Herpes simplex keratitis is one of the important causes of blindness and its early diagnosis is essential to the treatment of the respective patients accordingly. Herpes neonatorum can be categorized as follows6, 7, 8, 9, 10:. The TK gene of each sample virus strain is amplified and isolated under the control of a T7 promoter by PCR. HSE is due to HSV type 1 (HSV-1) in most cases but HSV type 2 (HSV-2) may be also implicated, especially in infants in the context of neonatal herpes. Although viruses resistant to either vidarabine or acyclovir developed readily in cell culture, no evidence of cross-resistance was obtained. Supported by contracts (NO1-AI-15113, NO1-AI-62554, and NO1-AI-12667) with the Virology Branch, Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases; by a grant (RR-032) from the Division of Research Resources of the National Institutes of Health; and by a grant from the state of Alabama. Therefore, the phenotypic screening of the virus in skin lesions has become increasingly important when choosing the appropriate therapy, especially in the case of patients who have a risk factor(s) for ACVr viral infection, such as immunodeficiency and long duration of ACV treatment (9, 23).
Latency is characteristic for all herpesviruses. Twenty nine of the 34 survivors were assessed six months to 11 years after herpes simplex encephalitis. Herpes simplex encephalitis (HSE) is a life-threatening consequence of herpes simplex virus (HSV) infection of the central nervous system (CNS). Latent virus has been isolated from trigeminal, sacral, and vaginal ganglia in human beings. In animals HSV can become latent directly within the brain; so far this has not been found in human beings. Neurovirulence is the consequence of peripheral multiplication, invasion of the CNS, and growth in the CNS, but HSV isolated from encephalitic brains often differs genetically from HSV isolated from peripheral blood.