International Scholarly Research Notices / 2013 / Article / Fig 4

Review Article

The Pathogenesis of Alphaviruses

Figure 4

Diagrammatic representation of SFV pathogenesis. The dotted lines represent partial inhibition. Following peripheral (intramuscular, intraperitoneal, or subcutaneous) infection, the virus produces a transient viremia, largely through multiplication in muscle. It then crosses the blood-brain barrier and multiplies in the CNS. All strains of SFV show a tropism for neurons and oligodendrocytes. Infection of neurons with the virulent L10 and SFV4 strains results in a lethal threshold of damage to neurons. Multiplication of the avirulent A7, A7 [49], and M9 strains is partially restricted in neurons and immune intervention occurs to clear the virus before lethal damage can occur. The result of oligodendrocyte infection is myelin damage leading to the presentation of myelin antigens to the immune system and inflammatory demyelination, which could also occur by molecular mimicry. Remyelination occurs in BALB/c mice, but small lesions of demyelination and proinflammatory cytokine secretion occur in SJL mice for up to a year.
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