1. Identification of a new control region in the genome of the DDP strain of BK virus isolated from PBMC
- Author
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Valeria Pietropaolo, Paola Cordiali-Fei, Anna Marta Degener, Cristiana Di Taranto, Nicola Orsi, L. Sinibaldi, Li Jin, Franco Ameglio, and Elisabetta Trento
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Molecular Sequence Data ,HIV Infections ,Genome, Viral ,Biology ,Origin of replication ,medicine.disease_cause ,chemistry.chemical_compound ,Capsid ,Transcription (biology) ,Sequence Homology, Nucleic Acid ,Virology ,medicine ,human polyomavirus BK (BKV) ,non-coding control region (NCCR) ,new BKV strain (DDP ,U91605) ,Humans ,Point Mutation ,Genomic organization ,Polyomavirus Infections ,Base Sequence ,Nucleic acid sequence ,Sequence Analysis, DNA ,Molecular biology ,BK virus ,Tumor Virus Infections ,Infectious Diseases ,chemistry ,Regulatory sequence ,BK Virus ,GenBank ,DNA, Viral ,Leukocytes, Mononuclear ,Capsid Proteins ,Sequence Alignment ,DNA - Abstract
The various strains of human polyomavirus BK (BKV) show a marked heterogeneity in the noncoding control region (NCCR), which includes the origin of replication and the regulatory region for early and late transcription. A new BKV strain (DDP, U91605) was identified by direct detection and sequencing of PCR products of BKV-NCCR DNA obtained from PBMC samples of HIV-positive or -negative subjects. The DDP strain NCCR sequence showed an organisation not described previously in vivo with the maximum homology with the archetypal strain (WW) (M34048), as compared with those collected in GenBank. Structurally, P68, Q39, and S68 boxes were perfectly conserved, whereas the R63 box was completely deleted. This deletion involves the loss of sequences able to bind cellular factors essential for the DNA transcription, such as NF1 binding sites, normally present twice in the R box and the modification of SP1. It is possible that these rearrangements represent a cause of the loss of the VP1 region observed in 9/22 PBMC samples and never observed in urine isolates, which are similar to the WW strain. J. Med. Virol. 58:413–419, 1999. © 1999 Wiley-Liss, Inc.
- Published
- 1999
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