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The Lancet. Neurology Mar 2019
Topics: Humans; JC Virus; Leukoencephalopathy, Progressive Multifocal; Multiple Sclerosis; Natalizumab; Retrospective Studies
PubMed: 30784549
DOI: 10.1016/S1474-4422(19)30022-5 -
Transplant Infectious Disease : An... Feb 2011We report JC virus (JCV)-associated nephropathy in a renal allograft recipient and summarize the clinical and laboratory data of the 8 previous cases. A 28-year-old male... (Comparative Study)
Comparative Study Review
We report JC virus (JCV)-associated nephropathy in a renal allograft recipient and summarize the clinical and laboratory data of the 8 previous cases. A 28-year-old male renal allograft recipient received a preemptive transplant from his father. Six months later, a kidney biopsy was performed because of deterioration of allograft function. Biopsy revealed tubulointerstitial mononuclear infiltrates with normal glomeruli; on hematoxylin and eosin staining, basophilic nuclear inclusions were seen in the nucleus of tubular cells. Urinary cytology failed to demonstrate decoy cells, but polymerase chain reaction of a urinary sample was positive for JCV 3.15 × 10(10) copies/mL. Additionally, polyomavirus (SV40) immunohistochemical staining was performed and was positive in the enlarged nuclei of tubular epithelial cells in the kidney biopsy sample. After the diagnosis of polyomavirus-associated nephropathy (PVAN) was confirmed by kidney biopsy, immunosuppressive agents were reduced. Intravenous immunoglobulin was administered 5 times at a dose of 500 mg/kg every other 3 weeks. Two months after diagnosis, the serum creatinine became stable and urinary viral load of JCV was decreased. Because viruria was still present, tacrolimus was converted to sirolimus. Four months after immunosuppressive agent conversion from tacrolimus to sirolimus, the viruria had disappeared. Review of the literature and our case demonstrates that male gender, previous acute rejection episode, low incidence of JCV viremia, PVAN pattern B histology, and reducing immunosuppression are the diagnostic touchstones for PVAN due to JCV.
Topics: Adult; DNA, Viral; Humans; JC Virus; Kidney; Kidney Diseases; Kidney Transplantation; Male; Polymerase Chain Reaction; Polyomavirus Infections; Tumor Virus Infections
PubMed: 21299772
DOI: 10.1111/j.1399-3062.2010.00567.x -
Methods in Molecular Biology (Clifton,... 2005JC virus (JCV) belongs to the family of double-stranded DNA polyomaviruses and in humans causes a demyelinating disease of the central nervous system, progressive...
JC virus (JCV) belongs to the family of double-stranded DNA polyomaviruses and in humans causes a demyelinating disease of the central nervous system, progressive multifocal leukoencephalopathy (PML). It has been reported that sialic acids play a pivotal role in hemagglutination of red blood cells and entry into host cells of JCV and that JCV can enter a wide variety of cell types and localize to the nuclei. The outer shell of the JCV virion comprises the major capsid protein VP1, and a virus-like particle (VLP) consisting of recombinant VP1 made from Escherichia coli exhibit a virion-like structure and physiological functions (cellular attachment and intracytoplasmic trafficking) similar to those of JCV virions. To examine the mechanism of cell attachment of JCV, an overlay assay using a VLP has been developed, revealing that sialoglycoproteins, including alpha1 acid-glycoprotein, fetuin, and transferrin receptor bind with VLP. In addition, VLPs bind to glycolipids, such as lactosylceramide and gangliosides including GM3, GD2, GD3, GD1b, GT1b, and GQ1b, and VLP weakly bind to GD1a. In this section, detailed procedures for the synthesis of VLP from E. coli and VLP overlay assay are described.
Topics: Electrophoresis, Polyacrylamide Gel; Hemagglutination Tests; Humans; Immunoblotting; JC Virus; Microscopy, Electron
PubMed: 15507708
DOI: 10.1385/1-59259-848-x:175 -
Current Clinical Topics in Infectious... 1989
Review
Topics: Animals; Brain Neoplasms; Disease Models, Animal; Humans; JC Virus; Leukoencephalopathy, Progressive Multifocal
PubMed: 2553062
DOI: No ID Found -
No To Shinkei = Brain and Nerve Feb 2002
Review
Topics: Animals; DNA-Binding Proteins; Genetic Vectors; Genome, Viral; Humans; JC Virus; Leukoencephalopathy, Progressive Multifocal; Organ Specificity; Receptors, Virus; Species Specificity; Transcription Factors; Transcription, Genetic; Viral Proteins; Viral Regulatory and Accessory Proteins; Virion
PubMed: 11889755
DOI: No ID Found -
Journal of Virology Feb 2020JC polyomavirus (JCPyV) infects 50 to 80% of the population and is the causative agent of a fatal demyelinating disease of the central nervous system (CNS). JCPyV...
JC polyomavirus (JCPyV) infects 50 to 80% of the population and is the causative agent of a fatal demyelinating disease of the central nervous system (CNS). JCPyV presents initially as a persistent infection in the kidneys of healthy people, but during immunosuppression, the virus can reactivate and cause progressive multifocal leukoencephalopathy (PML). Within the CNS, JCPyV predominately targets two cell types, oligodendrocytes and astrocytes. Until recently, the role of astrocytes has been masked by the pathology in the myelin-producing oligodendrocytes, which are lytically destroyed by the virus. To better understand how astrocytes are impacted during JCPyV infection, the temporal regulation and infectious cycle of JCPyV were analyzed in primary normal human astrocytes (NHAs). Previous research to define the molecular mechanisms underlying JCPyV infection has mostly relied on the use of cell culture models, such as SVG-A cells (SVGAs), an immortalized, mixed population of glial cells transformed with simian virus 40 (SV40) T antigen. However, SVGAs present several limitations due to their immortalized characteristics, and NHAs represent an innovative approach to study JCPyV infection Using infectivity assays, quantitative PCR, and immunofluorescence assay approaches, we have further characterized JCPyV infectivity in NHAs. The JCPyV infectious cycle is significantly delayed in NHAs, and the expression of SV40 T antigen alters the cellular environment, which impacts viral infection in immortalized cells. This research establishes a foundation for the use of primary NHAs in future studies and will help unravel the role of astrocytes in PML pathogenesis. Animal models are crucial in advancing biomedical research and defining the pathogenesis of human disease. Unfortunately, not all diseases can be easily modeled in a nonhuman host or such models are cost prohibitive to generate, including models for the human-specific virus JC polyomavirus (JCPyV). JCPyV infects most of the population but can cause a rare, fatal disease, progressive multifocal leukoencephalopathy (PML). There have been considerable advancements in understanding the molecular mechanisms of JCPyV infection, but this has mostly been limited to immortalized cell culture models. In contrast, PML pathogenesis research has been greatly hindered because of the lack of an animal model. We have further characterized JCPyV infection in primary human astrocytes to better define the infectious process in a primary cell type. Albeit a cell culture model, primary astrocytes may better recapitulate human disease, are easier to maintain than other primary cells, and are less expensive than using an animal model.
Topics: Animals; Antigens, Viral, Tumor; Astrocytes; Cell Culture Techniques; Cell Line; Disease Models, Animal; Disease Progression; Female; Humans; JC Virus; Leukoencephalopathy, Progressive Multifocal; Neuroglia; Polyomavirus Infections; Simian virus 40; Viral Proteins
PubMed: 31826993
DOI: 10.1128/JVI.01331-19 -
Virology Feb 2019JCV is a human polyomavirus (PyV) that establishes a persistent infection in its host. Current immunomodulatory therapies, such as Natalizumab for multiple sclerosis,...
JCV is a human polyomavirus (PyV) that establishes a persistent infection in its host. Current immunomodulatory therapies, such as Natalizumab for multiple sclerosis, can result in JCV reactivation, leading to the debilitating brain disease progressive multifocal leukoencephalopathy (PML). JCV is among the viruses that recruit and modulate the host DNA damage response (DDR) to replicate its genome. We have identified host proteins recruited to the nuclear sites of JC viral DNA (vDNA) replication using three cell types susceptible to infection in vitro. Using confocal microscopy, we found that JCV recruited a similar repertoire of host DDR proteins to these replication sites previously observed for other PyVs. Electron tomography of JCV "virus factories" showed structural features like those described for murine PyV. These results confirm and extend previous observations for PyVs to JCV emphasizing a similar replication strategy among members of this virus family.
Topics: Astrocytes; Cell Line; Choroid Plexus; DNA Damage; DNA Replication; DNA, Viral; Epithelial Cells; Humans; JC Virus; Microscopy, Confocal; Microscopy, Electron; Virus Replication
PubMed: 30811999
DOI: 10.1016/j.virol.2018.12.014 -
PloS One 2023JC Polyomavirus (JCV) is a human polyomavirus encoding T-antigen protein, which is implicated in carcinogenesis. JCV is prevalent in the upper and lower gastrointestinal... (Meta-Analysis)
Meta-Analysis
JC Polyomavirus (JCV) is a human polyomavirus encoding T-antigen protein, which is implicated in carcinogenesis. JCV is prevalent in the upper and lower gastrointestinal track. Several studies have reported JCV associations with the risk of developing colorectal cancer (CRC), however, these findings remain controversial. Since JCV DNA may be present in healthy tissues as well as transformed tissues, JCV T-antigen expression could be a more useful measure of JCV's association with cancer development. The aim of this study is to conduct a meta-analysis of case-control studies to investigate if there is a significant association between JCV T-antigen protein expression and risk of CRC. A systematic review was performed to identify studies reporting JCV DNA prevalence in CRC and JCV T-antigen expression. The strength of the association was estimated by odds ratios (ORs). Five (of 66) studies satisfied analysis inclusion criteria, and spanned years 1999 to 2022. Random effects meta-analysis of CRC cases versus controls showed an 11-fold increased risk of CRC development in JCV DNA positive samples with JCV T-antigen expression versus normal tissues (OR 10.95; 95% CI: 2.48-48.24; P = 0.0016). The results of this meta-analysis of JCV infection followed by JCV T-antigen protein expression for the risk of CRC support the argument that JCV infection significantly increases the risk of colorectal cancer in tissues where the JCV T-antigen protein is expressed. Further research with JCV T-antigen expression in relation to CRC development is needed.
Topics: Humans; Colorectal Neoplasms; JC Virus; Antigens, Viral, Tumor; Odds Ratio; Case-Control Studies; DNA, Viral; Polyomavirus Infections
PubMed: 37000859
DOI: 10.1371/journal.pone.0283642 -
Virology Journal Feb 2010JCV infection occurs early in childhood and last throughout life. JCV has been associated to colorectal cancer and might contribute to the cancer phenotype by several... (Review)
Review
JCV infection occurs early in childhood and last throughout life. JCV has been associated to colorectal cancer and might contribute to the cancer phenotype by several mechanisms. Among JCV proteins, particularly two of them, large T-antigen and agnoprotein, can interfere with cell cycle control and genomic instability mechanisms, but other viral proteins might also contribute to the process. Part of viral DNA sequences are detected in carcinoma lesions, but less frequently in adenomas, and not in the normal surrounding tissue, suggesting they are integrated in the host cell genome and these integrations have been selected; in addition viral integration can cause a gene, or chromosomal damage. The inflammatory infiltration caused by a local chronic viral infection in the intestine can contribute to the selection and expansion of a tumor prone cell in a cytokine rich microenvironment. JCV may not be the cause of colorectal cancer, but it can be a relevant risk factor and able to facilitate progression at one or several stages in tumor progression. JCV transient effects might lead to selective expansion of tumor cells. Since there is not a direct cause and effect relationship, JCV infection may be an alternative to low frequency cancer predisposition genes.
Topics: Colorectal Neoplasms; Humans; JC Virus; Polyomavirus Infections; Tumor Virus Infections
PubMed: 20167111
DOI: 10.1186/1743-422X-7-42 -
Asian Pacific Journal of Cancer... Oct 2020JC virus (JCV) , and BK virus (BKV) can remain latency in kidney and excrete via urine asymptomatically. JCV has been associated with colorectal and bladder cancers. BKV...
UNLABELLED
JC virus (JCV) , and BK virus (BKV) can remain latency in kidney and excrete via urine asymptomatically. JCV has been associated with colorectal and bladder cancers. BKV has been linked with lung, pancreas, liver, urogenital tract, head and neck cancers. Therefore, the frequency of JCV DNA and BKV DNA are essential to evaluate in urine samples of healthy individuals.
MATERIALS AND METHODS
Hundred sixty four urine samples were collected from healthy subjects [96 females and 68 males]. DNA was extracted and detection of JCV DNA and BKV DNA was carried out by PCR . The analysis of sequencing and construction of phylogenetic tree were performed for the samples positive for JCV DNA and BKV DNA.
RESULTS
Ten (6.09%) urine samples [5/96(5.2%) females and 5/68( 8.82) males] were tested positive for JCV DNA (P= 0.814). The results of sequencing and phylogenetic tree showed the isolated JCV DNA were cluster with 3A genotype. 21/164 (12.8%) samples were tested positive for BKV DNA [11/96(11.45%) females and males 10/68(14.7%)] ( P= 0.63). The results of sequencing and phylogenetic tree showed that the isolated BKV was cluster with genotype III.
CONCLUSION
In the present study 6.09% and 12.8% of the healthy individuals showed positive for JCV DNA (genotype 3A) and BKV DNA(genotype III) respectively. With regard to life threating diseases by BKV and JCV in immunocomprsied patients , the screening BKV DNA and JCV DNA should be implemented for patients with cancer /autoimmune diseases /organ recipient/ multiple sclerosis (MS), prior to immunosuppression therapy or immunomodulatory agents treatment.
.Topics: Adolescent; Adult; Aged; BK Virus; Child; Child, Preschool; DNA, Viral; Female; Genotype; Healthy Volunteers; Humans; Iran; JC Virus; Male; Middle Aged; Phylogeny; Polyomavirus Infections; Prevalence; Tumor Virus Infections; Young Adult
PubMed: 33112543
DOI: 10.31557/APJCP.2020.21.10.2877