Herpes simplex virus type 1 (HSV-1) is a ubiquitous virus, included in the Herpesviridae family, Alphaherpesvirinae subfamily, associated with lifelong and mostly asymptomatic infections. After the primary infection, HSV-1 genome persists in neurons in a latent state from which it reactivates periodically to resume replication and produce infectious virus. Because of this stable permanence in the central nervous system (CNS), a relationship between HSV-1 infection and neurodegenerative diseases has been hypothesized. In particular, there is a growing body of literature linking HSV-1 infection with the development of Alzheimer's disease (AD). Different mechanisms have been outlined, such as the accumulation of misfolded proteins, the local chronic parainflammation and the lysosome system damage. Moreover, analyses performed on cotton rats Sigmodon Hispidus neural cells showed an active replication of the virus, enhancing the disruption of myelin fibres, typical lesions associated to multifocal demyelination pathologies, such as multiple sclerosis (MS) and disseminated encephalomyelitis (ADEM). This scenario opens the way for the identification of potential targets for new treatments that could be successfully applied against neurodegenerative disorders.
Herpes simplex virus type 1 (HSV-1) is a ubiquitous virus, included in the Herpesviridae family, Alphaherpesvirinae subfamily, associated with lifelong and mostly asymptomatic infections. After the primary infection, HSV-1 genome persists in neurons in a latent state from which it reactivates periodically to resume replication and produce infectious virus. Because of this stable permanence in the central nervous system (CNS), a relationship between HSV-1 infection and neurodegenerative diseases has been hypothesized. In particular, there is a growing body of literature linking HSV-1 infection with the development of Alzheimer's disease (AD). Different mechanisms have been outlined, such as the accumulation of misfolded proteins, the local chronic parainflammation and the lysosome system damage. Moreover, analyses performed on cotton rats Sigmodon Hispidus neural cells showed an active replication of the virus, enhancing the disruption of myelin fibres, typical lesions associated to multifocal demyelination pathologies, such as multiple sclerosis (MS) and disseminated encephalomyelitis (ADEM). This scenario opens the way for the identification of potential targets for new treatments that could be successfully applied against neurodegenerative disorders.
Contributions of human herpesviruses herpes simplex virus 1 (HSV-1) to neurodegenerative disease pathology
CAT GENOVA, ELENA
2019/2020
Abstract
Herpes simplex virus type 1 (HSV-1) is a ubiquitous virus, included in the Herpesviridae family, Alphaherpesvirinae subfamily, associated with lifelong and mostly asymptomatic infections. After the primary infection, HSV-1 genome persists in neurons in a latent state from which it reactivates periodically to resume replication and produce infectious virus. Because of this stable permanence in the central nervous system (CNS), a relationship between HSV-1 infection and neurodegenerative diseases has been hypothesized. In particular, there is a growing body of literature linking HSV-1 infection with the development of Alzheimer's disease (AD). Different mechanisms have been outlined, such as the accumulation of misfolded proteins, the local chronic parainflammation and the lysosome system damage. Moreover, analyses performed on cotton rats Sigmodon Hispidus neural cells showed an active replication of the virus, enhancing the disruption of myelin fibres, typical lesions associated to multifocal demyelination pathologies, such as multiple sclerosis (MS) and disseminated encephalomyelitis (ADEM). This scenario opens the way for the identification of potential targets for new treatments that could be successfully applied against neurodegenerative disorders.File | Dimensione | Formato | |
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https://hdl.handle.net/20.500.14240/125041