Lymphotropism of Merkel Cell Polyomavirus Infection, Nova Scotia, Canada

Toracchio, Sonia; Foyle, Annette; Šroller, Vojtěch; Reed, Jon A.; Wu, Jun; Kozinetz, Claudia A.; Butel, Janet S.

doi:10.3201/eid1611.100628

Cited by 44 publications

(40 citation statements)

References 32 publications

(29 reference statements)

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“…These results are consistent with a previous serologic study from Tolstov and colleagues (20) on 18 CLL cases where they found no median differences when compared with 18 acute lymphoblastic leukemia subjects. Our serologic data are also in agreement with previous studies where almost null viral DNA and/or antigen were detected (13)(14)(15)(16)). An exception to the above is a report from Pantulu and colleagues (17) and complemented by Haugg and colleagues (18) describing the detection of DNA encoding a mutated MCV LT-Ag in CLL cells.…”

Section: Discussionsupporting

confidence: 93%

“…Among subjects with lymphoproliferative disorders, CLL subjects have been shown to have higher MCV DNA detection rates, although prevalences and viral load are low (13)(14)(15)(16). LT-Ag detection is almost null in lymphomas but in purified CD5þ/CD19þ CLL cells a mutated DNA sequence encoding for MCV LT-Ag has been reported (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

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Antibody Response to Merkel Cell Polyomavirus Associated with Incident Lymphoma in the Epilymph Case–Control Study in Spain

Robles

Poloczek

Casabonne

et al. 2012

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Merkel cell polyomavirus (MCV) has been identified as the cause of Merkel cell carcinoma. The increased incidence of chronic lymphocytic leukemia in Merkel cell cancer cohorts and the lymphotropic properties of the virus suggest a possible viral association with lymphomagenesis. To investigate this potential role, we explored seroreactivity against MCV VP1 capsids within the Epilymph case-control study in Spain.Methods: Serum samples from 468 incident lymphomas, categorized into up to 11 entities, and 522 controls frequency matched by age, sex, and recruitment center were tested for MCV antibodies by enzyme immunoassay using Virus-Like-Particles. Adjusted multinomial logistic regression was used to estimate the OR and 95% confidence interval (CI) associated to MCV seroprevalence. Immunosuppressed subjects were excluded.Results: MCV seroprevalence was 82% in controls and 85% in lymphoma cases. Among 11 lymphoma categories, MCV seropositivity was significantly higher in diffuse large B-cell lymphomas (DLBCL; 96.4%; OR ¼ 6.1, 95%CI ¼ 1.9-19.8), as compared with controls. MCV prevalences were also higher in follicular lymphoma, lymphoplasmacytic lymphoma, chronic lymphocytic leukemia, Hodgkin lymphoma, and mature T-cell lymphoma but differences did not reach statistical significance. Lower prevalences were observed for multiple myeloma and other B-cell lymphoma. Exclusion of samples collected after start of treatment did not change the results. In a subset analysis, no significant association was observed between BKV and JCV seroprevalence and DLBCL.Conclusion: The association observed between serologic evidence of MCV exposure and DLBCL warrants further research. Impact: MCV might be involved in the pathway of DLBCL and other lymphomas. Cancer Epidemiol Biomarkers Prev; 21(9); 1592-8. Ó2012 AACR.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Antibody Response to Merkel Cell Polyomavirus Associated with Incident Lymphoma in the Epilymph Case–Control Study in Spain

Robles

Poloczek

Casabonne

et al. 2012

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…In this study, autopsy brain tissue samples of HIV-positive patients with KIPyV/WUPyV reactivation were examined. No specific histopathological lesions were found associated with the presence of KIPyV and WUPyV (41) unlike MCPyV (8,42).…”

Section: Histopathologymentioning

confidence: 99%

The human polyomaviruses KI and WU: virological background and clinical implications

Babakir‐Mina

Ciccozzi²,

Perno

et al. 2013

APMIS

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Babakir-Mina M, Ciccozzi M, Perno CF, Ciotti M. The human polyomaviruses KI and WU: virological background and clinical implications. APMIS 2013; 121: 746-54. In 2007, two novel polyomaviruses KI and WU were uncovered in the respiratory secretions of children with acute respiratory symptoms. Seroepidemiological studies showed that infection by these viruses is widespread in the human population. Following these findings, different biological specimens and body compartments have been screened by real-time PCR in the attempt to establish a pathogenetic role for KI polyomavirus (KIPyV) and WU polyomavirus (WUPyV) in human diseases. Although both viruses have been found mainly in respiratory tract samples of immunocompromised patients, a clear causative link with the respiratory disease has not been established. Indeed, the lack of specific clinical or radiological findings, the frequent co-detection with other respiratory pathogens, the detection in subjects without signs or symptoms of respiratory disease, and the variability of the viral loads measured did not allow drawing a definitive conclusion. Prospective studies carried out on a large sample size including both immunocompromised and immunocompetent patients with and without respiratory symptoms are needed. Standardized quantitative real-time PCR methods, definition of a clear clinical cutoff value, timing in the collection of respiratory samples, are also crucial to understand the pathogenic role, if any, of KIPyV and WUPyV in human pathology.

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“…The primary target cells and the host cells that can function as reservoir are not known, but the virus seems to be common in healthy skin, skin lesions, eyebrow hairs, and warts, indicating a dermatotropism of this virus [Wieland et al, 2009;van der Meijden et al, 2010;Mertz et al, 2010a;Faust et al, 2011;Wieland et al, 2011]. MCPyV DNA is also found in blood, gall bladder, appendix, liver, lung, lymphoid, and intestine tissue [Feng et al, 2008;Sharp et al, 2009;Goh et al, 2009;Shuda et al, 2009;Foulongne et al, 2010a;Husseiny et al, 2010;Loyo et al, 2010;Toracchio et al, 2010;Campello et al, 2011;Pancaldi et al, 2011;reviewed in Moens et al, 2010 and. Another study has suggested that MCPyV may persist in and spread through inflammatory monocytes [Mertz et al, 2010b].…”

Section: Mcpyv: Route Of Infection Cell Tropism and Transmissionmentioning

confidence: 99%