Vaccination News Home Page

http://jvi.asm.org/cgi/content/abstract/76/22/11447

Full Text of this Article Reprint (PDF) Version of this Article Similar articles found in: JVI Online PubMed PubMed Citation Search Medline for articles by: Gomi, Y. || Yamanishi, K. Alert me when: new articles cite this article   Download to Citation Manager

Books from ASM Press

Journal of Virology, November 2002, p. 11447-11459, Vol. 76, No. 22
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.22.11447-11459.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
 

Comparison of the Complete DNA Sequences of the Oka Varicella Vaccine and Its Parental Virus

Yasuyuki Gomi,¹ Hiroki Sunamachi,¹ Yasuko Mori,² Kazuhiro Nagaike,^1,2 Michiaki Takahashi,³ and Koichi Yamanishi^2*

Kanonji Institute, The Research Foundation for Microbial Diseases of Osaka University, Kanonji, Kagawa,¹ The Research Foundation for Microbial Diseases of Osaka University,³ Department of Microbiology, Osaka University Medical School, Suita, Osaka, Japan²

Received 25 March 2002/ Accepted 14 August 2002

The DNA sequences of the Oka varicella vaccine virus (V-Oka) and its parental virus (P-Oka) were completed. Comparison of the sequences revealed 42 base substitutions, which led to 20 amino acid conversions and length differences in tandem repeat regions (R1, R3, and R4) and in an origin of DNA replication. Amino acid substitutions existed in open reading frames (ORFs) 6, 9A, 10, 21, 31, 39, 50, 52, 55, 59, 62, and 64. Of these, 15 base substitutions, leading to eight amino acid substitutions, were in the gene 62 region alone. Further DNA sequence analysis showed that these substitutions were specific for V-Oka and were not present in nine clinical isolates. The immediate-early gene 62 product (IE62) of P-Oka had stronger transactivational activity than the mutant IE62 contained in V-Oka in 293 and CV-1 cells. An infectious center assay of a plaque-purified clone (S7-01) from the V-Oka with 8 amino acid substitutions in ORF 62 showed smaller plaque formation and less-efficient virus-spreading activity than did P-Oka in human embryonic lung cells. Another clone (S-13) with only five substitutions in ORF 62 spread slightly faster than S7-01 but not as effectively as P-Oka. Moreover, transient luciferase assay in 293 cells showed that transactivational activities of IE62s of S7-01 and S7-13 were lower than that of P-Oka. Based on these results, it appears that amino acid substitutions in ORF 62 are responsible for virus growth and spreading from infected to uninfected cells. Furthermore, the Oka vaccine virus was completely distinguishable from P-Oka and 54 clinical isolates by seven restriction-enzyme fragment length polymorphisms that detected differences in the DNA sequence.

* Corresponding author. Mailing address: Department of Microbiology, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan. Phone: 81-6-6879-3321. Fax: 81-6-6879-3329. E-mail: yamanisi@micro.med.osaka-u.ac.jp.

Journal of Virology, November 2002, p. 11447-11459, Vol. 76, No. 22
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.22.11447-11459.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




 

Copyright © 2002 by the American Society for Microbiology. All rights reserved.

Vaccination News Home Page

ALL INFORMATION, DATA, AND MATERIAL CONTAINED, PRESENTED, OR PROVIDED HERE IS FOR GENERAL INFORMATION PURPOSES ONLY AND IS NOT TO BE CONSTRUED AS REFLECTING THE KNOWLEDGE OR OPINIONS OF THE PUBLISHER, AND IS NOT TO BE CONSTRUED OR INTENDED AS PROVIDING MEDICAL OR LEGAL ADVICE.  THE DECISION WHETHER OR NOT TO VACCINATE IS AN IMPORTANT AND COMPLEX ISSUE AND SHOULD BE MADE BY YOU, AND YOU ALONE, IN CONSULTATION WITH YOUR HEALTH CARE PROVIDER.