| Research Abstract |
1. We generated UL51-null mutants(FDL51) in HSV to uncover the function of UL51 protein The mutant plaques were much smaller in size and maximal titers of FDL51 were reduced nearly 100-fold compared to wild-type virus. In FDL51-infected cells, a large number of envelope nucleocapsids were observed in the perinuclear space, but envelope mature virions were rarely detectable, suggesting that UL51 protein is involved in the maturation and egress of HSV-1 particles downstream of the initial envelopment step.
2. UL56, a tail-anclcored type II membrane protein, associated with KIF1A, a neuron-specific kinesin involved in the axonal transport of synaptic vesicle precursors. UL56 protein also interacted with UL11 protein which is though to be involved in nuclear capsid envelopment and egress.
3. In the absence of US3 protein kinase(PK), UL46 tegment protein was quite unstable, being much more susceptible to degradation. UL46 protein was undetectable in the extracellular virions of US3-deficient virus. We also found that US3PK can directy phosphorylate UL46 protein as well as UL34, UL31, ICP22, and US9.
4. We have determined the complete nucleotide sequences of the genome of HF10, a highly attenuated, non-neuroinvasive HSV-1, and found that HF10 lacks the expression of UL56, UL55, UL43, UL49.5 and latency-associated transcripts(LAT).
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