Abstract
Recurrent intraoral herpes simplex virus infection, which was first described by Griffin in 1965, is an uncommon type of herpes simplex virus (HSV) infection. To determine whether this is caused by reactivation of HSV in the oral cavity latently infected with HSV, we isolated the viruses from primary and recurrent lesions of intraoral HSV infection in the same patient and analyzed the DNA of the isolated HSV viruses.
A 48-year-old woman came to our clinic on July 15, 1982 with severe pain in the oral cavity. On examination, numerous ulcerative lesions were observed in the mucosa of lower alveolus and hard palate. HSV was isolated by tissue culture work from the swab of lesions. Although the antibodies against HSV were not detected by complement-fixation test in the serum harvested from the patient at acute phase of the disease, the titer was increased to ×16 at the convalescent stage. Therefore, it was diagnosed as a primary herpetic gingivostomatitis. This disease was healed completely by topical administration of interferon-β. About 11 months later, ulcerative lesions occurred again in the lower gum and were treated with interferon-β. Virus was isolated from the lesions and proved to be HSV as demonstrated by a fluorescent antibody staining method for HSV antigen.
The two isolates obtained at different time from this patient, including standard HSV type 1 and 2, were grown in Vero cells. DNA was extracted from the infected cells according to the method of Hirt and was digested with various restriction endonucleases. The DNA fragments were submitted to agarose gel electrophoresis, stained with ethidium bromide and then the electrophoretic patterns were observed under UV illumination. The cleavage pattern of DNA from all the HSV isolates was found to be similar to that of HSV type 1, but not to the HSV type 2. Therefore, these isolates can be considered to be HSV type 1. Moreover, the two viruses isolated from the present case gave almost same DNA cleavage pattern. From these findings, it can be concluded that the intraoral HSV infection which occurred after complete remission of the primary HSV infection in the present case is caused by the same virus, implying that the second onset of intraoral HSV infection is of recurrent form.
