| Research Abstract |
I. To study on mechanisms of in vitro reactivation of latent herpes simplex virus (HSV) in sensory ganglia, we investigated on the effect of neurotransmitters, gamma aminobutyric acid (GABA), glutamine and glutamate, similar biochemical structure to butyrate, in cultured ganglia of mice. We found that GABA enhanced virus replication slightly but did not enhance viral reactivation per se. Glutamine and glutamate however, did not enhance both viral reactivation and replications. These results indicated that these neurotransmitter had no effect on the reactivation of latent HSV in the nervous system. II. In 1983, Openshaw described on latency of HSV in ocular tissue especially in the retina. The latency of HSV in human ocular tissue, however, has not been fully documented although there have been evidences of reactivation of varicella zoster virus manifested by acute retinal necrosis. We report here on acute retinitis two years after recovery from herpes simplex encephalitis. The HSE case
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was 30 year old man who developed a fluent dysphasia., poor recent memory, inappropriate behavior, hyperreflexia and bilateral extensor planter responses along with 1:64 of anti HSV-1 neutralizing antibody, pleocytosis, and increased protein in the cerebrospinal fluid (CSF). CT scan showed hypodence in both temporal lobes. Funduscopic examination was normal. Five months after onset, the patient had a stable memory and cognitive deficit but was able to carry out simple physical chores in a family-managed business. 2.5 year after recovery from encephalitis, the patient noted pain and sudden decrease in vision in the left eye. Funduscopically there were yellow- white patches of retinal necrosis and perivascular infiltrates and hemorrhages in the left eye. Viral antibody titer in the vitreum was 1:1280 for HSV-1 and less than 1:4 for varicella zoster virus and cytomegalovirus. The visual acuity of the left eye was improved following aciclovir therapy. This is the first case caused by reactivation of HSV in the retina demonstrated clearly. We will further investigate on neurological and ophthalmological disorders with HSV infection that have never demonstrated. III. We described on the mechanism of elevation of anti-HSV antibody in Guillain-Barre syndrome (GBS) of which phenomenon had been reported by Melnick & olivarius et al (1964 and 1975). This was caused by reactivation of HSV by axonal degenerations as well as demyelinations often seen in severe GBS. IV. Non invasive diagnosis of HSV is often difficult. We evaluated newly additional method for diagnosis for HSE, "capture ELIZA". Results showed that all the HSV previously diagnosed by routine method were all positive for capture ELIZA but 17.6% of non HSE such as demyelinative and degenerative disorders showed positive, indicating that capture ELIZA might not be always useful but useful as a confirmation of HSE as additional evidence of HSE. Less
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