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职称:professor
所属学校:University of Southern California
所属院系: School of Medicine
所属专业:Cell/Cellular Biology and Anatomical Sciences, Other
联系方式:(323) 442-1619
Herpes simplex Type 1 (HSV1), the cold sore virus, can cause relatively innocuous infections of oral mucous membranes and sensory nerves innervating those membranes in a large portion of the adult general population. HSV1, as with all herpesviruses, is capable of achieving latency, and can be reactivated by various factors such as stress, or exposure to UV light. Though relatively rare, HSV1 can also cause more serious encephalitic or systemic disseminated infections. Demonstrating increased risk for these more serious sequelae of HSV1 infection is the portion of the population that is relatively immunosuppressed (neonates, transplant patients, or those with immune-suppressive disorders). In addition, ocular herpetic keratitis, a recurrent infection and scarring of the corneal epithelium and stroma is herpetic infection. The multiple deleterious effects of herpesvirus infection thus motivate us to attempt a better understanding of neuronal cell responses to viral infection. The intracellular transport of HSV1 within the host neuron is required for cell-cell transmission of infection: newly synthesized virus in infected cell bodies is targeted to the plasma membrane of long axons or dendrites prior to release of mature infective virus near cells with which it forms synapses. The synaptic connections of the infected cell, and transneuronal transfer of virus, thus provide a unique route by which virus can be presented to the internal regions of the relatively immunoprotected CNS. The goal of our research is to identify the mechanisms used by HSV1 for targeted movement within neurons. Our hypothesis for this work is that HSV1 uses endogenous host mechanisms to accomplish intracellular transport. It is our bias that the study of how this virus may make use of host mechanisms will have implications for both the pathogenesis of herpes infection, as well as more broad implications for the cell biology of intracellular trafficking. Molecular mechanisms of intraneuronal viral transport; axonal transport of neural cytoskeleton; biochemistry and structure of the presynaptic terminal
Herpes simplex Type 1 (HSV1), the cold sore virus, can cause relatively innocuous infections of oral mucous membranes and sensory nerves innervating those membranes in a large portion of the adult general population. HSV1, as with all herpesviruses, is capable of achieving latency, and can be reactivated by various factors such as stress, or exposure to UV light. Though relatively rare, HSV1 can also cause more serious encephalitic or systemic disseminated infections. Demonstrating increased risk for these more serious sequelae of HSV1 infection is the portion of the population that is relatively immunosuppressed (neonates, transplant patients, or those with immune-suppressive disorders). In addition, ocular herpetic keratitis, a recurrent infection and scarring of the corneal epithelium and stroma is herpetic infection. The multiple deleterious effects of herpesvirus infection thus motivate us to attempt a better understanding of neuronal cell responses to viral infection. The intracellular transport of HSV1 within the host neuron is required for cell-cell transmission of infection: newly synthesized virus in infected cell bodies is targeted to the plasma membrane of long axons or dendrites prior to release of mature infective virus near cells with which it forms synapses. The synaptic connections of the infected cell, and transneuronal transfer of virus, thus provide a unique route by which virus can be presented to the internal regions of the relatively immunoprotected CNS. The goal of our research is to identify the mechanisms used by HSV1 for targeted movement within neurons. Our hypothesis for this work is that HSV1 uses endogenous host mechanisms to accomplish intracellular transport. It is our bias that the study of how this virus may make use of host mechanisms will have implications for both the pathogenesis of herpes infection, as well as more broad implications for the cell biology of intracellular trafficking. Molecular mechanisms of intraneuronal viral transport; axonal transport of neural cytoskeleton; biochemistry and structure of the presynaptic terminal
