ライフサイエンスコーパス: MCPyV

1 MCPyV cell entry is unique among members of the polyomav

2 MCPyV copy number averaged 891 copies/ng in anophthalmic

3 MCPyV differs from other known polyomaviruses concerning

4 MCPyV DNA was present in 13 of 18 samples, and HPV, HPyV

5 MCPyV has been difficult to propagate in vitro.

6 MCPyV infection and transformation of pro-/pre-B cells a

7 MCPyV infection is highly prevalent in adults, with age

8 MCPyV infection is widespread in the general population.

9 MCPyV infection showed the highest prevalence (65.1% of

10 MCPyV infections are highly prevalent in the human popul

11 MCPyV is associated with a highly aggressive form of ski

12 MCPyV is the first polyomavirus to be clearly associated

13 MCPyV isolated from MCC typically contains wild-type ST

14 MCPyV large T antigen could bind to Rb but was unable to

15 MCPyV small T (sT) antigen has emerged as the key oncoge

16 MCPyV sT translocates to nuclear foci containing activel

17 MCPyV sT, when coexpressed with ATOH1, is thus sufficien

18 MCPyV-negative tumors also displayed high overall mutati

19 MCPyV-negative tumors showed decreased RB1 expression, w

20 nistically, expression of YAP1 or WWTR1 in a MCPyV-positive MCC cell line induced cell-cycle arrest a

21 Although MCPyV is constantly shed from healthy skin, the MCC inci

22 when a replication-defective LT mutant or an MCPyV-origin mutant was introduced in place of wild-type

23 tochemistry with two distinct antibodies and MCPyV DNA using quantitative PCR.

24 tween the host DNA damage response (DDR) and MCPyV replication.

25 ecause these tumors often express PD-L1, and MCPyV-specific T cells express PD-1.

26 ntially expressed between MCPyV-negative and MCPyV-positive MCCs, with significant differential expre

27 tatus was concordant for all tumor pairs and MCPyV positive tumors harbored predominatly subclonal mu

28 analysis showed that these DDR proteins and MCPyV LT in fact colocalized at the actively replicating

29 HIV, solid organ transplant, CLL, UVR, and MCPyV.

30 understand why approximately 20% of MCCs are MCPyV-negative.

31 As MCPyV has been shown to be the etiologic cause of Merkel

32 In the Janus Serum Bank, MCPyV infection was associated with a higher risk of gli

33 Despite deep genetic differences between MCPyV-positive and -negative subtypes, current clinical

34 e sets were differentially expressed between MCPyV-negative and MCPyV-positive MCCs, with significant

35 Although the causative link between MCPyV and Merkel cell carcinoma is well established, the

36 have investigated any potential link between MCPyV T antigen expression and the highly metastatic nat

37 Beyond MCPyV, NTAR motifs are conserved in other polyomavirus A

38 imilar to native MCPyV infection, where both MCPyV origin and LT are present, the host DDR machinery

39 e within a subset of dermal fibroblasts, but MCPyV DNA has also been detected in a variety of other t

40 y the host genes specifically deregulated by MCPyV, as opposed to other PyVs, in order to better unde

41 evealed 28 genes specifically deregulated by MCPyV.

42 approximately 20% of MCCs are not driven by MCPyV and that such virus-negative MCCs, which can be qu

43 the skin cell type productively infected by MCPyV remains a central question.

44 Tumors were called MCPyV-positive if two or more of these three assays indi

45 vovirus B19, six herpesviruses, Merkel cell (MCPyV) and JC polyomaviruses, totaling 127 genomes.

46 ercentage of Australian MCC cases containing MCPyV may be lower than that of North American cases.

47 ib as an effective inhibitor for controlling MCPyV infection.

48 cidofovir as a possible drug for controlling MCPyV infection.

49 sT is a potential drug target for dampening MCPyV infection.

50 oss-of-function screens in a patient-derived MCPyV-positive cell line and identified MYCL and the non

51 We did not detect MCPyV in any matched normal blood DNA (0/57), but observ

52 rt that a novel monoclonal antibody detected MCPyV large T antigen expression in 56 of 58 (97%) uniqu

53 We detected MCPyV in 15% (26/177) of SCC DNA samples and 17% (11/63)

54 To address these controversies, we detected MCPyV large T antigen using immunohistochemistry with tw

55 h similar mechanisms of pathogenesis, either MCPyV-mediated or ultraviolet light-mediated.

56 GAS or NF-kB pathway factors led to elevated MCPyV replication.

57 to occur in MCC tumors that fail to express MCPyV large T antigen.

58 generated mice that conditionally expressed MCPyV TAgs and ATOH1 in epidermal cells, yielding micros

59 estored STING, cocultured T cells expressing MCPyV-specific T cell receptors (TCRs) show increased cy

60 Mice expressing MCPyV T antigens developed hyperplasia, hyperkeratosis,

61 hat these host DDR factors are important for MCPyV DNA replication, providing new insight into the ho

62 his, we established a cell culture model for MCPyV infection, which will facilitate investigation of

63 cation of a potential host cell receptor for MCPyV will aid in the elucidation of its entry mechanism

64 e identify a putative host cell receptor for MCPyV.

65 ire of quantitative PCR primers specific for MCPyV to improve the detection of viral DNA in MCC.

66 Epidemiological surveys for MCPyV seropositivity and sequencing analyses of healthy

67 biology could inform targeted therapies for MCPyV-associated MCC.

68 Furthermore, MCPyV-truncated large T antigen was more effective than

69 We describe how MCPyV replication and/or transcription elicit an innate

70 The present study aims to explore how MCPyV interfaces with innate immunity during its infecti

71 Our findings provide new insight into how MCPyV may regulate early infection dynamics and suggest

72 However, MCPyV appears different from other polyomaviruses, as it

73 RG1) in MCPyV gene-expressing NIKs and hTERT-MCPyV gene-expressing human keratinocytes (HK) compared

74 In addition, NDRG1 overexpression in hTERT-MCPyV gene-expressing HK or MCC cells resulted in a decr

75 decrease in wound healing capacity in hTERT-MCPyV gene-expressing HK was observed.

76 nctional inhibition of p53 reported in human MCPyV-positive MCCs.

77 on microscopic structures of the icosahedral MCPyV capsid and analysis of its glycan interactions via

78 In this report, we identify MCPyV sT as a novel Fe/S cluster protein and show that c

79 ottleneck during infectious entry.IMPORTANCE MCPyV is the first polyomavirus directly implicated in t

80 In MCPyV-positive MCC cells, the expression of NDRG1 was do

81 and ATR-mediated DDR pathways accumulate in MCPyV large T antigen (LT)-positive nuclear foci in cell

82 and ATR-mediated DDR pathways accumulate in MCPyV LT-positive nuclear foci.

83 The discovery of Fe/S clusters in MCPyV sT opens new avenues to the study of the structure

84 ns of Fe/S cluster-coordinating cysteines in MCPyV sT abolish its ability to stimulate viral replicat

85 ration of decreased RB protein expression in MCPyV-negative tumors and increased peritumoral CD8+ T l

86 An unusual C-terminal extension in MCPyV VP1 projects from the recessed capsid regions.

87 utations in PRUNE2 and NOTCH family genes in MCPyV-negative MCC.

88 In contrast, mutation burden was low in MCPyV-positive tumors (0.40 +/- 0.09 mutations/Mb) and l

89 N-myc downstream-regulated gene 1 (NDRG1) in MCPyV gene-expressing NIKs and hTERT-MCPyV gene-expressi

90 r, the mechanisms underlying pathogenesis in MCPyV-negative MCCs remain poorly understood.

91 Overall, NDRG1 plays an important role in MCPyV-induced cellular proliferation.IMPORTANCE Merkel c

92 e microtubule-associated protein stathmin in MCPyV ST-mediated microtubule destabilization and cell m

93 These included MCPyV integrations and truncations resembling clonally e

94 encoded by several polyomaviruses including MCPyV, but also provides insight into de novo protein ev

95 tinct human polyomaviruses (PyVs), including MCPyV.

96 To date, the events connecting initial MCPyV infection and subsequent transformation still rema

97 ases of MCC reported to date, the integrated MCPyV genome has undergone mutations in the large T anti

98 The high seroprevalence of about 60% makes MCPyV a serious health care burden and illustrates the n

99 pment of Merkel cell carcinoma (MCC), making MCPyV the first polyomavirus to be clearly associated wi

100 Similar to native MCPyV infection, where both MCPyV origin and LT are pres

101 we show that, in cells infected with native MCPyV virions, components of the ATM- and ATR-mediated D

102 e nuclear foci in cells infected with native MCPyV virions.

103 ormed integrative sequencing on two cases of MCPyV-negative MCC, as well as a validation cohort of 14

104 irst report demonstrating the coexistence of MCPyV and HPV-17 in cutaneous SCC.

105 Coexpression of MCPyV tLT did not appreciably alter the phenotype driven

106 y polymerase chain reaction for detection of MCPyV and epidermodysplasia verruciformis HPV (EV-HPV) t

107 to increase the sensitivity of detection of MCPyV in MCC by developing antibodies capable of detecti

108 analyzed the cell biological determinants of MCPyV entry into A549 cells, a highly transducible lung

109 cycle could contribute to the development of MCPyV-associated MCC.

110 ilencing as essential for the development of MCPyV-positive MCC.FundingUS Public Health Service grant

111 stly inhibits the sT-mediated enhancement of MCPyV replication but has little effect on the basal vir

112 competent individuals warrants evaluation of MCPyV as an etiologic agent in the carcinogenesis of SCC

113 Our data establish that expression of MCPyV sTAg alone is sufficient for rapid neoplastic tran

114 recombinase expression induced expression of MCPyV T antigens in stratified squamous epithelial cells

115 Our data establish that expression of MCPyV TAgs in ATOH1-reprogrammed epidermal cells and the

116 We tested 21 MCCs for the expression of MCPyV, TdT, PAX5, IgG, IgM, IgA, kappa, and lambda by im

117 or immunodeficiency might alter the fate of MCPyV and its host cell to encourage carcinogenesis.

118 ted, and alternatively spliced 57kT forms of MCPyV large T antigen.

119 nst the large T (LT) antigen and VP1 gene of MCPyV.

120 The importance of MCPyV sT led us to investigate sT functions and to ident

121 criptional subtypes that were independent of MCPyV status.

122 The present study reveals that the onset of MCPyV replication and early gene expression induces an i

123 antigens, but the molecular pathogenesis of MCPyV-negative MCC is largely unexplored.

124 te genes contributing to the pathogenesis of MCPyV-negative MCCs, we performed DNA microarray analysi

125 n reaction products revealed the presence of MCPyV and HPV-17 DNA.

126 ood DNA (0/57), but observed the presence of MCPyV DNA in 1 of 12 normal mouthwash DNAs.

127 The presence of MCPyV in approximately 15% of SCCs from immunocompetent

128 To test for the presence of MCPyV in immunocompetent SCC patients, we used PCR prime

129 Studies reporting the prevalence of MCPyV in MCC specimens collected in the US were combined

130 With the high prevalence of MCPyV infection and the increasing amount of MCC diagnos

131 e associated with an increased prevalence of MCPyV infection in eyebrow hair and normal skin swab spe

132 To explore the infectious entry process of MCPyV, we analyzed the cell biological determinants of M

133 identify the unique oncogenic properties of MCPyV, we analyzed the gene expression profiles in human

134 EAD-dependent) transcriptional repression of MCPyV LT.ConclusionThese findings identify what we belie

135 Insufficient restriction of MCPyV by normal cellular processes, for example, could p

136 has emerged to support the etiologic role of MCPyV in Merkel cell carcinoma (MCC), an extremely letha

137 However, the precise host cell tropism(s) of MCPyV remains unclear: MCPyV is able to replicate within

138 also eliminates TBK1-mediated suppression of MCPyV replication during early infection of human dermal

139 imply that the deletion of the C terminus of MCPyV large T antigen found in MCC serves not only to di

140 ve an important role in the tumorigenesis of MCPyV-negative MCCs.

141 A greater understanding of MCPyV biology could inform targeted therapies for MCPyV-

142 veries that have shaped our understanding of MCPyV oncogenic mechanism and host cellular tropism, as

143 at type I IFN exerts a more direct effect on MCPyV infection postentry by repressing early viral tran

144 also explore the effects of this response on MCPyV replication.

145 mple, could promote the incidental oncogenic MCPyV integration events and/or entry into the original

146 were attributable to ambient UVR exposure or MCPyV, with a small fraction due to immunosuppressive co

147 hat we call Merkel cell polyomavirus (MCV or MCPyV).

148 s provides a mechanism to support persistent MCPyV infection.

149 irst case in which Merkel cell polyomavirus (MCPyV) and human papillomavirus subtype 17 (HPV-17) were

150 ally caused by the Merkel cell polyomavirus (MCPyV) and recurs in 40% of patients.

151 ) that contain the Merkel cell polyomavirus (MCPyV) and the clinical significance of tumor viral stat

152 Infection with Merkel cell polyomavirus (MCPyV) can lead to Merkel cell carcinoma (MCC), a lethal

153 Merkel cell polyomavirus (MCPyV) causes the majority of cases of Merkel cell carci

154 Merkel cell polyomavirus (MCPyV) causes the majority of MCC cases due to the expre

155 A Virus (IAV), and Merkel Cell Polyomavirus (MCPyV) could be targeted.

156 frequently contain Merkel cell polyomavirus (MCPyV) DNA and express viral transforming antigens, sT a

157 st 80% of all MCC, Merkel cell polyomavirus (MCPyV) DNA has undergone clonal integration into the hos

158 Merkel cell polyomavirus (MCPyV) expressing viral T antigens is a common feature o

159 ries an integrated Merkel cell polyomavirus (MCPyV) genome and expresses viral transforming antigens

160 The Merkel cell polyomavirus (MCPyV) genome undergoes clonal integration into the host

161 Merkel cell polyomavirus (MCPyV) has been associated with approximately 80% of Mer

162 5, 24, 49, 76 and Merkel cell polyomavirus (MCPyV) having incidence rates greater than 20 per 1000 p

163 dicates a role for Merkel cell polyomavirus (MCPyV) in the development of Merkel cell carcinoma (MCC)

164 Merkel cell polyomavirus (MCPyV) infects most of the human population asymptomatic

165 Merkel cell polyomavirus (MCPyV) is a common infectious agent that is likely invol

166 Merkel cell polyomavirus (MCPyV) is a human double-stranded DNA tumor virus.

167 Merkel cell polyomavirus (MCPyV) is a small, nonenveloped tumor virus associated w

168 The Merkel cell polyomavirus (MCPyV) is an oncogenic driver in the majority of MCC tum

169 Merkel cell polyomavirus (MCPyV) is an oncogenic human polyomavirus that latently

170 Merkel cell polyomavirus (MCPyV) is frequently associated with Merkel cell carcino

171 Merkel cell polyomavirus (MCPyV) is the first human polyomavirus etiologically ass

172 Merkel cell polyomavirus (MCPyV) is the newest member of the human oncogenic virus

173 s or expression of Merkel cell polyomavirus (MCPyV) large and small T antigens (LT and ST).

174 ominine hosts, the Merkel cell polyomavirus (MCPyV) lineage.

175 Merkel cell polyomavirus (MCPyV) may contribute to tumorigenesis in a subset of tu

176 Merkel cell polyomavirus (MCPyV) plays an important role in Merkel cell carcinoma

177 r alterations, and Merkel cell polyomavirus (MCPyV) sequence were analyzed and compared between clini

178 The Merkel cell polyomavirus (MCPyV) was identified recently in human Merkel cell carc

179 rus 6 (HPyV6), and Merkel cell polyomavirus (MCPyV) with glioma risk within the Cancer Prevention Stu

180 of a polyomavirus, Merkel cell polyomavirus (MCPyV), and MCC tumor cells express putative polyomaviru

181 The Merkel cell polyomavirus (MCPyV), discovered in 2008, drives the development of mo

182 Merkel cell polyomavirus (MCPyV), identified in the majority of MCCs, may drive tu

183 ormation for SV40, Merkel cell polyomavirus (MCPyV), murine polyomavirus (MuPyV), and JC polyomavirus

184 he early region of Merkel cell polyomavirus (MCPyV), the causative agent of most Merkel cell carcinom

185 sed by a PyV named Merkel cell polyomavirus (MCPyV), the first PyV linked to human cancer.

186 Merkel cell polyomavirus (MCPyV), the only human polyomavirus that causes cancer,

187 bed polyoma virus, Merkel cell polyomavirus (MCPyV), was found in Merkel cell carcinoma (MCC), a rare

188 ssion of different Merkel cell polyomavirus (MCPyV)-derived truncated large T antigens induced ATOH1

189 t higher levels in Merkel cell polyomavirus (MCPyV)-positive (MCCP) relative to MCPyV-negative (MCCN)

190 decade, including Merkel cell polyomavirus (MCPyV).

191 ften caused by the Merkel cell polyomavirus (MCPyV).

192 is associated with Merkel cell polyomavirus (MCPyV).

193 ype 1 (HTLV1), and Merkel cell polyomavirus (MCPyV).

194 only driven by the Merkel cell polyomavirus (MCPyV).

195 olet light and the Merkel-cell polyomavirus (MCPyV).

196 DNA from a new polyomavirus, MCPyV, was recently shown to be clonally integrated in s

197 alence, and persistence of 9 polyomaviruses (MCPyV, BK polyomavirus, KI polyomavirus, JC polyomavirus

198 Similar to other polyomaviruses, MCPyV encodes early T antigen genes, viral oncogenes req

199 Like other polyomaviruses, MCPyV engages sialic acid as a (co)receptor.

200 blistering sunburn (P = .019), and prevalent MCPyV SSW infections persisted more often in those with

201 ntibodies to the viral capsid indicate prior MCPyV infection, they provide limited clinical insight i

202 s natural host cells that support productive MCPyV infection.

203 human dermal fibroblasts support productive MCPyV infection.

204 It has also been shown to promote MCPyV LT-mediated replication by stabilizing LT.

205 ulate infected dermal fibroblasts to promote MCPyV propagation.

206 By qPCR, MCPyV was detected in 19/20 anophthalmic samples compare

207 investigated whether antibodies recognizing MCPyV large and small tumor-associated antigens (T-Ag) w

208 We found that recombinant MCPyV VP1 pentameric capsomeres both hemagglutinated she

209 sly established system, in which recombinant MCPyV episomal DNA is autonomously replicated in culture

210 ty, may restrict viral propagation to reduce MCPyV burden.

211 ll interfering RNA (siRNA) knockdown reduced MCPyV DNA replication without significantly affecting LT

212 fact colocalized at the actively replicating MCPyV replication complexes, which were absent when a re

213 Verhaegen et al. report MCPyV small T-antigen-expressing transgenic mice that no

214 ckout of the receptor dramatically repressed MCPyV infection-induced ISG expression but did not signi

215 roteins are important for maintaining robust MCPyV DNA replication.

216 Moreover, we show that sT sensitizes MCPyV replication to cidofovir inhibition.

217 Here, we show MCPyV ALTO acts as a tumor suppressor and is silenced in

218 iated human skin can significantly stimulate MCPyV gene expression and replication.

219 pathway and other growth factors stimulates MCPyV infection.

220 To further study MCPyV replication, we employed our previously establishe

221 In summary, MCPyV-associated carcinogenesis is likely to induce the

222 mary human dermal fibroblasts (HDFs) support MCPyV infection has made it possible to closely model ce

223 d peritumoral CD8+ T lymphocytes surrounding MCPyV-positive tumors.

224 aracterized by tumor sequencing and targeted MCPyV sequencing to distinguish independent primary tumo

225 plication and promote viral latency and that MCPyV ALTO must be silenced for MCC to develop.

226 n this issue, Becker et al. demonstrate that MCPyV DNA can be isolated from 85% of primary European M

227 Intriguingly, we demonstrate that MCPyV ST expression promotes microtubule destabilization

228 Indeed, we demonstrated that MCPyV sT enhances LT-mediated replication in a manner th

229 In this study, we further discovered that MCPyV infection of human dermal fibroblasts (HDFs) induc

230 We discovered that MCPyV sT purified from bacteria contains iron-sulfur (Fe

231 Regardless of clonality, we found that MCPyV status was concordant for all tumor pairs and MCPy

232 n, our results suggested the hypothesis that MCPyV sT might be directly involved in viral replication

233 We hypothesized that MCPyV would be present in SCCs.

234 Our results indicate that MCPyV enters cells via caveolar/lipid raft-mediated endo

235 These results indicate that MCPyV is present in MCC tumors more frequently than prev

236 These results indicate that MCPyV T antigens are tumorigenic in vivo, consistent wit

237 This finding further indicates that MCPyV sT plays a direct role in stimulating viral DNA re

238 These reports support the possibility that MCPyV is etiologically involved in at least some cases o

239 ious studies have consistently reported that MCPyV can be detected in approximately 80% of all MCC tu

240 We previously reported that MCPyV stimulates the host's STING-TBK1 signaling axis to

241 We further show that MCPyV ST induces this process by regulating the phosphor

242 quantitative proteomic approach to show that MCPyV ST promotes differential expression of cellular pr

243 paramagnetic resonance analysis showed that MCPyV sT coordinates a [2Fe-2S] and a [4Fe-4S] cluster.

244 ing host-virus interactions and suggest that MCPyV latency is actively maintained through a finely tu

245 analyses of healthy human skin suggest that MCPyV may represent a common component of the human skin

246 tween the analyzed gangliosides suggest that MCPyV VP1 likely interacts with sialic acids on both bra

247 The present study suggests that MCPyV infection may increase glioma risk.

248 The MCPyV status of MCCs was determined by PCR for viral DNA

249 sis between the host immune response and the MCPyV infectious cycle could contribute to the developme

250 f DDR factor/LT replication complexes at the MCPyV origin but also provides a platform for further st

251 lowing activation, NF-kappaB dimers bind the MCPyV noncoding control region (NCCR) and downregulate e

252 expression of NDRG1 was downregulated by the MCPyV early gene, as T antigen knockdown rescued the lev

253 ost cell genome, and most tumors express the MCPyV large and small T antigens.

254 However, the MCPyV life cycle and its oncogenic mechanism remain poor

255 ble for receptor interactions.IMPORTANCE The MCPyV genome was found to be clonally integrated in 80%

256 mechanistic role of host DDR factors in the MCPyV life cycle and virus-associated oncogenesis.

257 ight into the host machinery involved in the MCPyV life cycle.

258 ng, but not required for, replication of the MCPyV genome.

259 ral genome with persistent expression of the MCPyV large T (LT) and small T (ST) antigen.

260 In contrast, expression of the MCPyV large T antigen C-terminal 100 residues could inhi

261 process at play during the evolution of the MCPyV lineage.

262 ty of MCC cases due to the expression of the MCPyV small and large tumor antigens (ST and LT, respect

263 In particular, the MCPyV early gene downregulated the expression of the tum

264 Serum antibodies recognizing the MCPyV capsid protein VP1 are detectable at high titer in

265 We previously reported that the MCPyV early protein ALTO is a key modulator of the STING

266 We demonstrate that the MCPyV small tumor antigen (ST) promotes the destabilizat

267 served physical interaction of MYCL with the MCPyV small T viral antigen, supporting a mechanism of v

268 f of patients with MCC produce antibodies to MCPyV oncoproteins, the titers of which rise with diseas

269 I, 54.5%-70.9%) of MCCs were attributable to MCPyV.

270 molecular mechanisms have been attributed to MCPyV tumor antigen-mediated cellular transformation or

271 ed that the PYHIN protein IFI16 localizes to MCPyV replication centers but does not contribute to the

272 n their tracking of CD8+ T cells reactive to MCPyV T antigen (T-Ag) in the peripheral blood of 26 pat

273 omavirus (MCPyV)-positive (MCCP) relative to MCPyV-negative (MCCN) tumors.

274 ulates inflammatory cytokines in response to MCPyV infection by an alternative mechanism.

275 FN-mediated induction of ISGs in response to MCPyV infection is not crucial to viral control.

276 rming functions of full-length and truncated MCPyV large T antigen are unknown.

277 Tumor MCPyV status, PD-L1 expression, and tumor mutational bur

278 Responses were observed regardless of tumor MCPyV, PD-L1, or TMB status.

279 logical conditions could result in unbridled MCPyV replication that licenses MCC tumorigenesis.

280 st cell tropism(s) of MCPyV remains unclear: MCPyV is able to replicate within a subset of dermal fib

281 Progress toward understanding MCPyV biology has been hindered by its narrow cellular t

282 ue teno virus and Merkel cell polyoma virus (MCPyV) were detected frequently in healthy and anophthal

283 sociated with the Merkel cell polyoma virus (MCPyV).

284 reviously established system for visualizing MCPyV replication complexes in cells.

285 ors showed decreased RB1 expression, whereas MCPyV-positive tumors were enriched for immune response

286 in our knowledge remains the basis by which MCPyV, among all 12 human polyomaviruses, is the only on

287 avirus) and examined factors associated with MCPyV infection in a prospective cohort of 209 men initi

288 st, nonsignificant positive association with MCPyV infection was also observed in CPS-II (OR: 1.29; 9

289 he response rate was 62% among patients with MCPyV-positive tumors (10 of 16 patients) and 44% among

290 ghly prevalent in the human population, with MCPyV virions being continuously shed from human skin.

291 polyomaviruses (BKPyV, JCPyV, KIPyV, WUPyV, MCPyV, HPyV6, HPyV7, TSPyV, HPyV9, HPyV10) and 5 herpesv