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====Pathogenesis====
 
====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 producedViral 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.
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Upon entry to the host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes.  In macrophages and neutrophils viral replication leads to shedding and significant clearance of viral particles.  No further clinical signs develop if this clearance is successful.  Erythrocyte and leukocyte absorption are used to circumvent the immune defences of the host.  After incomplete elimination, residual virus infects endothelial cells and accumulates in highly vascular organs such as the liver and spleen.  In these organs, viral replication produces circulating virus and a second viraemic period, typically associated with early clinical signs.  Neuroinvasion and replication occurs within a weekAn incubation period of 7-21days has been demonstrated after experimental infection with Eastern or Western EEV, but the incubtion is often shorter for EEE compared with WEE.
 
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Viraemia during the acute phase of EEE and WEEIncubation period of 1-3weeks after experimental infection with EEE or WEE.  Incubtion often shorter with EEE.  Central nervous system (CNS) replication within a week
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3 key phases of the pathogenesis of alphavirus encephalitis. These are the early extraneural phase, the process of neuroinvasion itself, and virus and host factors related to neurovirulence.
      
====Signalment====
 
====Signalment====
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