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Genetic variations of human herpesvirus 7 by analysis of glycoproteins B and H, and R2-repeat regions

✍ Scribed by Duanthanorm Thawaranantha; Kanittha Chimabutra; Kruavon Balachandra; Paijit Warachit; Somsak Pantuwatana; Keiko Tanaka-Taya; Reiko Inagi; Takeshi Kurata; Koichi Yamanishi

Publisher: John Wiley and Sons
Year: 2002
Tongue: English
Weight: 206 KB
Volume: 66
Category: Article
ISSN: 0146-6615
DOI: 10.1002/jmv.2154

No coin nor oath required. For personal study only.

✦ Synopsis

Abstract

Clinical isolates of human herpesvirus 7 (HHV‐7) from the saliva of healthy individual were investigated for genetic variations in the regions of two immediate‐early (IE) genes, the glycoprotein B (gB) and glycoprotein H (gH) genes, and in R2‐repeat. The genomic DNA of 24 isolates from citizens of Thailand, Japan, and the United States was amplified to detect size variations in the IE‐1 and IE‐2 loci, but none was observed, suggesting that there was no deletion or insertion in these genes, in contrast with an IE gene of human herpesvirus 6 (HHV‐6). The sequences of the gB gene from isolates acquired from 5 Japanese and 8 Thai subject were then compared with those of American strains JI and RK with respect to codons that are known to differentiate gB alleles. All the isolates were found to have gB allele C except for the JI strain, which has allele F. Variability was also observed in five specific gH codons, resulting in 6 different groups. The HHV‐7 isolates might be classified into two major genetic variants by combining their gB and gH allelic groupings. In the present study, only JI belonged to variant 1, while the rest of the isolates appeared to belong to variant 2. In the R2‐repeat region, size heterogeneities were observed among the 24 isolates, due to different repeat numbers (17, 15, 14, 13, or 12 repeats). Therefore, we used the R2‐repeat to identify the origins of isolates in a study of HHV‐7 transmission, and found HHV‐7 to be transmitted within a family from both mothers and fathers to their children. J. Med. Virol. 66:370‐377, 2002. © 2002 Wiley‐Liss, Inc.

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