Characterization of an HPV33 natural variant with enhanced transcriptional activity suggests a role for C/EBPbeta in the regulation of the viral early promoter.
Introduction: In further support of this notion, we observed that the C7732G variation that is present in some A2-sublineage variants and which we previously found to be associated with high grade squamous intraepithelial lesion (HSIL), also increases the activity of the HPV33 EP approximately 2-fold in PHK.
Naturally Occurring Variations Modulate the Activity of the HPV33 Early Promoter and its Affinity for the E2 Transcription Factor.
Result: The HSIL-associated C7732G variation and 79-bp duplication increase EP activity in PHK.
Result: This can be attributed to the C7732G variation which is the only difference between LCR6 and LCR5 and is also present in LCR14.
Result: While C7732G certainly accounts for the higher activity of LCR6 and LCR14 in PHK, compared to
Discussion: Interestingly, the LCRs with the highest activities in PHK (white or lighter shades of red in Fig._7) were the A1-sublineage LCR-PT and LCR12, and the two A2-variants LCR6 and LCR14 which contain the C7732G variation.
Human papillomavirus type 33 polymorphisms and high-grade squamous intraepithelial lesions of the uterine cervix.
PMID: 16960775
2006
The Journal of infectious diseases
Abstract: The C7732G variation, which results in the loss of a putative binding site for the cellular upstream stimulatory factor, was associated with HSILs (age- and site-adjusted OR, 8.0 [95% CI, 1.5-42.8]).
HPV mutation literature information.
PMID: 
2019
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