Multiorgan WU Polyomavirus Infection in Bone Marrow Transplant Recipient

Siebrasse, Erica A.; Nguyen, Nang L.; Willby, Melisa J.; Erdman, Dean D.; Menegus, Marilyn A.; Wang, David

doi:10.3201/eid2201.151384

Cited by 23 publications

(23 citation statements)

References 23 publications

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“…PCR-based studies of 30 lung cancer patients compared to healthy individuals indicated no direct association between WUV infection and lung adenocarcinoma (38). However, recently, a lung transplant patient with Job’s syndrome and a bone marrow transplant recipient with severe acute respiratory distress syndrome were reported to have WUV pulmonary infection (29, 39). In the present study, we have identified a case of WUV-associated bronchitis with the demonstration of both early and late viral antigens in intact dysplastic lung epithelia.…”

Section: Discussionmentioning

confidence: 99%

Survey for human polyomaviruses in cancer

Toptan¹,

Yousem²,

Ho³

et al. 2016

JCI Insight

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Over the past 8 years, the discovery of 11 new human polyomaviruses (HPyVs) has revived interest in this DNA tumor virus family. Although HPyV infection is widespread and largely asymptomatic, one of these HPyVs, Merkel cell polyomavirus (MCV), is a bona fide human tumor virus. JC virus (JCV), BK virus, HPyV7, and trichodysplasia-spinulosa virus (TSV) can cause nonneoplastic diseases in the setting of immunosuppression. Few specific reagents are available to study the biology of the newly discovered HPyVs. We developed a pan-HPyV-screening method using a cocktail of 3 antibodies that, when combined, recognize T antigen proteins of all HPyVs. We validated detection characteristics of the antibody cocktail by immunoblotting and immunohistochemistry and screened 1,184 cases, including well-defined diseases and tumor tissue microarrays. This assay robustly detected MCV, TSV, JCV, and HPyV7 in etiologically related diseases. We further identified WU polyomavirus in a case of chronic lymphocytic lymphoma-associated bronchitis. Except for scattered, incidentally infected cells in 5% of lung squamous cell carcinomas and colon adenocarcinomas, a broad panel of tumor tissues was largely negative for infection by any HPyV. This method eliminates known HPyVs as suspected causes of cancers investigated in this study. Pan-HPyV survey can be applied to identify diseases associated with recently discovered polyomaviruses.

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Section: Discussionmentioning

confidence: 99%

Survey for human polyomaviruses in cancer

Toptan¹,

Yousem²,

Ho³

et al. 2016

JCI Insight

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“…Toptan et al [13] developed a panhuman PyV immunohistochemistry test and analysed 1,250 samples from various, also lung, tumours and normal tissues (detailed in Table 3), and antigen positivity was revealed in a lung tissue sample from a patient with chronic lymphocytic leukaemia, then the presence of WUPyV DNA was also proved. Siebrasse et al[14, 15] studied KIPyV and WUPyV in lung tissue samples from 2 patients not only by PCR, but also by antibodies, revealing antigen positivity. KIPyV-positive cells were identified as CD68+, suggesting that alveolar macrophages might be infected by the virus.…”

Section: Resultsmentioning

confidence: 99%

“…Immunohistochemistry was performed on lung, trachea, liver, kidney, and gastrointestinal tract tissue sections from a bone marrow transplant patient by anti-VP1 WUPyV antibody. Viral antigen-positive cells were found in trachea and lung sections; some cells were CD68+ and showed macrophage morphology [15]. …”

Section: Resultsmentioning

confidence: 99%

“…Later, both viruses were found mainly in respiratory samples: the viruses were detected (positivity rates are shown in brackets) in respiratory secretions (0.5–6.5% for KIPyV and 0.35–16.4% for WUPyV) and in tonsillar tissue samples (2% for KIPyV and 2.2–12% for WUPyV) [4-10], and both viruses were demonstrated in non-cancerous lung tissues (3.3 and 9.5% for KIPyV and case studies to detect antigens of WUPyV and KIPyV) [11-15], while WUPyV was found in 7.8 and 27.7% of adenoids studied [6, 7] as well. The MW polyomavirus (MWPyV) genome was discovered from stool samples in 2012 [16], but beside stool samples (2.3%), it was also detected in a condyloma specimen [17], nasal swab and nasopharyngeal aspirate samples (1.5–9.2%) [18, 19], tonsils (2 and 6%) and adenoid tissue (1%) [8, 20].…”

Section: Introductionmentioning

confidence: 99%

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Survey of KI, WU, MW, and STL Polyomavirus in Cancerous and Non-Cancerous Lung Tissues

et al. 2017

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Background/Aims: The pathogenesis of the human polyomavirus (PyV) KI, WU, MW, and STL has not been elucidated yet. Respiratory transmission is suggested, but the site of the replication, tissue, and cell tropism is not clarified. KIPyV and WUPyV DNA and/or antigen were detected in normal lung tissues previously by others. In fact, a KIPyV DNA sequence was found in lung cancer samples. Up to date, there is no publication about the DNA prevalence of MWPyV and STLPyV neither in normal nor in cancerous lung tissues. The aim of the present study was to examine the DNA prevalence of these polyomaviruses in cancerous and non-cancerous lung tissue samples, in order to study the possible site for viral replication and/or persistence, and the potential association of these viruses with lung carcinogenesis as well. Methods: 100 cancerous and 47 non-cancerous, formalin-fixed paraffin-embedded lung tissue samples were studied for KIPyV, WUPyV, MWPyV, and STLPyV by real-time PCR. Results and Conclusion: Neither of the viruses was found in samples from small-cell, non-small-cell (adenocarcinoma, squamous-cell carcinoma and large-cell neuroendocrine lung cancer), mixed-type and non-differentiated lung carcinoma, and non-cancerous lung tissues (from patients with pneumonia, emphysema and fibrosis).

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“…KIPyV and WUPyV have been detected worldwide in respiratory specimens and clinical samples (Babakir-Mina et al 2008Kiasari et al 2008;Bialasiewicz et al 2008;Foulongne et al 2008;Payungporn et al 2008;Abed et al 2007;Han et al 2007;Le et al 2007), suggesting a widespread infection, but their involvement in human disease or tumor development is not clear (Giraud et al 2008(Giraud et al , 2009). Reactivation and excretion of KIPyV and WUPyV have also been reported in the gastrointestinal tract of immunosuppressed transplanted patients (Siebrasse et al 2016) and in HIV patients.…”

Section: Kipyv and Wupyvmentioning

confidence: 99%

Entry, infection, replication, and egress of human polyomaviruses: an update

Bhattacharjee

Chattaraj

2017

Can. J. Microbiol.

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Polyomaviruses (PyVs), belonging to the family Polyomaviridae, are a group of small, nonenveloped, double-stranded, circular DNA viruses widely distributed in the vertebrates. PyVs cause no apparent disease in adult laboratory mice but cause a wide variety of tumors when artificially inoculated into neonates or semipermissive animals. A few human PyVs, such as BK, JC, and Merkel cell PyVs, have been unequivocally linked to pathogenesis under conditions of immunosuppression. Infection is thought to occur early in life and persists for the lifespan of the host. Over evolutionary time scales, it appears that PyVs have slowly co-evolved with specific host animal lineages. Host cell surface glycoproteins and glycolipids seem to play a decisive role in the entry stage of viral infection and in channeling the virions to specific intracellular membrane-bound compartments and ultimately to the nucleus, where the genomes are replicated and packaged for release. Therefore the transport of the infecting virion or viral genome to this site of multiplication is an essential process in productive viral infection as well as in latent infection and transformation. This review summarizes the major findings related to the characterization of the nature of the interactions between PyV and host protein and their impact in host cell invasion.

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Multiorgan WU Polyomavirus Infection in Bone Marrow Transplant Recipient

Abstract: Virus was detected in the lung and trachea of a deceased patient.

Cited by 23 publications

References 23 publications

Survey for human polyomaviruses in cancer

Survey for human polyomaviruses in cancer

Survey of KI, WU, MW, and STL Polyomavirus in Cancerous and Non-Cancerous Lung Tissues

Entry, infection, replication, and egress of human polyomaviruses: an update

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