BK Virus, JC Virus and Simian Virus 40 Infection in Humans, and Association with Human Tumors

Barbanti‐Brodano, Giuseppe; Sabbioni, Silvia; Martini, Fernanda; Negrini, Massimo; Corallini, Alfredo; Tognon, Mauro

doi:10.1007/0-387-32957-9_23

Cited by 65 publications

(96 citation statements)

References 178 publications

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“…Polyomaviruses are generally species specific, and as mentioned above, five have been described as human polyomaviruses (23). However, in addition to these five, a sixth polyomavirus, SV40, from the rhesus monkey, has, to a variable but generally rare extent, been detected in humans (3). Both BKV and JCV establish latency after primary infection and can be reactivated under certain circumstances (21).…”

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confidence: 99%

DNA from BK Virus and JC Virus and from KI, WU, and MC Polyomaviruses as Well as from Simian Virus 40 Is Not Detected in Non-UV-Light-Associated Primary Malignant Melanomas of Mucous Membranes

et al. 2008

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The single most important causative factor for malignant melanomas of the skin is UV radiation. However, this is not true for melanomas on body surfaces sheltered from the sun; thus, it is important to seek new causative factors of melanoma genesis. Human papillomaviruses and gammaherpesviruses are associated with human skin cancer; for example, human papillomavirus types 5 and 8 are associated with epidermodysplasia verruciformis, and human herpesvirus 8 is associated with Kaposi's sarcoma. Recently, a newly described human polyomavirus, Merkel cell polyomavirus (MCPyV), has been associated with Merkel cell carcinoma, an unusual form of neurotropic skin cancer. Moreover, melanocytes are of neuroepithelial origin. This background impelled us to investigate if human polyomavirus DNA could play a role in the development of extracutaneous melanomas. Sixty-four extracutaneous melanomas were initially collected and dissected. Of these, 38 could be successfully used for further testing for the presence of the five human polyomaviruses known so far-BK virus (BKV), JC virus (JCV), KI polyomavirus (KIPyV), WU polyomavirus (WUPyV), and MCPyV-and of simian virus 40 (SV40). No polyomavirus DNA could be detected in any of the samples tested by use of a nested PCR detecting BKV, JCV, and SV40; a newly designed PCR detecting KIPyV and WUPyV; or a newly designed PCR for MCPyV. We conclude that since no human polyomavirus DNA was detected in primary malignant melanomas on non-sun-exposed body surfaces, these polyomaviruses presumably are not major factors for the development of extracutaneous melanomas.The single most important factor for the development of malignant melanomas of the skin is UV radiation. In addition, numerous other risk factors or cofactors have been demonstrated, such as, e.g., hereditary/familial predisposition, a large number of nevi, the skin phenotype, and the hair and eye colors (13). However, UV radiation presumably cannot be responsible for some subgroups of cutaneous melanomas on body surfaces more or less sheltered from the sun, such as the acral lentiginous melanomas of the palms, soles, and subungual areas. Moreover, melanomas can appear on body surfaces completely sheltered from the sun, e.g., mucosal membranes of the sinonasal cavity, the anus-rectum, the vulva-vagina, and the penis. These melanomas, sometimes named extracutaneous melanomas, are rare in absolute numbers compared to the cutaneous melanomas but are similar to them if density (i.e., the average number of tumors per square unit of body surface area) is taken into account (19). This similarity in melanoma density is compelling and demonstrates the necessity of finding new causative factors of melanoma genesis. Nevertheless, there are biological differences between cutaneous and extracutaneous melanomas, and it is possible that by comparing extracutaneous melanomas with cutaneous melanomas, we may find non-UV-light-associated factors or cofactors in melanoma genesis. Viruses could be such factors. It is possible that DNA viruses are ass...

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DNA from BK Virus and JC Virus and from KI, WU, and MC Polyomaviruses as Well as from Simian Virus 40 Is Not Detected in Non-UV-Light-Associated Primary Malignant Melanomas of Mucous Membranes

et al. 2008

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“…In the normal host, BK viral infection is asymptomatic, usually in childhood, with a prevalent seropositivity of up to 94% in healthy adults [1]. Primary infection is thought to be usually acquired via the respiratory tract, although infections can also occur through urinary shedding, semen, blood transfusion, and organ transplantation [5]. The natural history indicates that the virus is dormant after primary infection and reactivates during periods of reduced immunity.…”

Section: Discussion Epidemiology and Pathogenesismentioning

confidence: 99%

Late-Onset BK Viral Nephropathy in a Kidney Transplant Recipient

Mathew

Holanda

Figanbaum

et al. 2014

Transplantation Proceedings

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“…BKV has been associated with posttransplantation nephropathy and hemorrhagic cystitis in hematopoietic stem cell transplant (HSCT) recipients (7,17). In addition to JCV and BKV, there are reports on the presence of the primate polyomavirus simian virus 40 (SV40) in humans, possibly introduced by contaminated poliovirus vaccine produced in monkey cells (4), although other ways of transmission have also been suggested (10,27). SV40 genomic sequences have been detected in human malignant mesothelioma tumors, but its role in human tumor development remains debated (25).…”

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Identification of a Third Human Polyomavirus

Allander

Andreasson

Gupta

et al. 2007

J Virol

570

522

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We have previously reported on a system for large-scale molecular virus screening of clinical samples. As part of an effort to systematically search for unrecognized human pathogens, the technology was applied for virus screening of human respiratory tract samples. This resulted in the identification of a previously unknown polyomavirus provisionally named KI polyomavirus. The virus is phylogenetically related to other primate polyomaviruses in the early region of the genome but has very little homology (<30% amino acid identity) to known polyomaviruses in the late region. The virus was found by PCR in 6 (1%) of 637 nasopharyngeal aspirates and in 1 (0.5%) of 192 fecal samples but was not detected in sets of urine and blood samples. Since polyomaviruses have oncogenic potential and may produce severe disease in immunosuppressed individuals, continued searching for the virus in different medical contexts is important. This finding further illustrates how unbiased screening of respiratory tract samples can be used for the discovery of diverse virus types.

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BK Virus, JC Virus and Simian Virus 40 Infection in Humans, and Association with Human Tumors

Cited by 65 publications

References 178 publications

DNA from BK Virus and JC Virus and from KI, WU, and MC Polyomaviruses as Well as from Simian Virus 40 Is Not Detected in Non-UV-Light-Associated Primary Malignant Melanomas of Mucous Membranes

DNA from BK Virus and JC Virus and from KI, WU, and MC Polyomaviruses as Well as from Simian Virus 40 Is Not Detected in Non-UV-Light-Associated Primary Malignant Melanomas of Mucous Membranes

Late-Onset BK Viral Nephropathy in a Kidney Transplant Recipient

Identification of a Third Human Polyomavirus

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