Abstract
Human polyomavirus 9 (HPyV9) was originally detected in the serum of a renal transplant patient. Seroepidemiological studies showed that ~20–50% of the human population have antibodies against this virus. HPyV9 has not yet been associated with any disease and little is known about the route of infection, transmission, host cell tropism, and genomic variability in circulating strains. Recently, the HPyV9 variant UF-1 with an eight base-pair deletion, a thirteen base-pair insertion and with point mutations, creating three putative Sp1 binding sites in the late promoter was isolated from an AIDS patient. Transient transfection studies with a luciferase reporter plasmid driven by HPyV9 or UF1 promoter demonstrated that UF1 early and late promoters were stronger than HPyV9 promoters in most cell lines, and that the UF1 late promoter was more potently activated by HPyV9 large T-antigen (LTAg). Mutation of two Sp1 motifs strongly reduced trans-activation of the late UF1 promoter by HPyV9 LTAg in HeLa cells. In conclusion, the mutations in the UF1 late promoter seem to strengthen its activity and its response to stimulation by HPyV9 LTAg in certain cells. It remains to be investigated whether these promoter changes have an influence on virus replication and affect the possible pathogenic properties of the virus.
Highlights
Polyomaviruses, a family of small, double-stranded DNA viruses that infects mammals, birds, and fish, while polyomavirus-like sequences have been found in reptiles and invertebrates [1,2,3]
In an effort to determine the biological importance of the differences in non-coding control region (NCCR) between Human polyomavirus 9 (HPyV9) and UF-1, we examined their relative early and late promoter strength in seven different human cell lines and studied the effect of HPyV9 large T-antigen (LTAg) on the early and late promoter activities
HPyV9 DNA can be found in urine, throat swabs, skin, and blood from healthy individuals [13,27,28,29,30,31], while viremia was observed in renal recipients and in patients with both kidney and pancreas transplantation [20]
Summary
Polyomaviruses, a family of small, double-stranded DNA viruses that infects mammals, birds, and fish, while polyomavirus-like sequences have been found in reptiles and invertebrates [1,2,3]. In 1971, the first two human polyomaviruses BK polyomavirus (BKPyV) and JC polyomavirus (JCPyV) were described and named after the initials of the patients from which they were isolated [4,5] It was not until 2007 that a third human polyomavirus (Karolinska Institute polyomavirus, KIPyV) was isolated [6], and since another 11 not previously reported polyomaviruses have been detected in human samples. A third HPyV9 variant was isolated from peripheral blood monocytes of an AIDS patient [26] This variant, designated HPyV9 UF-1 (hereafter referred to as UF-1), differs by two amino acids in the VP2/3 proteins relative to the originally isolated HPyV9 genomes [13,14], and has several changes in its non-coding control region (NCCR). The possible role of additional Sp1 sites in UF-1 NCCR when compared to the HPyV9 NCCR in promoter activity was investigated
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