The role of polyomaviruses in human disease

Jiang, Mengxi; Abend, Johanna R.; Johnson, Silas F.; Imperiale, Michael J.

doi:10.1016/j.virol.2008.09.027

Cited by 253 publications

(269 citation statements)

References 180 publications

(221 reference statements)

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“…These viruses are involved in several human diseases (Jiang et al, 2009), but no conclusive evidence exists that they cause or act as a cofactor in human cancer. However, a wide range of reports have indicated the presence of viral genomic sequences in multiple human cancers such as osteosarcomas, mesotheliomas, brain tumors, gliomas, medulloblastomas, colorectal carcinomas and skin cancers (Table 1) (Goel et al, 2006;McCabe et al, 2006;Feng et al, 2008;Jiang et al, 2009).…”

Section: Polyomaviruses: Sv40 Jcv Bkv and MCVmentioning

confidence: 99%

Viral epigenomes in human tumorigenesis

Fernández

Esteller

2010

Oncogene

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Viruses are associated with 15-20% of human cancers worldwide. In the last century, many studies were directed towards elucidating the molecular mechanisms and genetic alterations by which viruses cause cancer. The importance of epigenetics in the regulation of gene expression has prompted the investigation of virus and host interactions not only at the genetic level but also at the epigenetic level. In this study, we summarize the published epigenetic information relating to the genomes of viruses directly or indirectly associated with the establishment of tumorigenic processes. We also review aspects such as viral replication and latency associated with epigenetic changes and summarize what is known about epigenetic alterations in host genomes and the implications of these for the tumoral process. The advances made in characterizing epigenetic features in cancer-causing viruses have improved our understanding of their functional mechanisms. Knowledge of the epigenetic changes that occur in the genome of these viruses should provide us with markers for following cancer progression, as well as new tools for cancer therapy.

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Section: Polyomaviruses: Sv40 Jcv Bkv and MCVmentioning

confidence: 99%

Viral epigenomes in human tumorigenesis

Fernández

Esteller

2010

Oncogene

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“…Up to 90% of adults have serologic evidence of exposure to BKV, but in most humans the virus remains latent (25,26). Almost all disease accompanied by BKV reactivation has been found in immunocompromised patients (22). In recent years, BKV has been associated with nephropathy (polyomavirus-associated nephropathy, or PVAN) in up to 10% of renal transplant patients.…”

mentioning

confidence: 99%

“…In BKV and in other polyomaviruses, three genomic areas have been distinguished: (i) a noncoding control region including the origin of viral DNA replication, (ii) the early genes encoding large and small T antigens (TAgs), and (iii) the late genes which code for the capsid proteins VP-1, VP-2, and VP-3 and the agnoprotein (22).…”

mentioning

confidence: 99%

Host-Specific Replication of BK Virus DNA in Mouse Cell Extracts Is Independently Controlled by DNA Polymerase α-Primase and Inhibitory Activities

Tikhanovich

Nasheuer

2010

J Virol

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The activation of the human polyomavirus BK causes polyomavirus-associated nephropathy in immunocompromised humans. Studies of the virus have been restricted since the virus DNA replication is species specific. Cell-based and cell-free DNA replication systems, including the BK virus (BKV) monopolymerase DNA replication system using purified proteins, reproduce the species specificity (28). Therefore, the major host proteins comprising this assay, DNA polymerase ␣-primase (Pol-prim) and replication protein A (RPA), were intensively studied here. We demonstrate that Pol-prim plays a major role in the species specificity of BKV DNA replication. Both large subunits p180 and p68 of the enzyme complex have central functions in modulating the host specificity. Recently, an inhibitory activity of BKV DNA replication was described (C. Mahon, B. Liang, I. Tikhanovich, J. R. Abend, M. J. Imperiale, H. P. Nasheuer, and W. R. Folk, J. Virol. 83:5708-5717, 2009), but neither mouse Pol-prim nor mouse RPA diminishes cell-free BKV DNA replication. However, the inhibition of BKV DNA replication in mouse extracts depends on sequences flanking the core origin. In the presence of human Pol-prim, the inhibitory effect of mouse cell factors is abolished with plasmid DNAs containing the murine polyomavirus early promoter region, whereas the late enhancer region and the core origin are supplied from BKV. Thus, BKV replication is regulated by both Pol-prim, as a core origin species-specific factor, and inhibitory activities, as origin-flanking sequence-dependent factor(s).

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“…It may also be non-specific which occurs secondary to tubular injury. Excessive tissue destruction might occur once the patient's immunity improves (26). Histopathology has difficulties in distinguishing between rejection and PVAN especially where there is co-existence of both the disease process (27).…”

Section: Bk Polyoma Virusmentioning

confidence: 99%

Prevalence of cytomegalovirus and BK polyoma virus infection in post-renal transplant patients in a tertiary care centre in

Manuel¹,

Ambroise²,

Varghese³

et al. 2017

J Nephropathol

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Background: Viral infections are a significant cause of graft loss and dysfunction in kidney transplant recipients. Cytomegalovirus and BK polyomavirus have often been explained as the most common viral etiological agents. Objectives: The current study was undertaken to assess the prevalence of cytomegalovirus and BK polyomavirus infection in post-renal transplant individuals in a tertiary care centre in South India and also to study the histopathological changes of such infections in the kidney allograft biopsies. Patients and Methods:We conducted a retrospective investigation of 100 cases using archival renal biopsy specimens which were subjected to immunohistochemical stains to detect cytomegalovirus and BK polyoma virus. These findings were then correlated with the histopathological alterations detected in H&E sections. Results: We detected the prevalence of cytomegalovirus in 7% and BK polyoma virus in 3%. Cytomegalovirus was statistically associated with pre-and post-transplant infections along with diabetic status. We noted that, out of the seven patients who were immunohistochemically cytomegalovirus positive, only five had positive cytomegalovirus IgM status. With BK polyoma virus, we noted a statistical significance with pre-and posttransplant infections. However, we did not find evidence of cytomegalovirus and BK polyoma virus co-infection in any of the renal allograft biopsies. Conclusions: Routine immunohistochemical evaluation of cytomegalovirus and BK polyoma viral infections in kidney allograft recipients must be done, especially in those with preand post-transplant infections and diabetes.

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The role of polyomaviruses in human disease

Cited by 253 publications

References 180 publications

Viral epigenomes in human tumorigenesis

Viral epigenomes in human tumorigenesis

Host-Specific Replication of BK Virus DNA in Mouse Cell Extracts Is Independently Controlled by DNA Polymerase α-Primase and Inhibitory Activities

Prevalence of cytomegalovirus and BK polyoma virus infection in post-renal transplant patients in a tertiary care centre in

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