| Summary: | 碩士 === 國立成功大學 === 微生物及免疫學研究所 === 91 === Herpes simplex virus type 1 (HSV-1), a member of Herpesviridae with double-stranded DNA genome, is able to multiply and spread in multiple organs, including nervous system, to cause death. However, the pathogenesis of HSV virulence is not clearly understood. Previous and my studies showed that different HSV-1 strains varied in their virulence to cause death in mice. My results showed that these two viruses replicated to the same degree but 294.1 persisted longer than KOS in peripheral and nervous tissues. How these two viruses affect the infected brains was also investigated and compared. I found the permeability of blood-brain barrier (BBB) was altered in infected mice. The change of BBB permeability is due to viral replication in the brain because 294.1Δtk, which cannot replicate in nervous tissues, failed to open BBB. The expression of pro-inflammatory cytokines were detected in infected brains. The number of inflammatory cells increased and the major type of inflammatory cells switched from lymphocytes to monocyte/marcopgage in the brain after infection. The change of BBB permeability and degree of cytokine expression as well as inflammatory responses observed in 294.1-infected brains were greater than those in KOS-infected brains. Moreover, histological examination and Nissl staining showed the neuron damage and loss, particularly in 294.1-infected brains. Taken together, the higher virulence of 294.1 in mice might result from neuron damage in the CNS caused by both viral as well as immune activities.
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