No Evidence for an Association between JC Polyomavirus Infection and Gastroduodenal Diseases

Cherati, Azadeh Yazdani; Yahyapour, Yousef; Ranaee, Mohammad; Rajabnia, Ramazan; Shokri‐Shirvani, Javad; Hajiahmadi, Mahmoud; Sadeghi, Farzin

doi:10.1159/000489928

Cited by 4 publications

(2 citation statements)

References 38 publications

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“…Interestingly, JCPyV was detected with higher load in the preneoplastic colon and in the adenocarcinoma, compared to the adjacent normal tissue, suggesting the oncogenic properties of JCPyV in this cancer type 10 . However, our study did not show any evidence of involvement of JCPyV in colon cancer pathogenesis, in accordance with Newcomb, and Yazdani Cherati 53,54 . Therefore, the causative role of JCPyV in colon cancers pathogenesis is still to be investigated.…”

Section: Discussionsupporting

confidence: 44%

Human polyomaviruses genomes in clinical specimens of colon cancer patients

Dolci

Signorini

Toumi

et al. 2021

Journal of Medical Virology

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Colon cancer is the third cause of cancer death in the developed countries. Some environmental factors are involved in its pathogenesis, including viral infections. The possible involvement of human polyomaviruses (HPyVs) in colon cancer pathogenesis has been previously reported, leading to inconsistent conclusions. Clinical specimens were collected from 125 colon cancer patients. Specifically, 110 tumor tissues, 55 negative surgical margins, and 39 peripheral blood samples were analyzed for the presence of six HPyVs: JC polyomavirus (JCPyV), BK polyomavirus (BKPyV), Merkel cell PyV (MCPyV), HPyV −6, −7, and −9 by means of DNA isolation and subsequent duplex Real Time quantitative polymerase chain reaction. HPyVs genome was detected in 33/204 samples (16.2%): the significant higher positivity was found in tumor tissues (26/110, 23.6%), followed by negative surgical margins (3/55, 5.5%, p < .05), and peripheral blood mononuclear cells (PBMCs) (4/39; 10.3%).HPyVs load was statistically higher only in the tumor tissues compared to negative surgical margins (p < .05). Specifically, MCPyV was detected in 19.1% (21/110) of tumor tissues, 3.6% (2/55) of negative surgical margins (p < .05), and 7.7% (3/39) of PBMCs; HPyV-6 in 2.7% (3/110) of tumor tissues, and 1.8% (1/55) of negative surgical margins; one tumor tissue (1/110, 0.9%) and one PBMCs sample (1/39, 2.6%) were positive for BKPyV; JCPyV was present in 0.9% (1/110) of tumor tissues.HPyV-7 and 9 were not detected in any sample. High prevalence and load of MCPyV genome in the tumor tissues might be indicative of a relevant rather than bystander role of the virus in the colon tumorigenesis.

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Section: Discussionsupporting

confidence: 44%

Human polyomaviruses genomes in clinical specimens of colon cancer patients

Dolci

Signorini

Toumi

et al. 2021

Journal of Medical Virology

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“…In addition, other investigations detected JCPyV DNA, Tag and the JCPyV-specific microRNA 5p (miR-J1-5p) in CRC biopsies, being their presence associated with the tumor development (7,(21)(22)(23). However, other studies did not identify JCPyV DNA sequences in hyperplastic polyps/adenoma and adenocarcinoma and normal tissues (11,(24)(25)(26). The reasons for these contrasting data reported by different investigations are not known.…”

Section: Introductionmentioning

confidence: 95%

Colorectal Carcinoma Affected Patients Are Significantly Poor Responders Against the Oncogenic JC Polyomavirus

et al. 2021

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BackgroundMany investigations reported the association between human tumors and JCPyV, a polyomavirus with oncogenic potential. The association has been supported by studies that found JCPyV footprints in CRC and gliomas of different types. Indeed, JCPyV footprints including its nucleic acids and Tag oncoprotein have been revealed in CRC tissues.MethodsHerein, sera from colorectal carcinoma (CRC) affected patients and healthy individuals (HS), employed as control, were analysed for immunoglobulin G (IgG) antibodies against specific JCPyV viral capsid protein 1 (VP1) antigens. The investigation was carried out employing an innovative immunological assay. Indeed, an indirect enzyme-linked immunosorbent assay (ELISA) with JCPyV VP1 mimotopes was used. JCPyV VP1 mimotopes consisted of synthetic peptides mimicking VP1 epitopes.ResultsSera from CRC affected patients, evaluated using indirect ELISAs with synthetic mimotopes, showed a significant lower prevalence of IgG antibodies against JCPyV VP1 mimotopes (26%) compared to HS (51%), p<0.005. These data were confirmed by another method, the hemagglutination inhibition (HAI) assay. Altogether these results, i.e. the prevalence of serum IgG antibodies against JCPyV VP1 mimotopes from patients with CRC is approximately 50% lower than in HS, are of interest.DiscussionOur data suggest that patients with CRC are significantly poor responders against JCPyV VP1 antigens. It is possible that CRC patients are affected by a specific immunological deregulation. This immunological dysfunction, revelled in CRC patients, may account for their predisposition to the colorectal carcinoma onset.

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Presence of JC Polyomavirus in Nonneoplastic Inflamed Colon Mucosa and Primary and Metastatic Colorectal Cancer

Esmailzadeh

Ranaee

Alizadeh

et al. 2019

Gastrointest Tumors

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Background: Despite decades of epidemiologic and histopathologic investigations, the association between JC polyomavirus (JCPyV) infection and colorectal cancer (CRC) remains controversial. Objective: This study tested the presence of JCPyV sequences and determined the viral load in a series of colorectal samples from Iranian patients. In total, 223 formalin-fixed paraffin-embedded samples from patients diagnosed with primary and metastatic CRC as well as with nonneoplastic inflamed colon mucosa were analyzed by quantitative real-time PCR for the presence of JCPyV large tumor antigen (LT-Ag) sequences. Results: JCPyV LT-Ag sequences were detected in 18.6% of the CRC tissues and in 15.5% of the nonneoplastic control group. Viral LT-Ag was quantified in 18/100 primary colon adenocarcinomas, 2/10 metastatic adenocarcinomas, and 1/3 primary adenocarcinomas of the rectum. Two JCPyV-positive metastatic tumors presented a negative test result for JCPyV in the corresponding primary tumor. The median JCPyV LT-Ag copy number was 64 × 10–2 per cell and 14 × 10–2 per cell in the CRC cases and the nonneoplastic samples, respectively. There was no statistically significant difference between the two study groups regarding median LT-Ag DNA load (p = 0.059). Among the JCPyV-positive samples, the LT-Ag DNA load was higher in 2 metastatic tumors (from a patient with lung metastasis: 232 × 10–2 copies per cell; from a patient with liver metastasis: 121 × 10–2 copies per cell). Conclusions: The detection of JCPyV DNA at low copy numbers (lower than 1 viral copy per cell equivalent) and the absence of viral sequences in the corresponding primary tumors of the JCPyV-positive metastatic samples weaken the hypothesis of an etiological role of JCPyV in primary CRC induction.

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No Evidence for an Association between JC Polyomavirus Infection and Gastroduodenal Diseases

Cited by 4 publications

References 38 publications

Human polyomaviruses genomes in clinical specimens of colon cancer patients

Human polyomaviruses genomes in clinical specimens of colon cancer patients

Colorectal Carcinoma Affected Patients Are Significantly Poor Responders Against the Oncogenic JC Polyomavirus

Presence of JC Polyomavirus in Nonneoplastic Inflamed Colon Mucosa and Primary and Metastatic Colorectal Cancer

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