ライフサイエンスコーパス: HPV

1 HPV E7 binds the putative tumor suppressor PTPN14 and ta

2 HPV status was also considered.

3 HPV vaccination and cervical cancer screening for women

4 HPV vaccines generate functional (neutralizing) antibodi

5 HPV-based screen and treat is the recommended approach f

6 HPV-EM achieved 97-100% accuracy when benchmarked using

7 HPV-specific ASC responses correlated with titres of pla

8 HPVs infect human keratinocytes, and we previously repor

9 Vaccine effectiveness of at least 1 HPV vaccine dose at age <=18 years or >18 years was 59%

10 cine effectiveness (VE) was computed as (1 - HPV prevalence ratio) for HPV among all women and among

11 We analyzed 87 samples (normal = 16, HPV +/- CIN = 50, cancer = 21 patients).

12 values from channels detecting HPV type 16, HPV types 18 or 45 (or both), and HPV types 31, 33, 35,

13 isk HPV types in five channels: HPV type 16; HPV types 18 or 45, or both; HPV types 31, 33, 35, 52, o

14 ere performed, detecting several STIs and 28 HPV genotypes.

15 onstrates long-term immunogenicity of the 2D HPV vaccine schedule.

16 human papillomavirus [HPV] positive, n = 34; HPV negative, n = 25) from November 2015 to October 2018

17 ine samples were collected and tested for 37 HPV genotypes.

18 In maternal cohorts with 60%-80% HPV vaccination coverage as achieved in Australia, there

19 Cumulative vaccine efficacy against HPV 16/18-associated CIN2+ over the 11-year period was 9

20 Women vaccinated against HPV have a lower incidence of cervical dysplasia compare

21 repeated cross-sectional survey, VE against HPV-16/18 was 89.9% (95% confidence interval, 63.0%-97.2

22 ohort study revealed no increased risk among HPV vaccine-exposed girls, with incidence rate ratios cl

23 Surprisingly, among HPV-negative cases, a gene signature for HPV status was

24 s were randomly assigned (1:1) to receive an HPV 16/18 AS04-adjuvanted vaccine or control hepatitis A

25 In conclusion, anal HPV-16 is more persistent than HPV-18, and its incidence

26 of ART and other HIV-related factors on anal HPV infection, anal intraepithelial neoplasia (AIN), and

27 Both BPV-1 and HPV-31 Y102E are similar in that neither binds the C ter

28 V type 16, HPV types 18 or 45 (or both), and HPV types 31, 33, 35, 52, or 58 (or more than one of the

29 hese types; HPV types 51 or 59, or both; and HPV types 39, 56, 66, or 68, or more than one of these t

30 from sexually active women for cytology and HPV testing.

31 ne populations from patients with HPV(-) and HPV(+) HNSCC and healthy donors.

32 lactic vaccines to prevent HPV infection and HPV assays that detect nucleic acids of the virus.

33 used an automated DNA extraction method and HPV genotyping was performed using the Linear Array geno

34 HNSCC can be separated into HPV-negative and HPV-positive HNSCC.

35 lted in tumor regression in HPV-positive and HPV-negative HNSCC PDXs.

36 However, comparing HPV-positive and HPV-negative oropharyngeal squamous cell carcinomas (OPS

37 Three studies provided rates by sex and HPV genotype; 2 favored a preponderance of F-M and 1 fav

38 comes were compared between unvaccinated and HPV-vaccinated women born 1994-2005.

39 The global scale-up of HPV vaccination and HPV-based screening-including self-sampling-has potentia

40 of Gal-9 on T cells in hepatitis B virus and HPV infections.

41 provide mechanistic insights into WEE1i and HPV+ HNSCC therapies.

42 in these hospital records in both girls and (HPV-unvaccinated) boys, with no relationship to the 2009

43 n the individual level other factors such as HPV exposure or antibody avidity could be important.

44 Changes in histone modification at HPV integration events were correlated with upregulation

45 n likely generates more aggressive tumors at HPV-associated oropharynx subsites than national average

46 A test at 6-month follow-up, if the baseline HPV test was negative.

47 beta-HPV 8E6 expression recapitulates some of these phenotype

48 y of keratinocytes to control cutaneous beta-HPV infection and a high risk for non-melanoma skin canc

49 After failed cytokinesis, beta-HPV 8E6 attenuates phosphorylation of the HP kinase (LAT

50 per offers mechanistic insight into how beta-HPV E6 causes this change in cell signaling.

51 Supporting this idea, beta-HPV's 8E6 protein attenuates p53 accumulation after fail

52 If beta-HPV infections do promote cSCCs, they are hypothesized t

53 These phenotypes were dependent on beta-HPV 8E6 destabilizing p300 and did not completely attenu

54 This system allowed us to show that beta-HPV 8E6 reduced activation of large tumor suppressor kin

55 We show that beta-HPV E6 more broadly impairs cellular signaling, indicati

56 ul to investigate CIB1 interaction with beta-HPV in future studies.

57 However, beta-HPVs are not necessary for tumor maintenance in the gene

58 rvational studies on the association between HPV and adverse pregnancy outcomes.

59 nsistent and significant association between HPV and preterm birth and preterm premature rupture of m

60 analyses, we observed no association between HPV vaccination and subsequent symptoms.

61 s: HPV type 16; HPV types 18 or 45, or both; HPV types 31, 33, 35, 52, or 58, or more than one of the

62 The finding that PTPN14 binding by HPV E7 impairs differentiation has significant implicati

63 uish between alterations directly induced by HPV or indirectly by the need for immortalization or sel

64 to anti-PD-1/PD-L1 immunotherapy mediated by HPV E5, which can be exploited using the HPV E5 inhibito

65 cular mechanism underlying transformation by HPV.

66 etects high-risk HPV types in five channels: HPV type 16; HPV types 18 or 45, or both; HPV types 31,

67 us particles (or capsids) of the most common HPV cancer-causing genotypes.

68 However, comparing HPV-positive and HPV-negative oropharyngeal squamous cel

69 We studied concurrent HPV infections in 17-year-old girls from two birth cohor

70 Contemporary HPV genotyping assays only detect < 25% of all known HPV

71 ed into L1/L2 of the HPV-31 genome, creating HPV-31neo.

72 Using HPV-EM, we demonstrated HPV genotypic differences in recurrence and patient outc

73 This is the first report that describes HPV E5 as a mediator of resistance to anti-PD-1/PD-L1 im

74 cle threshold values from channels detecting HPV type 16, HPV types 18 or 45 (or both), and HPV types

75 present a conserved feature across different HPV genera.

76 erminal arginine highly conserved in diverse HPV E7.

77 residue in the C-terminal domain of diverse HPV E7 mediates the interaction with PTPN14.

78 The E7 proteins from diverse HPVs bind to the host cellular nonreceptor protein tyros

79 inical outcomes of patients with HPV driven (HPV+) OPSCC, a significant subset of HPV tumors associat

80 P), namely LANA (KSHV), EBNA1 (EBV), and E2 (HPV).

81 ces of directionality preponderance for each HPV type.

82 ived their first dose at age <=18, estimated HPV vaccine effectiveness was high regardless of number

83 For HPV genotyping, cervical and anal samples were obtained

84 imilar over time: 32.6% for RWISA, 30.6% for HPV Demonstration, and 27.1% for U54 (P = .007).

85 ity, making this assay an optimal choice for HPV-based screen and treat in settings with a high preva

86 development of cellular immunotherapies for HPV-associated OPC patients.

87 erentiation has significant implications for HPV-mediated carcinogenesis and the HPV life cycle.

88 for women whose lesions tested positive for HPV-16/18 (vaccine-type cases) with that for women who h

89 ealth benefits and should be prioritised for HPV vaccination.

90 s computed as (1 - HPV prevalence ratio) for HPV among all women and among unvaccinated women.

91 k of health care provider recommendation for HPV vaccination is strongly associated with vaccine noni

92 Participants provided oral rinse samples for HPV genotyping.

93 ong HPV-negative cases, a gene signature for HPV status was predictive of survival, even after adjust

94 providers collected separate anal swabs for HPV detection and cytopathologic examination.

95 n for TZ tissue being the primary target for HPV infection and cervical carcinogenesis.

96 may represent a novel therapeutic target for HPV-induced cervical cancer.

97 following cytology processing and tested for HPV.

98 Publicly funded HPV vaccination of female adolescents began in Australia

99 we aim to evaluate the prevalence of genital HPV infection among adolescents and young adults in Braz

100 Current genomic HPV genotyping algorithms use a simple read-alignment an

101 cross our three models and suggest that high HPV vaccination coverage of girls can lead to cervical c

102 m induced by chronic infections such as HIV, HPV, lymphocytic choriomeningitis virus (LCMV), and schi

103 For the 7 HR-HPV types (16, 18, 31, 33, 45, 52, 58) in the nonavalent

104 ong men with HIV, the prevalence of the 7 HR-HPV types in the 9v vaccine was high and was associated

105 as associated with the presence of any 9v HR-HPV (relative risk [RR], 1.8 [95% confidence interval {C

106 as associated with the presence of any 9v HR-HPV (RR, 4.3 [95% CI, 1.6-11.5]; P < .001).

107 revalence, incidence, and clearance of 9v HR-HPV vaccine types, compared with other HR types, and ass

108 were at higher risk of having anogenital HR-HPV acquisition and persistence.

109 Factors associated with high-risk HPV (HR-HPV) persistence and incidence were assessed.

110 ssfully applied to quantitatively detect: i) HPV DNA in saliva and clinical vaginal swab samples, and

111 erally used in combination with radiation in HPV-negative HNSCC where comorbidities prevent the use o

112 th radiation resulted in tumor regression in HPV-positive and HPV-negative HNSCC PDXs.

113 cted promitotic transcriptional signature in HPV+ versus HPV- HNSCCs.

114 t correlate with patient overall survival in HPV-negative OPSCC, there was a strong correlation withi

115 Thus, HNSCC can be separated into HPV-negative and HPV-positive HNSCC.

116 Cervical screening involved HPV testing at age 35 years, or at ages 35 years and 45

117 typing assays only detect < 25% of all known HPV genotypes and are not accurate for low-risk or mixed

118 s and are not accurate for low-risk or mixed HPV genotypes.

119 Infection with multiple HPV types was more common among unvaccinated girls than

120 er 1000 vaccinated girls, and the nonavalent HPV vaccine was estimated to avert 19 cases, 14 deaths,

121 6, 18, 31, 33, 45, 52, 58) in the nonavalent HPV vaccine, PHIV had significantly higher incidence (P

122 and cases of cervical cancer and noncervical HPV-associated cancer by 82%, 80%, 59%, and 39%, respect

123 Antibodies against nonvaccine HPV types 31, 33, 45, 52, and 58 were lower but still si

124 previously reported that tyrosine (Y) 138 of HPV-31 E2 is phosphorylated by the fibroblast growth fac

125 The ability of HPV capsids to package non-viral DNA makes these a usefu

126 making about performance characteristics of HPV testing can be shifted to programme implementers and

127 sed to either a high or low concentration of HPV for various elapsed times.

128 critical risk factor for the development of HPV-induced malignancies.

129 -16/18-positive, 136 (4%) received 1 dose of HPV vaccine, 108 (3%) received 2 doses, and 325 (10%) re

130 against vaccine-type CIN2+ after 3 doses of HPV vaccine and lower but significant VE with 1 or 2 dos

131 CE The E7 oncoprotein is a primary driver of HPV-mediated carcinogenesis.

132 (HPV) E7 oncoprotein is a primary driver of HPV-mediated carcinogenesis.

133 However, the effect of HPV E6 on other pathways is still under investigation.

134 However, the establishment of HPV-harboring cell lines requires selection and immortal

135 Half of HPV positive cervical and pharyngeal cancers comprised a

136 determine carcinogenic effects and impact of HPV vaccinations are warranted, especially in sub-Sahara

137 The introduction of HPV vaccination does not seem to have had an effect on t

138 no relationship to the 2009 introduction of HPV vaccine to Denmark's vaccination program.

139 ignancies and reveal a powerful mechanism of HPV-mediated immunosuppression, which can be exploited t

140 nvolves three independent, dynamic models of HPV infection, cervical carcinogenesis, screening, and p

141 d whether girls have nonspecific outcomes of HPV vaccination, using triangulation from cohort, self-c

142 4.8%) specimens, with a different pattern of HPV infection between sexes.

143 keratinocytes are altered in the presence of HPV genomes.

144 Between the 2 surveys, the prevalence of HPV vaccine types decreased from 8.3% to 1.4%, whereas t

145 we have conducted proteome-wide profiling of HPV-16-specific T cell responses in a cohort of 66 patie

146 AMP) for the detection and quantification of HPV DNA.

147 months potentially conferring higher risk of HPV-OPC among these men.

148 fically, the breadth and overall strength of HPV-specific T cell responses were significantly higher

149 driven (HPV+) OPSCC, a significant subset of HPV tumors associated with tobacco exposure have diminis

150 t for cancer prevention and the treatment of HPV-related diseases.

151 inse specimens were assessed for 37 types of HPV.

152 rom CIN2+ lesions was tested for 37 types of HPV.

153 The global scale-up of HPV vaccination and HPV-based screening-including self-s

154 Naturally occurring variants of HPV have been classified into lineages and sublineages b

155 egnancy outcomes in cohorts of women offered HPV vaccination.

156 nt status had the most significant impact on HPV-specific CD8+ and CD4+ T cell immunity.

157 apsid proteins of vaccine-relevant oncogenic HPV genotypes.

158 the HPV capsid of vaccine-relevant oncogenic HPV genotypes.IMPORTANCE Human papillomavirus (HPV) is t

159 ariants of seven vaccine-relevant, oncogenic HPV genotypes by using a large panel of monoclonal antib

160 age has the potential to eradicate oncogenic HPVs, but such high coverage is hard to achieve.

161 Girls-only HPV vaccination was predicted to reduce the median age-s

162 6, -18, -31, -33/58, -45, or -52 positive or HPV negative).

163 Oral HPV persistence for individual and grouped high-risk HPV

164 estigated effects of HIV and smoking on oral HPV risk.

165 sociation between smoking and high-risk oral HPV: odds ratios for smoking 3.46 (95% confidence interv

166 oad clinical relevance beyond HNSCC to other HPV-associated malignancies and reveal a powerful mechan

167 C) medium (SurePath) using contrived panels (HPV genotype 16 [HPV16] positive, HPV18 positive, or HPV

168 apillomavirus BPV-1 and alpha papillomavirus HPV-31 E2.

169 quantitatively detect human papillomavirus (HPV) 16 and 18 DNAs with sensitivities of 10 and 100 cop

170 Human papillomavirus (HPV) 16 displays substantial sequence variation; four HP

171 ous abnormalities, and human papillomavirus (HPV) 16.

172 ce of the BD Onclarity human papillomavirus (HPV) assay (Onclarity) on the BD Viper LT platform using

173 The human papillomavirus (HPV) E7 oncoprotein is a primary driver of HPV-mediated

174 encing methylation and human papillomavirus (HPV) genotyping assays were performed on cervical cells

175 wledge that persistent human papillomavirus (HPV) infection is the main cause of cervical cancer has

176 ota (VMB) composition, human papillomavirus (HPV) infection, and cervical intraepithelial neoplasia (

177 Human papillomavirus (HPV) infection, and its sequelae of precancerous cervica

178 In human papillomavirus (HPV) infection, the cellular protein complex known as re

179 es resembling those of human papillomavirus (HPV) infection.

180 mechanism by which the human papillomavirus (HPV) inhibits the activity of CBI in head and neck squam

181 Human papillomavirus (HPV) is one of the most common sexually transmitted infe

182 Human papillomavirus (HPV) is the causative agent of cervical and other epithe

183 V genotypes.IMPORTANCE Human papillomavirus (HPV) is the causative agent of cervical and some other e

184 Human papillomavirus (HPV) L1 and L2 capsid proteins self-assemble into virion

185 the viral life cycle, human papillomavirus (HPV) needs to alter the transcriptional program of host

186 genital infection with human papillomavirus (HPV) relative to male-to-female (M-F).

187 ite low specificity of human papillomavirus (HPV) testing, particularly in women living with HIV, lea

188 ess, defined as either human papillomavirus (HPV) type-specific clearance among participants who were

189 Human papillomavirus (HPV) types differ by geographic location and the ethnici

190 cost-effectiveness of human papillomavirus (HPV) vaccination in girls.

191 s, the routine age for human papillomavirus (HPV) vaccination is 11 to 12 years, with catch-up vaccin

192 Human papillomavirus (HPV) vaccination of girls with very high (>90%) coverage

193 lemented a 2-dose (2D) human papillomavirus (HPV) vaccination schedule for adolescents based on immun

194 Highly effective human papillomavirus (HPV) vaccines are used in many national programs in 3- o

195 uted to infection with human papillomavirus (HPV), primarily HPV-16.

196 parity was confined to human papillomavirus (HPV)-associated oropharyngeal cancers, specifically the

197 specific biomarker of human papillomavirus (HPV)-associated oropharyngeal squamous cell carcinoma (O

198 organotypic rafts, and human papillomavirus (HPV)-immortalized keratinocytes are altered in the prese

199 nant transformation by human papillomavirus (HPV).

200 largely driven by the human papillomavirus (HPV).

201 y accrued 59 patients (human papillomavirus [HPV] positive, n = 34; HPV negative, n = 25) from Novemb

202 High-risk human papillomaviruses (HPV) are the causative agents of cervical cancer.

203 d with infections by human papillomaviruses (HPV).

204 SlipChip to quantify human papillomaviruses (HPVs) 16 and 18 and tested this method with fifteen anon

205 Human papillomaviruses (HPVs) infect keratinocytes of stratified epithelia.

206 To replicate, the human papillomaviruses (HPVs) that cause anogenital and oropharyngeal malignanci

207 smitted infections worldwide, and persistent HPV infection can cause warts and even cancer.

208 at elevated basal FOXM1 activity predisposes HPV+ HNSCC to WEE1i-induced toxicity and provide mechani

209 elopment of prophylactic vaccines to prevent HPV infection and HPV assays that detect nucleic acids o

210 n with human papillomavirus (HPV), primarily HPV-16.

211 reporting receipt of a health care provider HPV vaccine recommendation.

212 Lack of provider HPV vaccine recommendation was reported by 73% (95% CI,

213 In this study, 1 or 2 doses of quadrivalent HPV vaccine was associated with substantial protection a

214 s and women 10 to 30 years old, quadrivalent HPV vaccination was associated with a substantially redu

215 updated model, the bivalent or quadrivalent HPV vaccine was estimated to avert 15 cases, 12 deaths,

216 Women received quadrivalent HPV vaccine or placebo (1:1) at entry, week 4, and week

217 e expression signatures of radiosensitivity, HPV status, tumour hypoxia, and microsatellite instabili

218 The control group received HPV vaccine and was replaced with a new unvaccinated con

219 series, several gene signatures representing HPV and microsatellite instability remained significant

220 Factors associated with high-risk HPV (HR-HPV) persistence and incidence were assessed.

221 were positive for at least 1 of 13 high-risk HPV (hrHPV) types.

222 RT) on the natural history of anal high-risk HPV and anal lesion progression is not well established.

223 pes among 184 men positive for any high-risk HPV at their oral baseline visit was assessed at 6-month

224 e model that PTPN14 degradation by high-risk HPV E7 leads to repression of differentiation and contri

225 not impact the ability of several high-risk HPV E7 proteins to bind and degrade the retinoblastoma t

226 es to the carcinogenic activity of high-risk HPV E7 used variants of E7 unable to bind to UBR4.

227 nadir CD4 counts might reduce anal high-risk HPV infection and anal cancer risk.

228 Having a high-risk HPV infection was associated with sexual risk behavior a

229 Six months persistence of oral high-risk HPV infections was positively associated with age and gi

230 ported factor associated with oral high-risk HPV persistence.

231 d with a 10% reduction per year in high-risk HPV prevalence in two studies (adjusted OR 0.90, 0.85-0.

232 th HIV receiving ART had 35% lower high-risk HPV prevalence than ART-naive people (crude odds ratio [

233 istence for individual and grouped high-risk HPV types among 184 men positive for any high-risk HPV a

234 r Xpert HPV (an assay that detects high-risk HPV types in five channels: HPV type 16; HPV types 18 or

235 The prevalence of high-risk HPV types was significantly higher in women (38.6% vs. 2

236 roteins for low-risk HPV-11 E6 and high-risk HPV-16 E6.

237 90 potential substrate proteins for low-risk HPV-11 E6 and high-risk HPV-16 E6.

238 The model predicts that the current U.S. HPV vaccination program will reduce the number of diagno

239 participants who were positive for the same HPV type at baseline, or a negative VIA test at 6-month

240 ated quasiviruses containing G418-selectable HPV-31 genomes with phosphodeficient phenylalanine mutan

241 cells and plasma cells, we generated several HPV-specific human monoclonal antibodies, which exhibite

242 t birth year, maternal age, and age-specific HPV vaccination coverage as independent variables.

243 ve had an effect on the tendency of specific HPV types to cluster together.

244 val of Appalachian males with advanced-stage HPV-associated oropharyngeal cancers suggests pervasive

245 This study did not support HPV vaccination to prevent recurrent HSIL after LEEP in

246 ndirect adjusted VE against vaccine-targeted HPV types was 88% (95% CI, 80% to 92%) and 78% (CI, 61%

247 clusion, anal HPV-16 is more persistent than HPV-18, and its incidence correlates with a prior detect

248 mavirus-16 cleared significantly slower than HPV-18 (32% versus 54% by 24 months).

249 Here, we demonstrate that HPV-16 E2 Y138E bound to full-length Brd4 but not to the

250 For years it seemed that HPV oncogenes activated the homologous recombination pat

251 Retrospective studies suggest that HPV vaccination improves response to treatment of cervic

252 rovides an overview of the diverse ways that HPV oncogenes manipulate homologous recombination and id

253 The HPV types included in the quadrivalent vaccine were dete

254 of plasma IgG and were directed against the HPV proteins E2, E6 and E7, with the most dominant respo

255 ions for HPV-mediated carcinogenesis and the HPV life cycle.

256 gous recombination pathway to facilitate the HPV lifecycle.

257 Median follow-up time for the HPV group was 11.1 years (IQR 9.1-11.7), 4.6 years (4.3-

258 alterations thought to be important for the HPV life cycle are actually late events that may reflect

259 Data from the HPV Infection in Men (HIM) study which followed particip

260 ohort for years 0-4, and 2073 women from the HPV vaccine group and 2530 women from the new unvaccinat

261 2635 women in the HPV vaccine group and 2677 women in the control group we

262 unvaccinated control group and three in the HPV vaccine group died; no deaths were deemed to be rela

263 After the blinded phase, women in the HPV vaccine group were invited to enrol in the long-term

264 curring variation on the antigenicity of the HPV capsid of vaccine-relevant oncogenic HPV genotypes.I

265 occurring variation on the structure of the HPV capsid proteins of vaccine-relevant oncogenic HPV ge

266 llular factors to mediate replication of the HPV genome.

267 ctable marker was inserted into L1/L2 of the HPV-31 genome, creating HPV-31neo.

268 ore functional antigenic determinants on the HPV capsid.

269 er, the herd effect (HE) depends both on the HPV type and the vaccination strategy.

270 We conclude that the HPV infection model provides a valuable tool to distingu

271 We now show that the HPV oncoprotein E7 of HPV8, HPV11 and HPV16 directly int

272 Our findings demonstrate that the HPV+ OPSCC clinical outcomes are strongly correlated wit

273 ; no deaths were deemed to be related to the HPV vaccine.

274 by HPV E5, which can be exploited using the HPV E5 inhibitor rimantadine to improve outcomes for hea

275 DH isoform expression diversity, compared to HPV-/p53HRmut cases (p = 0.03).

276 orporates additional information relevant to HPV-positive disease.

277 mpse of the overall human T cell response to HPV in a clinical setting and offer groundbreaking insig

278 s were constructed to examine median time to HPV clearance overall, and by selected risk factors.

279 52, or 58, or more than one of these types; HPV types 51 or 59, or both; and HPV types 39, 56, 66, o

280 Unexpectedly, HPV-specific T cell responses from OPC patients were not

281 Using HPV-EM, we demonstrated HPV genotypic differences in rec

282 methods and present new protocols for using HPV capsids to deliver non-viral DNA thereby providing a

283 S. vaccination policy on use of the 9-valent HPV vaccine in adult women and men is being reviewed.

284 tic transcriptional signature in HPV+ versus HPV- HNSCCs.

285 es owing to increased human papilloma virus (HPV) exposure.

286 ciated with high-risk human papilloma virus (HPV) infection is a growing clinical problem.

287 ervical cancer cells, human papilloma virus (HPV) protein E7 binds to Rb, releasing it from E2F to pr

288 tis B virus (HBV) and human papilloma virus (HPV; for example, HPV16 or HPV18).

289 sults, and vaccine history, 1,561 (47%) were HPV-16/18-positive, 136 (4%) received 1 dose of HPV vacc

290 ty-five percent of the patients (18/51) were HPV-positive and current or past tobacco consumption was

291 We evaluated whether HPV type restriction and more stringent cutoffs on Xpert

292 plicate in a transient in vitro assay, while HPV-31 Y102E binds E1 and was able to replicate, albeit

293 lifetime protection against infections with HPV types 16, 18, 31, 33, 45, 52, and 58, and to scale u

294 favorable clinical outcomes of patients with HPV driven (HPV+) OPSCC, a significant subset of HPV tum

295 umoral immune populations from patients with HPV(-) and HPV(+) HNSCC and healthy donors.

296 ll responses in a cohort of 66 patients with HPV-associated OPC and 22 healthy individuals.

297 ntifying disease recurrence in patients with HPV-associated oropharyngeal cancer and may facilitate e

298 CR rates were 85.3% and 78.3% for those with HPV-positive and -negative HNSCC, respectively.

299 men had cervical samples collected for Xpert HPV (an assay that detects high-risk HPV types in five c

300 eshold cutoffs on selected channels in Xpert HPV improve specificity with only modest losses in sensi

301 triction and more stringent cutoffs on Xpert HPV optimise performance characteristics of this assay f