Abstract

BackgroundIt has been predicted that the UL31 gene originates from the positive strand of the human cytomegalovirus (HCMV) genome, whereas the UL30 and UL32 genes originate from the complementary strand. Except for the UL32 gene, the transcription of this gene region has not been investigated extensively.MethodsNorthern blotting, cDNA library screening, RACE-PCR,and RT-PCR were used.ResultsAt least eight transcripts of the antisense orientation of UL31 were transcribed from the UL30–UL32 region during the late phase of HCMV infection. The 3′ coterminus of these transcripts was located within the predicted UL30 gene. The longest 6.0-kb transcript was initiated upstream of the predicted UL32 gene. Other transcripts were derived from the predicted UL30 and UL31 gene region. Except for the previously predicted UL32 open reading frame (ORF), three novel ORFs, named UL31anti-1, UL31anti-2 and UL31anti-3, were located in the transcripts from the UL31anti-UL32 transcription unit. No transcription was found in UL31.ConclusionA family of novel 3′ coterminal transcripts was transcribed from the UL30–UL32 gene region.

Highlights

  • It has been predicted that the UL31 gene originates from the positive strand of the human cytomegalovirus (HCMV) genome, whereas the UL30 and UL32 genes originate from the complementary strand [2]

  • DNA sequence of UL30–UL32 in HCMV H genome The whole genome sequence of HCMV H isolate was obtained by high throughput sequencing

  • The sequence showed that the genome of HCMV H strain contained a completed UL30–UL32 gene region, which shared 99% homology with that of AD169 genome (X17403.1)

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Summary

Introduction

It has been predicted that the UL31 gene originates from the positive strand of the human cytomegalovirus (HCMV) genome, whereas the UL30 and UL32 genes originate from the complementary strand. Human cytomegalovirus (HCMV), a member of the Herpesviridae family, is a ubiquitous pathogen in the human population. HCMV infection in healthy individuals usually displays no signs or has only mild symptoms, and has no long-term health consequences during its life-long latency. HCMV causes severe congenital abnormalities in neonates and fatal opportunistic infections in immunosuppressed patients [1]. The HCMV genome consists of 230–235 kb of double stranded DNA and is predicted to encode 208 open reading frames (ORFs) in the laboratory strain AD169 [2]. Re-evaluation of HCMV coding potential has indicated that 37 previously annotated ORFs

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