Drug-resistance of herpes simplex virus (HSV) is caused most frequently by mutation of the viral thymidine kinase (TK) gene. To elucidate the significance of detecting nucleotide changes of the TK gene for screening drug-resistant viruses, the frequency and variation of the genetic polymorphisms in
Genotyping of herpes simplex virus type 1 strains isolated from ocular materials of patients with herpetic keratitis
✍ Scribed by Kenichi Umene; Tomoyuki Inoue; Yoshitsugu Inoue; Yoshikazu Shimomura
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 86 KB
- Volume
- 71
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
Abstract
Herpes simplex virus type 1 (HSV‐1) is the etiological agent of herpetic keratitis. The epithelial form (“epithelial keratitis”) is attributed mainly to destruction of the epithelium through active viral replication within the epithelium. The stromal form (“stromal keratitis”) is associated with immune reactions within the stroma and is the common cause of human blindness. In the present study, 29 HSV‐1 strains isolated from human ocular materials of herpetic keratitis were classified into 14 genotypes on the basis of DNA polymorphisms. Twenty‐one of 29 (72%) strains from eyes examined in the present study were of genotypes that were shown previously to be present in strains from non‐ocular lesions (including genital herpes). Five of nine (56%) strains from eyes related to stromal keratitis were of the F1 genotype, while four of twenty (20%) strains from eyes not related to stromal keratitis were of the F1 genotype. Thus, the proportion of F1 genotype was assumed to be larger in the group of strains related to stromal keratitis than in that not so related, suggesting an association of the F1 genotype with stromal keratitis. A connection of F1 genotype with recurrence was proposed previously; hence, F1 genotype seems to be associated to both stromal keratitis and the recurrence, thereby supporting the relationship between stromal keratitis and recurrence. J. Med. Virol. 71:75–81, 2003. © 2003 Wiley‐Liss, Inc.
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