The objectives of the research proposed in this application are to investigate the role of cellular functions in the establishment and maintenance of the latent herpes simplex virus (HSV) infection in mouse trigeminal ganglia, and to contrast these with pathways of ell control expressed by other herpesviruses.
The specific aims are as follows: The specific are as follows: (i) complete the identification of open reading frames (ORFs) that are expressed. The hypothesis that more than 84 ORFs are expressed is based on the unexpected discovery that 3 ORFs antisense to each other are expressed. (ii) Identify the viral genes expressed in trigeminal ganglia during the establishment and maintenance stages of HSV-1 latency. The decision whether virus initiates a latent or productive infection is probably made within a short time interval after infection. The objectives are to identify viral transcripts in trigeminal ganglia preclude meaningful examination of transcriptional activity within a very short time after infection. (iii) Identify maintenance stages of HSV-1 latency, and in the absence of such changes, identify neuronal proteins that interact with viral protein or viral promoters and test the significance of these interactions. The hypothesis to be tested is that cellular proteins play a major role in the establishment and maintenance of latent state. (iv) Identify cellular genes expressed during latency and determine their role in productive injection. In essence, the question being asked is whether alphaherpesviruses (e.g.HSV) and betaherpesviruses (e.g. CMV) and gammaherpesviruses (e.g. has been demonstrated in one case (hyperphosphorylation of the translation elongation factor 1delta). If common pathways are identified, viral gene exchanges in appropriate genetic backgrounds may identify the genes responsible for specific cellular responses to herpesviral infections.
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