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• W3003100241 abstract "Some human polyomaviruses (HPyVs) have been associated with inflammatory skin conditions (Ho et al., 2015Ho J. Jedrych J.J. Feng H. Natalie A.A. Grandinetti L. Mirvish E. et al.Human polyomavirus 7-associated pruritic rash and viremia in transplant recipients.J Infect Dis. 2015; 211: 1560-1565Crossref PubMed Scopus (60) Google Scholar, Nguyen et al., 2017Nguyen K.D. Lee E.E. Yue Y. Stork J. Pock L. North J.P. et al.Human polyomavirus 6 and 7 are associated with pruritic and dyskeratotic dermatoses.J Am Acad Dermatol. 2017; 76: 932-940.e3Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar). More investigation is needed to identify further presentations of pathological cases of patients with cutaneous HPyVs (Nguyen et al., 2019Nguyen K.D. Chamseddin B.H. Cockerell C.J. Wang R.C. The biology and clinical features of cutaneous polyomaviruses.J Invest Dermatol. 2019; 139: 285-292Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar, Sheu et al., 2019Sheu J.C. Tran J. Rady P.L. Dao Jr., H. Tyring S.K. Nguyen H.P. Polyomaviruses of the skin: integrating molecular and clinical advances in an emerging class of viruses.Br J Dermatol. 2019; 180: 1302-1311Crossref PubMed Scopus (10) Google Scholar). Kimura disease (KD) is a rare form of chronic inflammatory disorder that involves subcutaneous tissues and is frequently associated with regional lymphadenopathy (Leiferman and Peters, 2018Leiferman K.M. Peters M.S. Eosinophil-related disease and the skin.J Allergy Clin Immunol Pract. 2018; 6: 1462-1482.e6Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar). KD is observed predominantly in East Asian populations, especially Japanese and Chinese individuals (Chen et al., 2004Chen H. Thompson L.D. Aguilera N.S. Abbondanzo S.L. Kimura disease: a clinicopathologic study of 21 cases.Am J Surg Pathol. 2004; 28: 505-513Crossref PubMed Scopus (187) Google Scholar, Long et al., 2016Long H. Zhang G. Wang L. Lu Q. Eosinophilic skin diseases: a comprehensive review.Clin Rev Allergy Immunol. 2016; 50: 189-213Crossref PubMed Scopus (65) Google Scholar); however, its underlying cause is yet to be determined. A case study showed the presence of human polyomavirus 6 (HPyV6) DNA in a lymph node of a patient diagnosed as having KD or angiolymphoid hyperplasia with eosinophilia (ALHE) (Rascovan et al., 2016Rascovan N. Monteil Bouchard S. Grob J.J. Collet-Villette A.M. Gaudy-Marqueste C. Penicaud M. et al.Human polyomavirus-6 infecting lymph nodes of a patient with an angiolymphoid hyperplasia with eosinophilia or Kimura disease.Clin Infect Dis. 2016; 62: 1419-1421Crossref PubMed Scopus (25) Google Scholar). This observation raises the possibility that HPyV6 might have a role in the development of KD; however, further research is needed to demonstrate such a link. Given this background, we conducted the comprehensive study covering all the currently known cutaneous HPyVs— Merkel cell polyomavirus, HPyV6, HPyV7, trichodysplasia spinulosa-associated polyomavirus, HPyV9, HPyV10, New Jersey polyomavirus, and Lyon IARC polyomavirus—in terms of their prevalence by using biopsied formalin-fixed paraffin wax-embedded specimens from 80 Japanese patients with various inflammatory disorders presenting with subcutaneous nodules or lymphadenopathies. All of the specimens were tested two or three times for the presence of viral genomes by using qPCR in a blind manner. The PCR-targeted regions of the viral genomes and the sequences of primers and probes are listed in Supplementary Table S1. The study population and detailed methods are described in Supplementary Materials and Methods. As a result, HPyV6 was detected in four of five (80%) specimens of KD and its detection rate was significantly higher than those in other disorders tested including Kikuchi disease (3 of 38 [8%], P = 0.0046), dermatopathic lymphadenitis (1 of 28 [4%], P < 0.001), and Castleman disease (zero of four [0%], P = 0.048) (Supplementary Table S2). Likewise, a significantly higher detection rate was observed found in ALHE (four of five [80%]). Although Merkel cell polyomavirus DNA was present in one case of dermatopathic lymphadenitis, no samples harbored any viral DNAs of trichodysplasia spinulosa-associated polyomavirus, HPyV9, HPyV10, New Jersey polyomavirus, or Lyon IARC polyomavirus. Thus, because our blinded qPCR analysis showed the selective detection of HPyV6 in KD and ALHE, it is unlikely that our qPCR results represent a contamination of HPyV6 that might be ubiquitously present in the epidermis. Furthermore, both the cases of KD and ALHE had considerably higher HPyV6 loads than the other three diseases (Figure 1a). The viral loads for HPyV6-positive KD and ALHE were as follows: mean load of 38.4 copies/103 cells and median load of 21.0 copies/103 cells for KD; and mean load of 1.8 copies/103 cells and median load of 1.4 copies/103 cells for ALHE. Saláková et al., 2016Saláková M. Košlabová E. Vojtěchová Z. Tachezy R. Šroller V. Detection of human polyomaviruses MCPyV, HPyV6, and HPyV7 in malignant and non-malignant tonsillar tissues.J Med Virol. 2016; 88: 695-702Crossref PubMed Scopus (31) Google Scholar reported that the tonsils may be a site of HPyV6 latency, and the mean and median HPyV6 loads in this tissue were 0.13 copies/103 cells and 0.04 copies/103 cells, respectively. Because their study and ours used formalin-fixed paraffin wax-embedded tissues for HPyV6 DNA quantification, and despite some minor variations in the method used, the data from the two studies seem to be suitable for comparison. Our specimens of KD and ALHE harbored higher levels of HPyV6 DNA. We next performed immunohistochemistry by using the monoclonal antibody (2t10) against the HPyV6 small T antigen. Immunopositivity was found in three of four HPyV6 DNA-positive KD and three of four HPyV6 DNA-positive ALHE (Figure 1b and Table 1). Immunostaining was present in the nuclei and cytoplasm of scattered infiltrated lymphoid cells, which is consistent with the HPyV6 small T antigen expression pattern observed in the cells infected with polyomaviruses (Ellman et al., 1984Ellman M. Bikel I. Figge J. Roberts T. Schlossman R. Livingston D.M. Localization of the simian virus 40 small t antigen in the nucleus and cytoplasm of monkey and mouse cells.J Virol. 1984; 50: 623-628Crossref PubMed Google Scholar, Shuda et al., 2011Shuda M. Kwun H.J. Feng H. Chang Y. Moore P.S. Human Merkel cell polyomavirus small T antigen is an oncoprotein targeting the 4E-BP1 translation regulator.J Clin Invest. 2011; 121: 3623-3634Crossref PubMed Scopus (253) Google Scholar). The primary antibody did not react with HPyV6 DNA-negative tissues (Supplementary Figure S1), and control immunostaining with the isotype-matched antibody also showed negative results (Figure 1b), thereby indicating the specificity of the antibody.Table 1Clinical Features and Human Polyomavirus 6 Status in the Cases of KD and ALHEPatientAge/gender/raceBlood eosinophil ( ×106/L)IgE level (IU)TreatmentRecurrenceHPyV6 DNAHPyV6 antigenKD143/F/J9,400 ↑1The symbol ↑ indicates an elevated value.4,199 ↑Surgical excision/PSL+++KD255/M/J2,760 ↑629 ↑Surgical excision/PSL++−KD353/M/J14,940 ↑35,479 ↑Surgical excision/PSL+++KD444/M/J6,170 ↑3,350 ↑Surgical excision/PSL+++KD535/F/J837 ↑NTSurgical excision/PSL−−−ALHE165/M/J162327Surgical excision++−ALHE277/M/J1161,080 ↑Surgical excision+++ALHE378/F/J220NTSurgical excision+++ALHE431/M/J200NTSurgical excision−++ALHE552/M/J2902,804 ↑Surgical excision−−−Abbreviations: ALHE, angiolymphoid hyperplasia with eosinophilia; F, female; HPyV6, human polyomavirus 6; IU, international unit; J, Japanese; KD, Kimura disease; M, male; NT, not tested; PSL, prednisolone.1 The symbol ↑ indicates an elevated value. Open table in a new tab Abbreviations: ALHE, angiolymphoid hyperplasia with eosinophilia; F, female; HPyV6, human polyomavirus 6; IU, international unit; J, Japanese; KD, Kimura disease; M, male; NT, not tested; PSL, prednisolone. Our recent study revealed that HPyV6 have geographically distinct genotypes (Hashida et al., 2018Hashida Y. Higuchi T. Matsuzaki S. Nakajima K. Sano S. Daibata M. Prevalence and genetic variability of human polyomaviruses 6 and 7 in healthy skin among asymptomatic individuals.J Infect Dis. 2018; 217: 483-493Crossref PubMed Scopus (7) Google Scholar). Therefore, we then analyzed the genotypes of the HPyV6 strains recovered from the specimens of KD and ALHE. Phylogenetic analysis clearly showed that our studied strains had the Asian–Japanese genotype (Figure 1c). The sequencing analysis also demonstrated that our HPyV6 strains had genomic alterations specific to the Asian–Japanese strains (Hashida et al., 2018Hashida Y. Higuchi T. Matsuzaki S. Nakajima K. Sano S. Daibata M. Prevalence and genetic variability of human polyomaviruses 6 and 7 in healthy skin among asymptomatic individuals.J Infect Dis. 2018; 217: 483-493Crossref PubMed Scopus (7) Google Scholar), including point mutations resulting in amino acid substitution (Figure 1d). Of note, the HPyV6 strain LN1, detected in a patient with KD (Rascovan et al., 2016Rascovan N. Monteil Bouchard S. Grob J.J. Collet-Villette A.M. Gaudy-Marqueste C. Penicaud M. et al.Human polyomavirus-6 infecting lymph nodes of a patient with an angiolymphoid hyperplasia with eosinophilia or Kimura disease.Clin Infect Dis. 2016; 62: 1419-1421Crossref PubMed Scopus (25) Google Scholar), was also genetically close to the Asian–Japanese type, even though the patient was found in a hospital in France. Considering that KD and ALHE are mostly observed in Asians (Adler et al., 2016Adler B.L. Krausz A.E. Minuti A. Silverberg J.I. Lev-Tov H. Epidemiology and treatment of angiolymphoid hyperplasia with eosinophilia (ALHE): A systematic review.J Am Acad Dermatol. 2016; 74 (506–12.e11)Abstract Full Text Full Text PDF PubMed Scopus (61) Google Scholar, Chen et al., 2004Chen H. Thompson L.D. Aguilera N.S. Abbondanzo S.L. Kimura disease: a clinicopathologic study of 21 cases.Am J Surg Pathol. 2004; 28: 505-513Crossref PubMed Scopus (187) Google Scholar, Long et al., 2016Long H. Zhang G. Wang L. Lu Q. Eosinophilic skin diseases: a comprehensive review.Clin Rev Allergy Immunol. 2016; 50: 189-213Crossref PubMed Scopus (65) Google Scholar), whether the Asian–Japanese HPyV6 genotype is related preferentially to the incidence of these eosinophilic skin diseases with an ethnic predilection for Asian populations is an important issue. Both KD and ALHE tend to recur following treatment, and the recurrence rates may be up to 60% and 40%, respectively (Adler et al., 2016Adler B.L. Krausz A.E. Minuti A. Silverberg J.I. Lev-Tov H. Epidemiology and treatment of angiolymphoid hyperplasia with eosinophilia (ALHE): A systematic review.J Am Acad Dermatol. 2016; 74 (506–12.e11)Abstract Full Text Full Text PDF PubMed Scopus (61) Google Scholar, Chen et al., 2015Chen Q.L. Dwa S. Gong Z.C. Abasi K. Ling B. Liu H. et al.Kimura's disease: risk factors of recurrence and prognosis.Int J Clin Exp Med. 2015; 8: 21414-21420PubMed Google Scholar). Therefore, we followed up the medical histories of our patients for recurrence of the disease for at least 2 years. Four of the five patients with KD and three of the five patients with ALHE relapsed with a median recurrence time of 17 months (Table 1). Among these seven cases of recurrence, all of the patients harbored HPyV6 DNA in the initial affected tissues. Accordingly, we investigated the persistence of HPyV6 in the second biopsied specimens of patients with relapsed disease. Although the comparative HPyV6 loads between the two clinical stages varied for each case, the virus genome was clearly detected again at the second assessment (Supplementary Figure S2). Our challenge in demonstrating the significance of HPyV6 infection in KD and ALHE was somewhat limited by the relatively small number of subjects (10 patients), because both of the diseases are uncommon even in an endemic country such as Japan. However, this study raises the issues concerning an etiological role of HPyV6. It has been hypothesized that viral infection triggers a type I hypersensitivity, which results in the release of eosinophiliotropic cytokines (Chen et al., 2004Chen H. Thompson L.D. Aguilera N.S. Abbondanzo S.L. Kimura disease: a clinicopathologic study of 21 cases.Am J Surg Pathol. 2004; 28: 505-513Crossref PubMed Scopus (187) Google Scholar, Long et al., 2016Long H. Zhang G. Wang L. Lu Q. Eosinophilic skin diseases: a comprehensive review.Clin Rev Allergy Immunol. 2016; 50: 189-213Crossref PubMed Scopus (65) Google Scholar). Here, we showed persistent HPyV6 infections with relatively high loads of HPyV6 DNA and expression of HPyV6 antigen in the lesional tissues of KD and ALHE. These results support the idea of a possible role of HPyV6 as an allergen in a subject of patients with these eosinophilic skin diseases. Indeed, HPyV6 infection levels are significantly higher in skin swabs from Japanese patients with atopic dermatitis compared with skin swabs from healthy control individuals (Hashida et al., 2019Hashida Y. Higuchi T. Tanaka M. Shibata Y. Nakajima K. Sano S. et al.Prevalence and viral loads of cutaneous human polyomaviruses in the skin of patients with chronic inflammatory skin diseases.J Infect Dis. 2019; 219: 1564-1573Crossref PubMed Scopus (5) Google Scholar). Moreover, we here suggested that the potential mutant antigen is encoded by the HPyV6 genes with the Asian–Japanese-type mutation. Whether the mutant HPyV6 antigen might increase antigenic activity to lead to the hypersensitivity reaction compared with the wild-type antigen is also worth studying. The Ethics Committee of Kochi Medical School approved this retrospective study. Informed consent was obtained in the opt-out document on the website. The following information was presented to participants: the research procedures, including the data collection procedures and their aim; kinds of specimens and information that will be collected; protection of personal data; the right to refuse to be included in this study and to withdraw consent; the retention period for the personal data; and the name and contact details of the researchers involved, including a contact person. Yumiko Hashida: https://orcid.org/0000-0002-6300-3458 Tomonori Higuchi: https://orcid.org/0000-0003-1428-3040 Kimiko Nakajima: https://orcid.org/0000-0002-0341-3252 Takako Ujihara: https://orcid.org/0000-0002-8404-5534 Ichiro Murakami: https://orcid.org/0000-0001-7615-3503 Mikiya Fujieda: https://orcid.org/0000-0002-8975-0400 Shigetoshi Sano: https://orcid.org/0000-0002-9812-0216 Masanori Daibata: https://orcid.org/0000-0001-8714-2068 The data supporting the findings of this study are included in this published article and its supplementary materials. The authors state no conflict of interest. The authors thank Christopher B. Buck (National Cancer Institute, Bethesda, MD) for donating the mouse anti-HPyV6 antibody. This work was supported by the Japan Society for the Promotion of Science ( 19K17928 ) and the Takeda Science Foundation. Conceptualization: YH, IM, MF, SS, MD; Formal Analysis: YH, TH; Funding Acquisition: YH, MD; Investigation: YH, TH, TU; Methodology: YH, TH, MD; Resources: KN, IM, SS; Writing - Original Draft Preparation: YH, MD: Writing - Review and Editing: MD. This study cohort included 80 Japanese patients (persons of Japanese descent who reside in Japan) with subcutaneous nodules or lymphadenopathies. There were five patients diagnosed with Kimura disease (KD; denoted as cases KD1–5; median age, 44 years [range, 35–55]; three men and two women), five patients diagnosed with angiolymphoid hyperplasia with eosinophilia (ALHE; denoted as cases ALHE1–5, median age, 71 years [range, 31–78]; four men and one woman), 38 patients diagnosed with Kikuchi disease (denoted as cases KHNL1–38; median age, 26 years [range, 10–69]; 13 men and 25 women), 28 patients diagnosed with dermatopathic lymphadenitis associated with various skin disorders, including Sézary syndrome, psoriasis, eczema, atopic dermatitis, or allergic skin diseases (denoted as cases DL1–28; median age, 60 years [range, 16–82]; 17 men and 11 women), and four patients diagnosed with multicentric Castleman disease (denoted as cases CD1–4; median age, 41 years [range, 25–69]; one man and three women). H&E-stained slides of biopsied tissues were reviewed by pathologists and diagnosed by using strict morphologic criteria for each disease. Materials within the institute’s files were supplemented by a review of the patient demographics (age and gender), laboratory values (peripheral blood eosinophil count and IgE value), medical treatment, and the presence of recurrent disease. Peripheral blood eosinophilia was documented in all of the patients with KD, whereas none of the patients with ALHE had eosinophilia. Such differential clinical presentation also supported our diagnosis of the diseases (Chen et al., 2004Chen H. Thompson L.D. Aguilera N.S. Abbondanzo S.L. Kimura disease: a clinicopathologic study of 21 cases.Am J Surg Pathol. 2004; 28: 505-513Crossref PubMed Scopus (187) Google Scholar, Dhingra et al., 2019Dhingra H. Nagpal R. Baliyan A. Alva S.R. Kimura disease: case report and brief review of literature.Med Pharm Rep. 2019; 92: 195-199PubMed Google Scholar). Cases of KD were treated by surgical excision followed by corticosteroid therapy and cases of ALHE received surgical excision only. This study was approved by the Ethics Committee of Kochi Medical School and performed in accordance with the relevant guidelines and regulations. Informed consent was obtained from the patients in the form of opt-out on the website. DNA was extracted from formalin-fixed paraffin wax-embedded tissues by using a WaxFree DNA kit (TrimGen, Sparks, MD). In total, 200 ng aliquots of extracted DNA were analyzed for the detection and quantification of human polyomaviruses (HPyVs), using TaqMan-based qPCR, as described elsewhere (Hashida et al., 2013Hashida Y. Imajoh M. Nemoto Y. Kamioka M. Taniguchi A. Taguchi T. et al.Detection of Merkel cell polyomavirus with a tumour-specific signature in non-small cell lung cancer.Br J Cancer. 2013; 108: 629-637Crossref PubMed Scopus (40) Google Scholar). The reaction mixture was prepared in a total volume of 20 μl containing the TaqMan gene expression master mix (Thermo Fisher Scientific, Waltham, MA), 900 nM each primer, and 250 nM dual-labeled probe. The reaction conditions were 50 °C for 2 minutes and 95 °C for 10 minutes, followed by 50 cycles of 95 °C for 15 seconds and 60 °C for 1 minute. To calculate the viral copy numbers, the PCR product was cloned into the pMD20-T vector (Takara Bio Inc., Shiga, Japan), and then we prepared 10-fold serial dilutions by using the cloned plasmid DNA to generate a standard curve. Results are expressed as viral copies/μg DNA and viral copies/103 cells. Because samples with CT values below 40–41 were considered to be positive for targeted viral nucleic acids (Fuller et al., 2013Fuller J.A. Njenga M.K. Bigogo G. Aura B. Ope M.O. Nderitu L. et al.Association of the CT values of real-time PCR of viral upper respiratory tract infection with clinical severity, Kenya.J Med Virol. 2013; 85: 924-932Crossref PubMed Scopus (49) Google Scholar, Hashida et al., 2018Hashida Y. Higuchi T. Matsuzaki S. Nakajima K. Sano S. Daibata M. Prevalence and genetic variability of human polyomaviruses 6 and 7 in healthy skin among asymptomatic individuals.J Infect Dis. 2018; 217: 483-493Crossref PubMed Scopus (7) Google Scholar), we considered our specimens with CT values of ≤ 40 to be positive according to the published criteria. The PCR-targeted regions of the viral genomes and the sequences of primers and probes used in this study are listed in Supplementary Table S2. Immunohistochemistry was performed on formalin-fixed paraffin wax-embedded tissue sections by using the mouse monoclonal antibody 2t10 based on an indirect biotin-avidin system by using a biotinylated universal secondary antibody and 3,3′-diaminobenzidine substrate with hematoxylin counterstaining. 2t10 cross-reacts with the small T antigen of HPyV6 and HPyV7, but not with Merkel cell polyomavirus or HPyV10 (Ho et al., 2015Ho J. Jedrych J.J. Feng H. Natalie A.A. Grandinetti L. Mirvish E. et al.Human polyomavirus 7-associated pruritic rash and viremia in transplant recipients.J Infect Dis. 2015; 211: 1560-1565Crossref PubMed Scopus (60) Google Scholar). We used this antibody to detect HPyV6 in patients with KD and ALHE because initial PCR studies showed no evidence for HPyV7 infection in our patients, except for one patient (case KD3) diagnosed with KD. The specificity of staining with the primary antibody was controlled in parallel by testing the isotype-matched IgG2a control antibody. The HPyV6 sequences of the large T and small T genes (nucleotide positions 3,943–4,095 and 4,243–4,468 based on the GenBank HPyV6 sequence; accession number HM011560) were amplified by PCR by using the primer sets listed in Supplementary Table S1. The purified PCR products were sequenced directly, as described elsewhere (Hashida et al., 2013Hashida Y. Imajoh M. Nemoto Y. Kamioka M. Taniguchi A. Taguchi T. et al.Detection of Merkel cell polyomavirus with a tumour-specific signature in non-small cell lung cancer.Br J Cancer. 2013; 108: 629-637Crossref PubMed Scopus (40) Google Scholar). The nucleotide sequences were aligned by using Clustal W (Thompson et al., 1994Thompson J.D. Higgins D.G. Gibson T.J. CLUSTAL W. improving the sensitivity of progressive multiple sequence alignment through sequence weighting, position-specific gap penalties and weight matrix choice.Nucleic Acids Res. 1994; 22: 4673-4680Crossref PubMed Scopus (53470) Google Scholar). A phylogenetic tree was constructed by using the maximum likelihood method in MEGA 5.2 software (Tamura et al., 2011Tamura K. Peterson D. Peterson N. Stecher G. Nei M. Kumar S. MEGA5: molecular evolutionary genetics analysis using maximum likelihood, evolutionary distance, and maximum parsimony methods.Mol Biol Evol. 2011; 28: 2731-2739Crossref PubMed Scopus (33370) Google Scholar). Bootstrap values were based on 1,000 replicates for the tree. Representative sequences of the HPyV6 strains recovered from the specimens of KD and ALHE have been deposited in the GenBank database under accession numbers LC496078/LC496080 and LC496079/LC496081, respectively. Possible correlations between viral positivity rates were analyzed by using Fisher’s exact test. The differences in viral loads were compared by using the Mann–Whitney nonparametric U test. A P-value of < 0.05 was considered statistically significant. Abbreviations: F, forward; HPyV, human polyomavirus; LIPyV, Lyon IARC polyomavirus; MCPyV, Merkel cell polyomavirus; NJPyV, New Jersey polyomavirus; R, reverse; TSPyV, trichodysplasia spinulosa- associated polyomavirus. Abbreviations: ALHE, angiolymphoid hyperplasia with eosinophilia; HPyV, human polyomavirus; LIPyV, Lyon IARC polyomavirus; MCPyV, Merkel cell polyomavirus; NJPyV, New Jersey polyomavirus; TSPyV, trichodysplasia spinulosa-associated polyomavirus." @default.
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• W3003100241 title "Human Polyomavirus 6 with the Asian–Japanese Genotype in Cases of Kimura Disease and Angiolymphoid Hyperplasia with Eosinophilia" @default.
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