2007 Fiscal Year Final Research Report Summary
Molecular basis of host responses through herpes simplex virus US3 protein kinase
| Project/Area Number |
18590456
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | Aichi Medical University |
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Principal Investigator |
MORI Isamu Aichi Medical University, Department of Microbiology and Immunology, Associate Professor (80283167)
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| Project Period (FY) |
2006 – 2007
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| Keywords | herpes simplex virus / US3 protein kinase / apoptosis / olfactory neuron / microglia / neurovirulence |
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| Research Abstract |
1 We have investigated the molecular basis of herpes simplex virus US3, an accessory gene, in terms of its functions such as regulation of apoptosis, immunity and neumvirulence.
2 We used a highly neumvirulent strain (186), US3-deficient mutants (L1BR1 and LB101) and US3-rescued virus (L1B-11) in order to analyze the functions of US3 comprehensively.
3 With refarence to the molecular basis of US3 for regulation of apoptosis in peripheral neurons and neurovirulence, 186 and L1B-11 did not induce apoptosis (i.e., TUNEL negative) in olfactory neurons, while L1BR1 induced apoptosis in these peripheral neurons (TUNEL positive).
4 These results suggest that L1BI1 can promote viral entry and spread via the natural mute of infretion through negatively regulating virus-induced apoptosis and augment neurovirulence.
5 A newly developed mutant, LB101, did not infect olfactory neurons, the reason remaining unknown.
6 The molecular mechanisms of L1BR1 to induce apoptosis remain unknown. JNK, a protein kinase, may be involved in a process of apoptosis induction.
7 Ibal-immunopositive microglia can not be detected in olfactory neurons.
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