Detection of Quebec Polyomavirus DNA in Samples from Different Patient Groups

Prezioso, Carla; Ghelue, Marijke Van; Pietropaolo, Valeria; Moens, Ugo

doi:10.3390/microorganisms9051082

Cited by 8 publications

(9 citation statements)

References 61 publications

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“…For more than three decades, the BKV and JCV were the only well-known polyomaviruses associated with clinical diseases in specific groups of people. With the technological progress of modern molecular methods and next-generation sequencing technique, 13 polyomaviruses were included in the list of human polyomaviruses during the past 20 years ( Prezioso et al., 2021 ) ( Zhou et al., 2019 ). The previous epidemiological and phylogenetic studies suggest that BKV prevailed and co-evolved with humans, leading to its high seroprevalence all over the world ( Viscidi et al., 2011 ; Gaboriaud et al., 2018 ; Zhou et al., 2019 ; Zhou et al., 2020 ).…”

Section: Introductionmentioning

confidence: 99%

BK polyomavirus: latency, reactivation, diseases and tumorigenesis

Zhou,

Zhu,

2023

Front. Cell. Infect. Microbiol.

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The identification of the first human polyomavirus BK (BKV) has been over half century, The previous epidemiological and phylogenetic studies suggest that BKV prevailed and co-evolved with humans, leading to high seroprevalence all over the world. In general, BKV stays latent and symptomless reactivation in healthy individuals. BKV has been mainly interlinked with BKV-associated nephropathy (BKVAN) in kidney-transplant recipients and hemorrhagic cystitis (HC) in hematopoietic stem cell transplant recipients (HSCTRs). However, the mechanisms underlying BKV latency and reactivation are not fully understood and lack of extensive debate. As Merkel cell polyomavirus (MCV) was identified as a pathogenic agent of malignant cutaneous cancer Merkel cell carcinoma (MCC) since 2008, linking BKV to tumorigenesis of urologic tumors raised concerns in the scientific community. In this review, we mainly focus on advances of mechanisms of BKV latency and reactivation, and BKV-associated diseases or tumorigenesis with systematical review of formerly published papers following the PRISMA guidelines. The potential tumorigenesis of BKV in two major types of cancers, head and neck cancer and urologic cancer, was systematically updated and discussed in depth. Besides, BKV may also play an infectious role contributing to HIV-associated salivary gland disease (HIVSGD) presentation. As more evidence indicates the key role of BKV in potential tumorigenesis, it is important to pay more attention on its etiology and pathogenicity in vitro and in vivo.

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Section: Introductionmentioning

confidence: 99%

BK polyomavirus: latency, reactivation, diseases and tumorigenesis

Zhou,

Zhu,

2023

Front. Cell. Infect. Microbiol.

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“…LIPyV and QPyV have not yet been listed as an HPyV by the ICTV. QPyV DNA has been detected in urine from systemic lupus erythematosus patients, multiple sclerosis patients, and pregnant women, but more studies are required to confirm whether this is a genuine HPyV (Prezioso et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Functional Domains of the Early Proteins and Experimental and Epidemiological Studies Suggest a Role for the Novel Human Polyomaviruses in Cancer

2022

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As their name indicates, polyomaviruses (PyVs) can induce tumors. Mouse PyV, hamster PyV and raccoon PyV have been shown to cause tumors in their natural host. During the last 30 years, 15 PyVs have been isolated from humans. From these, Merkel cell PyV is classified as a Group 2A carcinogenic pathogen (probably carcinogenic to humans), whereas BKPyV and JCPyV are class 2B (possibly carcinogenic to humans) by the International Agency for Research on Cancer. Although the other PyVs recently detected in humans (referred to here as novel HPyV; nHPyV) share many common features with PyVs, including the viral oncoproteins large tumor antigen and small tumor antigen, as their role in cancer is questioned. This review discusses whether the nHPyVs may play a role in cancer based on predicted and experimentally proven functions of their early proteins in oncogenic processes. The functional domains that mediate the oncogenic properties of early proteins of known PyVs, that can cause cancer in their natural host or animal models, have been well characterized and we examined whether these functional domains are conserved in the early proteins of the nHPyVs and presented experimental evidence that these conserved domains are functional. Furthermore, we reviewed the literature describing the detection of nHPyV in human tumors.

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“…QPyV is the most recently discovered HPyV [15], and it was isolated for the first time in the feces of an 85-year-old man. Recently, although it was found in the urine of individuals affected by systemic lupus erythematosus (SLE) and multiple sclerosis (MS) patients [24], its DNA was not detected in urine and plasma samples from HIV-1 positive patients [24].…”

Section: Introductionmentioning

confidence: 99%

“…In this latter condition, the decrease in CD4+ can favor persistence or reactivation of HPyVs, influencing clinical outcomes of HIV/AIDS patients. JCPyV, BKPyV and MCPyV detection in HIV-1-infected individuals has been widely described in the literature, whereas little information is available about HPyV6, HPyV7 and QPyV prevalence in these patients [24,31].…”

Section: Introductionmentioning

confidence: 99%

Detection Analysis and Study of Genomic Region Variability of JCPyV, BKPyV, MCPyV, HPyV6, HPyV7 and QPyV in the Urine and Plasma of HIV-1-Infected Patients

Passerini

Prezioso

Prota

et al. 2022

Viruses

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Since it was clearly established that HIV/AIDS predisposes to the infection, persistence or reactivation of latent viruses, the prevalence of human polyomaviruses (HPyVs) among HIV-1-infected patients and a possible correlation between HPyVs and HIV sero-status were investigated. PCR was performed to detect and quantify JCPyV, BKPyV, MCPyV, HPyV6, HPyV7 and QPyV DNA in the urine and plasma samples of 103 HIV-1-infected patients. Subsequently, NCCR, VP1 and MCPyV LT sequences were examined. In addition, for MCPyV, the expression of transcripts for the LT gene was investigated. JCPyV, BKPyV and MCPyV’s presence was reported, whereas HPyV6, HPyV7 and QPyV were not detected in any sample. Co-infection patterns of JCPyV, BKPyV and MCPyV were found. Archetype-like NCCRs were observed with some point mutations in plasma samples positive for JCPyV and BKPyV. The VP1 region was found to be highly conserved among these subjects. LT did not show mutations causing stop codons, and LT transcripts were expressed in MCPyV positive samples. A significant correlation between HPyVs’ detection and a low level of CD4+ was reported. In conclusion, HPyV6, HPyV7 and QPyV seem to not have a clinical relevance in HIV-1 patients, whereas further studies are warranted to define the clinical importance of JCPyV, BKPyV and MCPyV DNA detection in these subjects.

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Detection of Quebec Polyomavirus DNA in Samples from Different Patient Groups

Cited by 8 publications

References 61 publications

BK polyomavirus: latency, reactivation, diseases and tumorigenesis

BK polyomavirus: latency, reactivation, diseases and tumorigenesis

Functional Domains of the Early Proteins and Experimental and Epidemiological Studies Suggest a Role for the Novel Human Polyomaviruses in Cancer

Detection Analysis and Study of Genomic Region Variability of JCPyV, BKPyV, MCPyV, HPyV6, HPyV7 and QPyV in the Urine and Plasma of HIV-1-Infected Patients

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