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1.
J Med Virol ; 89(12): 2230-2234, 2017 12.
Article in English | MEDLINE | ID: mdl-28667764

ABSTRACT

Human polyomaviruses such as JC polyomavirus and BK polyomavirus have long been well known pathogens of immunocompromised patients. Several new members of this viral family have been described during the last decade. Human polyomavirus 9 seems to be a novel pathogen of transplanted patients according to some studies. The aim of our study was to determine the presence of human polyomavirus 9 in patients after kidney or stem cell transplantation (SCT) at the University Hospital in Hradec Kralove, Czech Republic. Overall 100 patients, 65 after kidney transplantation and 35 after SCT, were included into the study. At least three follow-up samples from each patient were examined for human polyomavirus 9 DNA presentation with the two previously described in-house PCR protocols. Despite the frequent reactivation of human CMV (14.3% in kidney transplantation and 63.3% after SCT) or BK polyomavirus in our patient group, there was no positivity for human polyomavirus 9 either in blood samples or urine samples. One of the possible reasons for this discrepancy versus previous published studies could be a relatively low proportion of patients treated by induction therapy before kidney transplantation in our study cohort.


Subject(s)
Immunocompromised Host , Polyomaviridae/genetics , Polyomaviridae/isolation & purification , Polyomavirus Infections/epidemiology , Polyomavirus Infections/virology , Adult , Aged , Cohort Studies , Czech Republic/epidemiology , DNA, Viral/genetics , Female , Hospitals, University , Humans , Kidney Transplantation/adverse effects , Male , Middle Aged , Polymerase Chain Reaction , Polyomaviridae/pathogenicity , Stem Cell Transplantation/adverse effects , Young Adult
2.
J Clin Virol ; 76: 40-3, 2016 Mar.
Article in English | MEDLINE | ID: mdl-26809132

ABSTRACT

BACKGROUND: Merkel cell carcinoma (MCC) and trichodysplasia spinulosa (TS) are two proliferative cutaneous diseases caused by the Merkel cell polyomavirus (MCPyV) and trichodysplasia spinulosa-associated polyomavirus (TSPyV) respectively. Recently, studies have elucidated a key role of the small tumor (sT) antigen in the proliferative pathogenic mechanisms of MCPyV and likely TSPyV. While both sT antigens have demonstrated a capacity in regulating cellular pathways, it remains unknown whether MCPyV and TSPyV sT antigens contribute similarly or differentially to cell proliferation. OBJECTIVES: The present study aims to explore the proliferative potential of MCPyV and TSPyV sT antigens by investigating their regulatory effects on the retinoblastoma protein (pRb) tumor suppressor. STUDY DESIGN: Inducible cell lines expressing MCPyV sT or TSPyV sT were created using a lentiviral packaging system. Cellular proteins were extracted and subjected to SDS-PAGE followed by Western blot detection and densitometric analysis. RESULTS: Expression of TSPyV sT markedly enhanced the phosphorylation of pRb in Western blot experiments. In contrast, expression of MCPyV sT did not alter pRb phosphorylation under the same experimental conditions. Densitometric analysis revealed that TSPyV sT antigen expression nearly doubled the ratio of phosphorylated to total pRb (P<0.001, Student's T-test), while MCPyV sT antigen expression did not cause significant change in pRb phosphorylation status. CONCLUSION: Given that hyperphosphorylation of pRb is associated with dysregulation of the cell cycle, S-phase induction, and increased cell proliferation, our findings support an important role of TSPyV-mediated pRb deactivation in the development of TS. The observation that the pRb tumor suppressor is inactivated by TSPyV sT but not MCPyV sT provides further insights into the distinct pathobiological mechanisms of MCC and TS.


Subject(s)
Antigens, Polyomavirus Transforming/physiology , Carcinoma, Merkel Cell/virology , Cell Cycle , Hair Diseases/virology , Ichthyosis/virology , Merkel cell polyomavirus/pathogenicity , Polyomaviridae/pathogenicity , Retinoblastoma Protein/metabolism , Antigens, Polyomavirus Transforming/genetics , Carcinoma, Merkel Cell/physiopathology , Cell Line , DNA, Viral , HEK293 Cells , Humans , Merkel cell polyomavirus/genetics , Phosphorylation , Polyomaviridae/genetics , Polyomavirus Infections/complications , Polyomavirus Infections/virology , Skin Neoplasms
3.
Food Environ Virol ; 6(4): 260-8, 2014 Dec.
Article in English | MEDLINE | ID: mdl-24952878

ABSTRACT

Disinfection by low-pressure monochromatic ultraviolet (UVC) radiation (253.7 nm) became an important technique to sanitize drinking water and also wastewater in tertiary treatments. In order to prevent the transmission of waterborne viral diseases, the analysis of the disinfection kinetics and the quantification of infectious viral pathogens and indicators are highly relevant and need to be addressed. The families Adenoviridae and Polyomaviridae comprise human and animal pathogenic viruses that have been also proposed as indicators of fecal contamination in water and as Microbial Source Tracking tools. While it has been previously suggested that dsDNA viruses may be highly resistant to UVC radiation compared to other viruses or bacteria, no information is available on the stability of polyomavirus toward UV irradiation. Here, the inactivation of dsDNA (HAdV2 and JCPyV) and ssRNA (MS2 bacteriophage) viruses was analyzed at increasing UVC fluences. A minor decay of 2-logs was achieved for both infectious JC polyomaviruses (JCPyV) and human adenoviruses 2 (HAdV2) exposed to a UVC fluence of 1,400 J/m(2), while a decay of 4-log was observed for MS2 bacteriophages (ssRNA). The present study reveals the high UVC resistance of dsDNA viruses, and the UV fluences needed to efficiently inactivate JCPyV and HAdV2 are predicted. Furthermore, we show that in conjunction with appropriate mathematical models, qPCR data may be used to accurately estimate virus infectivity.


Subject(s)
Adenoviridae/radiation effects , DNA, Viral/radiation effects , Disinfection/methods , Polyomaviridae/radiation effects , RNA, Viral/radiation effects , Adenoviridae/metabolism , Adenoviridae/pathogenicity , Adenoviridae/ultrastructure , Adenoviruses, Human/metabolism , Adenoviruses, Human/pathogenicity , Adenoviruses, Human/radiation effects , Adenoviruses, Human/ultrastructure , Cell Line , DNA, Viral/metabolism , Humans , JC Virus/metabolism , JC Virus/pathogenicity , JC Virus/radiation effects , JC Virus/ultrastructure , Kinetics , Levivirus/metabolism , Levivirus/pathogenicity , Levivirus/radiation effects , Levivirus/ultrastructure , Microbial Viability/radiation effects , Microscopy, Electron, Transmission , Polyomaviridae/metabolism , Polyomaviridae/pathogenicity , Polyomaviridae/ultrastructure , RNA Stability/radiation effects , RNA, Viral/metabolism , Radiation Tolerance , Real-Time Polymerase Chain Reaction , Reverse Transcriptase Polymerase Chain Reaction , Ultraviolet Rays , Virion/metabolism , Virion/pathogenicity , Virion/radiation effects , Virion/ultrastructure , Virus Inactivation/radiation effects
4.
Clin Dev Immunol ; 2013: 373579, 2013.
Article in English | MEDLINE | ID: mdl-23737811

ABSTRACT

JC and BK polyomaviruses were discovered over 40 years ago and have become increasingly prevalent causes of morbidity and mortality in a variety of distinct, immunocompromised patient cohorts. The recent discoveries of eight new members of the Polyomaviridae family that are capable of infecting humans suggest that there are more to be discovered and raise the possibility that they may play a more significant role in human disease than previously understood. In spite of this, there remains a dearth of specific therapeutic options for human polyomavirus infections and an incomplete understanding of the relationship between the virus and the host immune system. This review summarises the human polyomaviruses with particular emphasis on pathogenesis in those directly implicated in disease aetiology and the therapeutic options available for treatment in the immunocompromised host.


Subject(s)
Antiviral Agents/pharmacology , BK Virus/pathogenicity , Immunocompromised Host , JC Virus/pathogenicity , Polyomaviridae/pathogenicity , Polyomavirus Infections/drug therapy , Tumor Virus Infections/drug therapy , BK Virus/drug effects , BK Virus/genetics , BK Virus/immunology , Genome, Viral/immunology , Humans , Immune Evasion , Immune System/drug effects , Immune System/immunology , Immune System/virology , JC Virus/genetics , JC Virus/immunology , Phylogeny , Polyomaviridae/classification , Polyomaviridae/genetics , Polyomaviridae/immunology , Polyomavirus Infections/immunology , Polyomavirus Infections/pathology , Polyomavirus Infections/virology , RNA, Viral/antagonists & inhibitors , RNA, Viral/biosynthesis , Tumor Virus Infections/immunology , Tumor Virus Infections/pathology , Tumor Virus Infections/virology , Virus Activation/immunology
5.
Enferm. infecc. microbiol. clín. (Ed. impr.) ; 30(supl.2): 70-75, mar. 2012. ilus, tab
Article in English | IBECS | ID: ibc-105879

ABSTRACT

Viral infections are a major cause of morbidity and even mortality in solid organ transplant recipients. This article reviews key aspects of infections in solid organ transplant recipients from respiratory viruses, such as influenza, polyomavirus, erythrovirus B19 and measles (AU)


Las infecciones víricas constituyen una causa importante de morbilidad y, en ocasiones, también de mortalidad en el receptor de un trasplante de órgano sólido. En este artículo se revisan aspectos fundamentales acerca de las infecciones por virus respiratorios, incluyendo el virus de la gripe, poliomavirus, erythrovirus B19 y sarampión en el receptor de un trasplante de órgano sólido (AU)


Subject(s)
Humans , Organ Transplantation/adverse effects , Herpesviridae Infections/complications , Erythrovirus/pathogenicity , Orthomyxoviridae/pathogenicity , Measles virus/pathogenicity , Polyomaviridae/pathogenicity , Severe acute respiratory syndrome-related coronavirus/pathogenicity
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