The Experts below are selected from a list of 251553 Experts worldwide ranked by ideXlab platform
Diethilde Theil - One of the best experts on this subject based on the ideXlab platform.
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Latency of Herpes simplex virus type-1 in human geniculate and vestibular Ganglia is associated with infiltration of CD8+ T-cells
Journal of Medical Virology, 2010Co-Authors: Diethilde TheilAbstract:Herpes simplex virus type-1 latency and CD8+ T-cell occurence were investigated in the trigeminal, geniculate, and vestibular Ganglia from seven deceased humans. The HSV-1 ''latency-associated transcript'' was assessed by in situ-hybridization and quantitative RT-PCR. Infiltration of CD8+ T-cell was detected by immunohistochemistry and quantitative RT-PCR. The data show that HSV-1 latency and CD8+ T-cell infiltration are not solely confined to the trigeminal Ganglia but can also occur in other cranial Ganglia along the neuroaxis. However, the HSV-1 latency transcripts in the geniculate and vestibular Ganglia were expressed at a very low level. The difference in CD8 transcript levels among HSV-1 latently infected trigeminal Ganglia, geniculate, and vestibular Ganglia was less conspicuous. Colocalisation of latent HSV-1 and CD8+ T-cells in geniculate and vestibular Ganglia supports further the hypothesis that HSV-1 reactivation is possible in these Ganglia and is the cause of Bell's palsy and vestibular neuritis.
K. Nagashima - One of the best experts on this subject based on the ideXlab platform.
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Latent herpes simplex virus type 1 in human geniculate Ganglia
Acta Neuropathologica, 1992Co-Authors: Y. Furuta, T. Takasu, K. C. Sato, S. Fukuda, Y. Inuyama, K. NagashimaAbstract:Viral infection, especially by reactivation of herpes simplex virus (HSV) has been considered to be a possible explanation for the pathogenesis of idiopathic peripheral facial nerve palsy (Bell's palsy). We investigated whether the geniculate Ganglia of man contain latent HSV type 1 (HSV-1), and compared the frequency of HSV-infected Ganglia and that of latently infected neurons in human geniculate Ganglia and in trigeminal Ganglia. From autopsy specimens of eight adults 15 geniculate Ganglia and 16 trigeminal Ganglia were examined by means of in situ hybridization and immunohistochemical staining. The HSV-1 genome was detected in 11 of the 15 (71%) geniculate Ganglia and in 13 of the 16 (81%) trigeminal Ganglia. No HSV antigen was noted in any of the Ganglia. The incidence of latently infected neurons was 0.9% in the trigeminal Ganglia and 5.3% in the geniculate Ganglia. The difference in percentages between the two types of Ganglia was significant. Our results suggest that reactivation of latent HSV in the geniculate Ganglia is a probable cause of some cases of herpetic stomatitis and of idiopathic peripheral facial nerve palsy.
Tatsuya Habaguchi - One of the best experts on this subject based on the ideXlab platform.
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role of basal Ganglia brainstem systems in the control of postural muscle tone and locomotion
Progress in Brain Research, 2004Co-Authors: Kaoru Takakusaki, Junko Oohinatasugimoto, Kazuya Saitoh, Tatsuya HabaguchiAbstract:Abstract This chapter argues that a basal Ganglia–brainstem system throughout the mesopontine tegmentum contributes to an automatic control of movement that operates in conjunction with voluntary control processes. Activity of a muscle tone inhibitory system and the locomotion executing system can be steadily balanced by a net excitatory cortical input and a net inhibitory basal Ganglia input to these systems. We further propose that dysfunction of the basal Ganglia–brainstem system, together with that of the cortico-basal Ganglia loop, underlies the pathogenesis of motor disturbances expressed in basal Ganglia diseases.
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Role of basal Ganglia–brainstem systems in the control of postural muscle tone and locomotion
Progress in Brain Research, 2004Co-Authors: Kaoru Takakusaki, Kazuya Saitoh, Junko Oohinata-sugimoto, Tatsuya HabaguchiAbstract:Abstract This chapter argues that a basal Ganglia–brainstem system throughout the mesopontine tegmentum contributes to an automatic control of movement that operates in conjunction with voluntary control processes. Activity of a muscle tone inhibitory system and the locomotion executing system can be steadily balanced by a net excitatory cortical input and a net inhibitory basal Ganglia input to these systems. We further propose that dysfunction of the basal Ganglia–brainstem system, together with that of the cortico-basal Ganglia loop, underlies the pathogenesis of motor disturbances expressed in basal Ganglia diseases.
Y. Furuta - One of the best experts on this subject based on the ideXlab platform.
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Latent herpes simplex virus type 1 in human geniculate Ganglia
Acta Neuropathologica, 1992Co-Authors: Y. Furuta, T. Takasu, K. C. Sato, S. Fukuda, Y. Inuyama, K. NagashimaAbstract:Viral infection, especially by reactivation of herpes simplex virus (HSV) has been considered to be a possible explanation for the pathogenesis of idiopathic peripheral facial nerve palsy (Bell's palsy). We investigated whether the geniculate Ganglia of man contain latent HSV type 1 (HSV-1), and compared the frequency of HSV-infected Ganglia and that of latently infected neurons in human geniculate Ganglia and in trigeminal Ganglia. From autopsy specimens of eight adults 15 geniculate Ganglia and 16 trigeminal Ganglia were examined by means of in situ hybridization and immunohistochemical staining. The HSV-1 genome was detected in 11 of the 15 (71%) geniculate Ganglia and in 13 of the 16 (81%) trigeminal Ganglia. No HSV antigen was noted in any of the Ganglia. The incidence of latently infected neurons was 0.9% in the trigeminal Ganglia and 5.3% in the geniculate Ganglia. The difference in percentages between the two types of Ganglia was significant. Our results suggest that reactivation of latent HSV in the geniculate Ganglia is a probable cause of some cases of herpetic stomatitis and of idiopathic peripheral facial nerve palsy.
Andrea S. Bertke - One of the best experts on this subject based on the ideXlab platform.
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Herpes Simplex Virus 1 Reactivates from Autonomic Ciliary Ganglia Independently from Sensory Trigeminal Ganglia To Cause Recurrent Ocular Disease
Journal of virology, 2015Co-Authors: Sungseok Lee, Angela M. Ives, Andrea S. BertkeAbstract:Herpes simplex virus 1 (HSV-1) and HSV-2 establish latency in sensory and autonomic neurons after ocular or genital infection, but their recurrence patterns differ. HSV-1 reactivates from latency to cause recurrent orofacial disease, and while HSV-1 also causes genital lesions, HSV-2 recurs more efficiently in the genital region and rarely causes ocular disease. The mechanisms regulating these anatomical preferences are unclear. To determine whether differences in latent infection and reactivation in autonomic Ganglia contribute to differences in HSV-1 and HSV-2 anatomical preferences for recurrent disease, we compared HSV-1 and HSV-2 clinical disease, acute and latent viral loads, and viral gene expression in sensory trigeminal and autonomic superior cervical and ciliary Ganglia in a guinea pig ocular infection model. HSV-2 produced more severe acute disease, correlating with higher viral DNA loads in sensory and autonomic Ganglia, as well as higher levels of thymidine kinase expression, a marker of productive infection, in autonomic Ganglia. HSV-1 reactivated in ciliary Ganglia, independently from trigeminal Ganglia, to cause more frequent recurrent symptoms, while HSV-2 replicated simultaneously in autonomic and sensory Ganglia to cause more persistent disease. While both HSV-1 and HSV-2 expressed the latency-associated transcript (LAT) in the trigeminal and superior cervical Ganglia, only HSV-1 expressed LAT in ciliary Ganglia, suggesting that HSV-2 is not reactivation competent or does not fully establish latency in ciliary Ganglia. Thus, differences in replication and viral gene expression in autonomic Ganglia may contribute to differences in HSV-1 and HSV-2 acute and recurrent clinical disease. IMPORTANCE Herpes simplex virus 1 (HSV-1) and HSV-2 establish latent infections, from which the viruses reactivate to cause recurrent disease throughout the life of the host. However, the viruses exhibit different manifestations and frequencies of recurrent disease. HSV-1 and HSV-2 establish latency in both sensory and autonomic Ganglia. Autonomic Ganglia are more responsive than sensory Ganglia to stimuli associated with recurrent disease in humans, such as stress and hormone fluctuations, suggesting that autonomic Ganglia may play an important role in recurrent disease. We show that HSV-1 can reactivate from autonomic Ganglia, independently from sensory Ganglia, to cause recurrent ocular disease. We found no evidence that HSV-2 could reactivate from autonomic Ganglia independently from sensory Ganglia after ocular infection, but HSV-2 did replicate in both Ganglia simultaneously to cause persistent disease. Thus, viral replication and reactivation in autonomic Ganglia contribute to different clinical disease manifestations of HSV-1 and HSV-2 after ocular infection.
