisms include erythrocyte and leukocyte absorption. After incomplete elimination, residual virus infects endothelial cells and concentrates in highly vascular organs such as the liver and spleen. In these organs, viral replication produces circulating virus. The second viraemic period is typically associated with early clinical signs. CNS infection occurs within 3-5 days.