HPV Genotypes distribution in Indian women with and without cervical carcinoma: Implication for HPV vaccination program in Odisha, Eastern India

Probably not a substantial claim: may not pass S3 (load-bearing).

In the Chinese population, HPV 16 is the most predominant followed by HPV 52 rather than 18.

“However, in the Chinese population, HPV 16 is the most predominant followed by HPV 52 rather than 18 [25].”

• cites [25] Chen Q, Xie L-X, Qing Z-R, Li L-J, Luo Z-Y, et al. Epidemiologic Characterization of Human Papillomavirus Infection in Rural Chaozhou, Eastern Guangdong Province of China. PLoS ONE. 2012;7(2):e32149. doi: 10.1371/journal.pone.0032149 . sourceDisputed

  The Results (Specific Prevalence of HR-HPV Types, Table 3) rank HPV-52 first at 33.40%, HPV-16 second at 20.95%, and HPV-18 at 8.36% in the study population. The Discussion likewise explicitly says HPV-52, rather than HPV-16, was the most commonly identified type in this rural Chaozhou population. The claim reverses the top two types and generalizes a regional finding to the Chinese population. (LLM, conf=0.90)

  Checked by a reasoning model — may be wrong.

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

The pattern of multiple infections in women without cancer corroborates with previous studies.

“In women without cancer multiple infections were most frequently observed in the age group 36–45 years and lowest in >55 years age group which corroborates with previous studies [25, 29].”

• cites [25] Chen Q, Xie L-X, Qing Z-R, Li L-J, Luo Z-Y, et al. Epidemiologic Characterization of Human Papillomavirus Infection in Rural Chaozhou, Eastern Guangdong Province of China. PLoS ONE. 2012;7(2):e32149. doi: 10.1371/journal.pone.0032149 . sourceDisputed

  The Discussion reports the opposite age pattern in the rural Chaozhou sample: women aged 55–60 had the highest multiple-infection prevalence, which increased with age. The Results (Figure 5C) also describe an increasing multiple-infection ratio with age. Our copy does not present this finding specifically for women without cancer; page numbers are not available in the supplied passages. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  Experimental — accuracy not yet measured
• cites [29] Resende LS, Rabelo-Santos SH, Sarian LO, Alves RR, Ribeiro AA, et al. A portrait of single and multiple HPV type infections in Brazilian women of different age strata with squamous or glandular cervical lesions. BMC Infect Dis. 2014;14:214. sourcePartly supported

  The Results (page unavailable) report that multiple-type HPV infections were most prevalent in women under 29, not those aged 36–45. They do report a decline in women aged 60 or older, which broadly supports the older-age part of the pattern. The reported age pattern is not specific to women without cancer. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

Among 184 different HPV genotypes, only 40 diverse types can infect the anogenital region.

“Among 184 different HPV genotypes, only 40 diverse types can infect anogenital region which can be classified into 3 classes based on their oncogenic potential.”

• cites [2] Trottier H, Burchell AN. Epidemiology of mucosal human papillomavirus infection and associated diseases. Public Health Genomics. 2009;12:291–307. sourceNot checked — no full text of the source
• cites [3] Bouvard V, Baan R, Straif K, Grosse Y, Secretan B, et al. A review of human carcinogens–Part B: biological agents. Lancet Oncol. 2009;10:321–2. sourceCould not verify

  The 'Historical aspects' passage links HPV types to anogenital cancers and mentions 120 fully sequenced genotypes, but it does not give the claimed total of 184 or say that 40 types can infect the anogenital region. Searches for those numbers and for anogenital HPV types found no decisive passage; the copy is truncated, so the relevant text may be missing. (LLM, conf=0.70)

  Experimental — accuracy not yet measured

May combine two claims.

Epidemiology of HPV infection and pattern of HPV genotype distribution are not well documented in the entire Indian subcontinent, which limits implementation of cervical cancer prevention programs.

“Epidemiology of HPV infection and pattern of HPV genotype distribution are not well documented in the entire Indian subcontinent which limits the implementation of cervical cancer prevention programs.”

• cites [5] Sreedevi A, Javed R, Dinesh A. Epidemiology of cervical cancer with special focus on India. Int J Womens Health. 2015;7:405–14.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [6] Bhatla N, Dar L, Patro AR, et al. Human Papillomavirus-Type Distribution in Women With and Without Cervical Neoplasia in North India. Int J Gynecol Pathol. 2008;27(3):426–30. sourcePartly supported

  The Abstract says that standardized data on HPV-type prevalence in India were limited, supporting the claim about incomplete documentation. It does not say that this data gap limits prevention programs; instead, it attributes difficulty implementing cytology-based screening to cost, infrastructure, false-negative tests, and underscreening. The study itself concerns symptomatic women in north India, not the entire subcontinent. (LLM, conf=0.86)

  Experimental — accuracy not yet measured
• cites [7] Basu P, Roychowdhury S, Bafna UD, Chaudhury S, et al. Human papillomavirus genotype distribution in cervical cancer in India: Results from a multi-center study. AsianPac J Cancer Prev. 2009;10:27–34.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [8] Deodhar K, Gheit T, Vaccarella S, Romao CC, et al. Prevalence of Human Papillomavirus Types in Cervical Lesions from Women in Rural Western India. J Med Virol. 2012;84:1054–60. sourceNot checked — no full text of the source
• cites [9] Srivastava S, Shahi UP, Dibya A, Gupta S, Roy JK. Distribution of HPV Genotypes and Involvement of risk factors in cervical lesions and invasive cervical cancer: a study in an indian population. Int J Mol Cell Med. 2014;3:2.Not checked — no full text of the source

May combine two claims.

Available reports from studies covering few parts of India show a wide variation in HPV infection prevalence and genotype distribution, attributed to diversified socio-economic and geo-climatic conditions.

“Available reports from studies covering few parts of India show a wide variation in the prevalence of HPV infection and genotypes distribution which is attributed to diversified socio-economic and geo-climatic condition [5–9].”

• cites [5] Sreedevi A, Javed R, Dinesh A. Epidemiology of cervical cancer with special focus on India. Int J Womens Health. 2015;7:405–14.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [6] Bhatla N, Dar L, Patro AR, et al. Human Papillomavirus-Type Distribution in Women With and Without Cervical Neoplasia in North India. Int J Gynecol Pathol. 2008;27(3):426–30. sourcePartly supported

  The Discussion reports differences in HPV genotype distribution between this north Indian study and a study from south India, and the Abstract notes that Indian data are limited. It does not attribute variation in HPV prevalence or genotype distribution to socioeconomic or geo-climatic conditions; the Results describe participants’ socioeconomic class without making that connection. No page numbers are available in our copy. (LLM, conf=0.86)

  Experimental — accuracy not yet measured
• cites [7] Basu P, Roychowdhury S, Bafna UD, Chaudhury S, et al. Human papillomavirus genotype distribution in cervical cancer in India: Results from a multi-center study. AsianPac J Cancer Prev. 2009;10:27–34.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [8] Deodhar K, Gheit T, Vaccarella S, Romao CC, et al. Prevalence of Human Papillomavirus Types in Cervical Lesions from Women in Rural Western India. J Med Virol. 2012;84:1054–60. sourceNot checked — no full text of the source
• cites [9] Srivastava S, Shahi UP, Dibya A, Gupta S, Roy JK. Distribution of HPV Genotypes and Involvement of risk factors in cervical lesions and invasive cervical cancer: a study in an indian population. Int J Mol Cell Med. 2014;3:2.Not checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

Cytological classification was done according to the Bethesda system.

“Cytological classification was done according to Bethesda system [10].”

• cites [10] Nayar R, Wilbur DC. The Pap test and Bethesda 2014. Cancer Cytopathol. 2015;123(5):271–81. sourceSupported

Classified as probably not a substantial claim.

Anogenital HPV genotypes are classified into high-risk, low-risk, and intermediate-risk groups based on oncogenic potential, with specific genotypes in each group.

“HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73 and 82 are included in high-risk group while HPV6, 11, 40, 42, 43, 44, 54, 61, 70, 72 and 81 are included in low-risk group whereas HPV 26, 53 and 66 belong to the group of intermediate risk [2, 3].”

• cites [2] Trottier H, Burchell AN. Epidemiology of mucosal human papillomavirus infection and associated diseases. Public Health Genomics. 2009;12:291–307. sourceNot checked — no full text of the source
• cites [3] Bouvard V, Baan R, Straif K, Grosse Y, Secretan B, et al. A review of human carcinogens–Part B: biological agents. Lancet Oncol. 2009;10:321–2. sourcePartly supported

  The section “Classification of weakly carcinogenic human papillomavirus types” (page unavailable) says HPV types vary in carcinogenic potential and identifies HPV16 and HPV18 as powerful carcinogens. The available copy does not substantiate the sentence’s remaining genotype lists or its specific high-, low-, and intermediate-risk assignments. (LLM, conf=0.82)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Reports from south India showed HPV 16 and HPV18 account for 58-69% and 5-19.4% of ICC cases respectively.

“Reports from south India showed HPV 16 and HPV18 accounts for 58–69% and 5–19.4% of ICC cases respectively [16, 18].”

• cites [16] Sowjanya AP, Jain M, Poli UR, et al. Prevalence and distribution of high-risk human papillomavirus (HPV) types in invasive squamous cell carcinoma of the cervix and in normal women in Andhra Pradesh. India BMC Infect Dis. 2005;5:116. sourceSupported
• cites [18] Pillai RM, Babu JM, Jissa VT, Lakshmi S, Chiplunkar SV, et al. Region-wise distribution of high-risk human papillomavirus types in squamous cell carcinomas of the cervix in India. Int J Gynecol Cancer. 2010;20:1046–51. sourceNot checked — no full text of the source

May combine two claims.

The genotype distribution with HPV 16 followed by HPV 18 as most prevalent in cervical cancer is in accordance with international and local data.

“The most prevalent genotype in cervical cancer was HPV 16 followed by18 is in accordance with international and local data [7, 8, 16].”

• cites [7] Basu P, Roychowdhury S, Bafna UD, Chaudhury S, et al. Human papillomavirus genotype distribution in cervical cancer in India: Results from a multi-center study. AsianPac J Cancer Prev. 2009;10:27–34.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [8] Deodhar K, Gheit T, Vaccarella S, Romao CC, et al. Prevalence of Human Papillomavirus Types in Cervical Lesions from Women in Rural Western India. J Med Virol. 2012;84:1054–60. sourceNot checked — no full text of the source
• cites [16] Sowjanya AP, Jain M, Poli UR, et al. Prevalence and distribution of high-risk human papillomavirus (HPV) types in invasive squamous cell carcinoma of the cervix and in normal women in Andhra Pradesh. India BMC Infect Dis. 2005;5:116. sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing).

Several reports show the association of multiple infections with cervical cancer.

“Though there are several reports showing the association of multiple infections with cervical cancer [39, 40] the biological effect of multiple infections on cervical diseases has not yet been established.”

• cites [39] Chagas BS, Comar M, Gurgel APAD, Paiva S, Seraceni S, de Freitas AC, et al. Association Study between Cervical Lesions and Single or Multiple Vaccine-Target and Non-Vaccine Target Human Papillomavirus (HPV) Types in Women from Northeastern Brazil. PLoS ONE. 2015;10(7):e0132570. doi: 10.1371/journal.pone.0132570 . sourceSupported
• cites [40] Chaturvedi AK, Katki HA, Hildesheim A, Rodríguez AC, Quint W, Schiffman M, et al. Human papillomavirus infection with multiple types: pattern of coinfection and risk of cervical disease. J Infect Dis. 2011;203:910–20. sourcePartly supported

  The Discussion reports that women with multiple HPV infections had significantly higher risks of CIN2-or-worse and HSIL-or-worse than women with single infections. The Statistical Analyses section shows that these were composite cervical-disease outcomes, not a separate analysis of invasive cervical cancer. Thus the paper supports an association with cervical disease, but not the claim specifically about cervical cancer. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

The bimodal shaped infection peak in noncancer cases is similar to many other reports.

“The age-specific trend of HPV infection among noncancer cases showed bimodal shaped infection peak which is similar to many other reports [28].”

• cites [28] Baloch Z, Li Y, Yuan T, Feng Y, et al. Epidemiologic characterization of human papillomavirus (HPV) infection in various regions of Yunnan Province of China. BMC Infect Dis. 2016;16:228. sourcePartly supported

  The Results section ('HPV genotypes and infection'; page unavailable) reports an early HPV-prevalence peak and a less pronounced second peak among women with normal results, supporting the bimodal pattern in noncancer cases. The passages found do not establish that this pattern is similar to many other reports. (LLM, conf=0.83)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

Bachtiary et al., in a study of 106 cervical cancer patients receiving radiation therapy, found that multiple-type HPV was an independent poor prognostic factor.

“Bachtiary et al. [38], in a study of 106 cervical cancer patients receiving radiation therapy, found that multiple-type HPV was an independent poor prognostic factor.”

• cites [38] Bachtiary B, Obermair A, Dreier B, Birner P, Breitenecker G, Knocke TH, et al. Impact of multiple HPV infection on response to treatment and survival in patients receiving radical radiotherapy for cervical cancer. Int J Cancer. 2002;102:237–43. sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing).

HPV infection at younger age reached its peak soon after sexual initiation.

“HPV infection at younger age reached its peak soon after sexual initiation [28].”

• cites [28] Baloch Z, Li Y, Yuan T, Feng Y, et al. Epidemiologic characterization of human papillomavirus (HPV) infection in various regions of Yunnan Province of China. BMC Infect Dis. 2016;16:228. sourcePartly supported

  The Results section (‘HPV genotypes and infection’; page unavailable) reports the highest overall HPV prevalence in women under 35, with prevalence declining thereafter, though it also notes a second peak in older women. The paper does not establish when those women initiated sexual activity, so it does not support the claim that the younger-age peak occurred soon after sexual initiation. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

Probably not a substantial claim: may not pass S3 (load-bearing).

Synergistic effect of multiple infections by HPV genotypes on carcinogenesis is supported by many studies.

“Synergistic effect of multiple infections by HPV genotypes on carcinogenesis is supported by many studies [7–9, 17, 26], while contradicting studies [25, 29, 31, 32, 35] invoke confusion.”

• cites [7] Basu P, Roychowdhury S, Bafna UD, Chaudhury S, et al. Human papillomavirus genotype distribution in cervical cancer in India: Results from a multi-center study. AsianPac J Cancer Prev. 2009;10:27–34.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [8] Deodhar K, Gheit T, Vaccarella S, Romao CC, et al. Prevalence of Human Papillomavirus Types in Cervical Lesions from Women in Rural Western India. J Med Virol. 2012;84:1054–60. sourceNot checked — no full text of the source
• cites [9] Srivastava S, Shahi UP, Dibya A, Gupta S, Roy JK. Distribution of HPV Genotypes and Involvement of risk factors in cervical lesions and invasive cervical cancer: a study in an indian population. Int J Mol Cell Med. 2014;3:2.Not checked — no full text of the source
• cites [17] Datta P, Bhatla N, Pandey RM, et al. Type-specific incidence and persistence of HPV infection among young women: a prospective study in North India. Asian Pac J Cancer Prev. 2012;13(3):1019–24. sourceCould not verify

  The Results (page unavailable) report that multiple HPV infections occurred in 3% of samples. The Introduction and Discussion (pages unavailable) link persistent high-risk HPV infection—not multiple-genotype infection or synergy—to cervical lesions and cancer. A search for multiple infections and carcinogenesis found no passage addressing the claimed synergistic effect. (LLM, conf=0.75)

  Experimental — accuracy not yet measured
• cites [26] Sanjosé SD, Diaz M, Castellsagué X, et al. Worldwide prevalence and genotype distribution of cervical human papillomavirus DNA in women with normal cytology: a meta-analysis. Lancet Infect Dis. 2007;7(7):453–9. sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

In Pakistan, HPV 16 and 18 account for 45.1-94.9% and 1.7-43.1% of ICC cases respectively.

“In Pakistan, HPV 16 and 18 accounts for 45.1–94.9% and 1.7–43.1% of ICC cases respectively [21–24].”

• cites [21] Gul S, Murad S, Javed A. Prevalence of High risk Human Papillomavirus in cervical dysplasia and cancer samples from twin cities in Pakistan. Int J Infect Dis. 2015;34:14–9. sourcePartly supported

  The Results and Discussion report HPV16 and HPV18 in cervical cancer samples from Islamabad and Rawalpindi, supporting the general point that both occur in Pakistani cases. They report 42% and 45%, respectively, in squamous cell carcinoma and 50% and 38.8% in adenocarcinoma; they do not establish the claimed nationwide ranges of 45.1–94.9% and 1.7–43.1%. (LLM, conf=0.87)

  Experimental — accuracy not yet measured
• cites [22] Siddiqa A, Zainab M, Qadri I, Bhatti MF, Parish JL. Prevalence and genotyping of high risk human papillomavirus in cervical cancer samples from Punjab, Pakistan. Viruses. 2014;6:2762–77. sourcePartly supported

  Results and Discussion §3.1 reports HPV16 in 64.94% of the Punjab samples and cites Karachi reports of 75–93%, consistent with the claimed HPV16 range. It reports HPV18 in 66.23% of the Punjab samples, above the claimed 43.1% upper limit. The paper does not state the quoted ranges for Pakistani ICC cases, and its Punjab sample includes non-invasive lesions. (LLM, conf=0.88)

  Experimental — accuracy not yet measured
• cites [23] Raza SA, Franceschi S, Pallardy S, Malik FR, Avan BI, Zafar A, Pervez S, Serajuddaula S, Snijders PJF, van Kemenade FJ, et al. Human papillomavirus infection in women with and without cervical cancer in Karachi, Pakistan. Br J Cancer. 2010;102:1657–60. sourcePartly supported

  The Results report that HPV16 and HPV18 were found in 75.8% and 6.6% of ICC cases, respectively, in the Karachi study. Both figures fall within the cited ranges, but this paper does not establish the ranges or their endpoints for Pakistan. (LLM, conf=0.87)

  Experimental — accuracy not yet measured
• cites [24] Khan S, Jaffer NN, Khan MN, Rai MA, Shafiq M, Ali A, Pervez S, Khan N, Aziz A, Ali SH. Human papillomavirus subtype 16 is common in Pakistani women with cervical carcinoma. Int J Infect Dis. 2007;11:313–7. sourceSupported

Probably not a substantial claim: may not pass S3 (load-bearing).

The potential vaccine impact in this study is similar to that in a French population study.

“It is similar to a study in French population [14].”

• cites [14] Riethmuller D, Jacquard A, Guily JL, Aubin F. Carcopino X et al Potential impact of a nonavalent HPV vaccine on the occurrence of HPV-related diseases in France. BMC Public Health. 2015;15:453. sourceSupported

Probably not a substantial claim: may not pass S2 (checkable).

The true potential impact of a vaccine lies somewhere between the high and low estimate.

“Since the true potential impact lies somewhere between the high and low estimate [14] the average value of the two was considered for convenience.”

• cites [14] Riethmuller D, Jacquard A, Guily JL, Aubin F. Carcopino X et al Potential impact of a nonavalent HPV vaccine on the occurrence of HPV-related diseases in France. BMC Public Health. 2015;15:453. sourceSupported

May combine two claims.

The potential impact of the nonavalent vaccine in Asia and worldwide is 91.5% and 89.5%, respectively.

“The potential impact of the nonavalent vaccine in Asia and worldwide are 91.5 and 89.5% respectively [44].”

• cites [44] Loya A, Serrano B, Rasheed F, Tous S, et al. Human Papillomavirus Genotype Distribution in Invasive Cervical Cancer in Pakistan. Cancers. 2016;8:72. sourcePartly supported

  The Results (§2.2; page unavailable) estimate that HPV types covered by the nonavalent vaccine account for 91.4% of invasive cervical cancer cases in Asia and 89.3% worldwide. This supports the claimed potential impact in substance, but neither cited percentage—91.5% or 89.5%—matches the paper. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

May combine two claims.

The most frequent genotype combination after HPV16+18 (9.4%) was HPV16+66+68 (2.7%) which was frequently observed in inflammatory cytology.

“The most frequent genotype combination after HPV16 + 18(9.4%) was HPV16 + 66 + 68(2.7%) which was frequently observed in inflammatory cytology.”

May combine two claims.

In inflammatory cytology, double genotypes were found in 19.31% of cases while 10.22% were infected with triple genotypes combinations.

“Infections with double genotypes found in 19.31% of cases while 10.22% cases were infected with triple genotypes combinations”

May combine two claims.

The most prevalent genotype combination as coinfection among ICC cases was HPV16+18 (4.32%) followed by HPV16+39 (2.16%).

“The most prevalent genotype combination as coinfection among ICC cases was HPV16 + 18(4.32%) followed by HPV16 + 39(2.16%)”

May combine two claims.

Other detected genotypes in descending order were HPV51 (3.46%), HPV39 (3.17%), HPV66 (2.8%), HPV68 (2.3%), HPV35 (1.7%), HPV45 (1.7%), HPV44 (1.1%), HPV58 (1.1%), HPV52 (0.57%), HPV6/11 (0.57%), HPV42 (1.1%), and HPV43 (0.57%).

“Other detected genotypes in descending order were HPV 51(3.46%), HPV 39(3.17%), HPV 66(2.8%), HPV 68(2.3%), HPV 35(1.7%), HPV 45(1.7%), HPV 44(1.1%), HPV 58 (1.1%), HPV 52(.57%), HPV 6/11(.57%), HPV 42(1.1%) and HPV 43(.57%)”

May combine two claims.

In inflammatory cytology, 70.45% cases were infected with single genotypes while 29.54% with multiple HPV types.

“In this group 70.45% cases were infected with single genotypes while 29.54% cases were infected with multiple HPV types”

May combine two claims.

The most common combination of coinfection in inflammatory cytology was HPV16+18 (14.72%) followed by HPV16+66+68 (6.81%).

“The most common combination of coinfection in this group was HPV 16 + 18 (14.72%) followed by HPV16 + 66 + 68(6.81%)”

May combine two claims.

The most prevalent genotype in cervical cancer was HPV 16 followed by HPV 18.

“The most prevalent genotype in cervical cancer was HPV 16 followed by18 is in accordance with international and local data [7, 8, 16].”

May combine two claims.

Low estimates of genotypes targeted by 2v, 4v, and 9v vaccines were 152 (82.16%), 152 (82.6%), and 156 (84.32%) respectively.

“Low estimates of genotypes targeted by 2v, 4v, and 9v vaccine were 152(82.16%), 152(82.6%) and156 (84.32%) respectively.”

May combine two claims.

High estimates of genotypes targeted by 2v, 4v, and 9v vaccines were 181 (97.83%), 183 (98.91%), and 185 (100%) respectively.

“High estimates of genotypes targeted by 2v, 4v, and 9v vaccines were 181(97.83%), 183(98.91%) and 185(100%) respectively.”

May combine two claims.

Among ICC cases, 78.9% were infected with single genotypes while 21.08% were with multiple genotypes including double (11.89%), triple (5.94%), and quadruple (3.24%) combinations.

“Among the ICC cases78.9% cases were infected with single genotypes while 21.08% cases were with multiple genotypes including double (11.89%), triple (5.94%) and quadruple (3.24%) combinations of genotypes”

May combine two claims.

No significant association was found between multiple HPV genotypes and age at diagnosis (≤50 vs >50), stage at diagnosis (early vs late), lymph node metastasis (yes vs no), or histopathology (SCC vs ADC).

“No significant association was found between multiple genotypes and clinicopathological variables such as age at diagnosis (≤50 years vs >50 years), stage at diagnosis (early stage or stage I-II vs late stage or stage III-IV), lymph node metastasis (yes vs no) and histopathology (Squamous cell carcinoma vs Adenocarcinoma).”

May combine two claims.

The frequency of HPV infection and multiple types increases with age.

“The frequency of HPV infection and multiple types increases with age explains cumulative lifetime exposure [33], relative incompetency in viral clearance and insufficient adaptive immune responses at this age caused by hormonal changes at menopausal transition, contributing to HPV persistence or reactivation of latent HPV infections [34, 35].”

May combine two claims.

No significant association of multiple infections with age, stage, lymph node metastasis, and histopathology was found in the present work.

“However, no significant association of multiple infections with other clinicopathological variables (age, stage, lymph node metastasis and histopathology) was found in the present work which agrees with the findings of Mungala et al [36].”

May combine two claims.

In the present study, the potential vaccine impact of bivalent and quadrivalent vaccines was 89.99% and 91.65%, respectively.

“The present study shows a potential vaccine impact of 2v and 4v vaccines were 89.99 and 91.65% respectively.”

Probably not a substantial claim: may not pass S2 (checkable).

Understanding HPV genotype distribution among different populations is essential for predicting the efficacy of current HPV vaccines and devising new vaccine strategies.

“Considering the limited cross protection offered by the current vaccines, understanding the genotype distribution among different population is essential in predicting the efficacy of current vaccine and devising new vaccine strategy [4].”

• cites [4] Herrero R. Human papillomavirus (HPV) vaccines: limited cross-protection against additional HPV types. J Infect Dis. 2009;199:919–22. sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

A total of 607 participants were enrolled in the study.

“A total of 607 participants were being enrolled in the study.”

Probably not a substantial claim: may not pass S3 (load-bearing).

12 cases were excluded from further analysis as they were negative for beta globin PCR.

“Among all the enrolled cases 12 cases were excluded from further analysis as they were negative for beta globin PCR.”

May combine two claims.

In Kolkata, 59-74% of ICC cases are infected with HPV 16 and 2-13.9% with HPV 18.

“In Kolkata, 59–74% of ICC cases are infected with HPV 16 and 2–13.9% cases infected with HPV 18 [7, 18].”

• cites [7] Basu P, Roychowdhury S, Bafna UD, Chaudhury S, et al. Human papillomavirus genotype distribution in cervical cancer in India: Results from a multi-center study. AsianPac J Cancer Prev. 2009;10:27–34.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [18] Pillai RM, Babu JM, Jissa VT, Lakshmi S, Chiplunkar SV, et al. Region-wise distribution of high-risk human papillomavirus types in squamous cell carcinomas of the cervix in India. Int J Gynecol Cancer. 2010;20:1046–51. sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

Cytological information was known for 440 cases only.

“Cytological information was known for 440 cases only which includes normal (n = 68), cervicities (n = 162), invasive carcinoma (n = 210).”

Probably not a substantial claim: may not pass S2 (checkable). May combine two claims.

This data would help planning an appropriate strategy for disease monitoring and provides baseline data for post-vaccination surveillance in the region.

“This data would help planning an appropriate strategy for disease monitoring and provides baseline data for post-vaccination surveillance in the region.”

Probably not a substantial claim: may not pass S3 (load-bearing).

The study did not look for bacterial, fungal or HIV infection which could make symptomatic women prone to HPV infection.

“This study, however, did not look for any bacterial, fungal or HIV infection which could make them prone to HPV infection in symptomatic cases.”

Probably not a substantial claim: may not pass S3 (load-bearing).

The prevalence of cancer cervix is high in India.

“The prevalence of cancer cervix is high in India [1]”

• cites [1] Globacan. Cervical cancer: estimated incidence mortality and prevalence worldwide in 2012. 2012; http://globocan.iarc.fr/old/FactSheets/cancers/cervix-new.asp . Accessed 5 Dec 2015.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

Probably not a substantial claim: may not pass S3 (load-bearing).

The lack of association of multiple infections with age, stage, lymph node metastasis, and histopathology agrees with the findings of Mungala et al.

“However, no significant association of multiple infections with other clinicopathological variables (age, stage, lymph node metastasis and histopathology) was found in the present work which agrees with the findings of Mungala et al [36].”

• cites [36] Munagala R, Donà MG, Rai SN, Jenson AB, Bala N, Ghim SJ, et al. Significance of multiple HPV infection in cervical cancer patients and its impact on treatment response. Int J Oncol. 2009;34:263–71.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

Probably not a substantial claim: may not pass S3 (load-bearing).

In a similar study from Delhi (north India), HPV 16 and 18 contributed 73.6 and 14.2% of cervical carcinoma cases.

“In a similar study from Delhi (north India) reported that HPV 16 and 18 contributing 73.6 and 14.2% cases of cervical carcinoma [19].”

• cites [19] Bhatla N, Dar L, Patro AR, Kriplani A, Gulati A, Verma K, Broor S, Shah KV, Gravitt PE. Human papillomavirus type distribution in cervical cancer in Delhi, India. Int J Gynecol Pathol. 2006;25(4):398–402. sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

The higher frequency of multiple infections at 36-45 years in both cancer and non cancer group might be due to multiple sexual partners at this age.

“The higher frequency of multiple infections at the 36–45 years in both cancer and non cancer group might be due to multiple sexual partners at this age.”

May combine two claims.

The increase in HPV infection and multiple types with age is explained by cumulative lifetime exposure, relative incompetency in viral clearance, and insufficient adaptive immune responses at menopausal transition, contributing to HPV persistence or reactivation.

“The frequency of HPV infection and multiple types increases with age explains cumulative lifetime exposure [33], relative incompetency in viral clearance and insufficient adaptive immune responses at this age caused by hormonal changes at menopausal transition, contributing to HPV persistence or reactivation of latent HPV infections [34, 35].”

• cites [33] Lin M, Yang LY, Li LJ, Wu JR, Peng YP, et al. Genital human papillomavirus screening by gene chip in Chinese women of Guangdong province. Aust N Z J Obstet Gynaecol. 2008;48:189–94. sourceNot checked — no full text of the source
• cites [34] Herrero R, Castle PE, Schiffman M, Bratti MC, Hildesheim A, Morales J, et al. Epidemiologic profile of type-specific human papillomavirus infection and cervical neoplasia in Guanacaste. Costa Rica J Infect Dis. 2005;191:1796–807. sourceNot checked — no full text of the source
• cites [35] Hildesheim A, Wang SS. Host and viral genetics and risk of cervical cancer: a review. Virus Res. 2002;89:229–40. sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

Prognosis of cervical carcinoma is related to clinical stage, lymph node metastasis, parametrial invasion, primary tumor size, histological type, depth of cervical stromal invasion and lymph vascular space involvement.

“Prognosis of cervical carcinoma is related to clinical stage, lymph node metastasis, parametrial invasion, primary tumor size, histological type, depth of cervical stromal invasion and lymph vascular space involvement [37].”

• cites [37] Kosary CL. FIGO stage, histology, histologic grade, age and race as prognostic factors in determining survival for cancers of the female gynecological system: an analysis of 1973-87 SEER cases of cancers of the endometrium, cervix, ovary, vulva, and vagina. Semin Surg Oncol. 1994;10(1):31–46. sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S3 (load-bearing).

The recently approved 9-valent HPV vaccine covers genotypes HPV16/18/31/33/45/52/58.

“The recently approved 9-valent vaccine covers HPV16/18/31/33/45/52/58 genotypes [42, 43].”

• cites [42] Press Announcements—FDA approves Gardasil 9 for Prevention of Certain Cancers Caused by Five Additional Types of HPV. Available online: http://www.fda.gov/newsevents/newsroom/pressannouncements/ucm426485.htm . Accessed 15 Feb 2016).Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [43] European Medicines Agency—News and Events—Gardasil 9 Offers Wider Protection against Cancers Caused by Human Papillomavirus (HPV). Available online: http://www.ema.europa.eu/ema/index.jsp?curl=pages/news_and_events/news/2015/03/news_detail_002295.jsp&mid=WC0b01ac058004d5c1 . Accessed 15 Feb 2016.Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

Probably not a substantial claim: may not pass S3 (load-bearing).

Approximately more than 70% of worldwide invasive cervical cancer could be prevented by the available bivalent and quadrivalent HPV vaccines.

“Approximately, more than 70% worldwide ICC could be prevented by the available bivalent HPV vaccines-CervarixTM (GlaxoSmithKline Biologicals, Rixensart, Belgium) and quadrivalent HPV vaccine- Gardasil® (4vHPV) (Merck & Co., Inc., Kenilworth, NJ, USA) [26, 27].”

• cites [26] Sanjosé SD, Diaz M, Castellsagué X, et al. Worldwide prevalence and genotype distribution of cervical human papillomavirus DNA in women with normal cytology: a meta-analysis. Lancet Infect Dis. 2007;7(7):453–9. sourceNot checked — no full text of the source
• cites [27] Guan P, Howell-Jones R, Li N, Bruni L, et al. Human papillomavirus types in 115,789 HPV-positive women: A meta-analysis from cervical infection to cancer Int. J Cancer. 2012;131:2349–59. sourceNot checked — no full text of the source

Probably not a substantial claim: may not pass S2 (checkable).

This study offers baseline data for future research and post-vaccination surveillance in the region.

“This study also offers the baseline data for future research and post-vaccination surveillance in the region.”

May combine two claims.

The study was unable to assess HIV status or other diseases in participants, which could strongly influence HPV infection prevalence.

“We were unable to assess HIV status or another disease for our participants, which could strongly influence the prevalence of HPV infection.”

May combine two claims.

Rural residential area reflects poor socio-economic condition possibly related to lack of access to proper care, which facilitates HPV infection and persistence and increases cancer risk.

“Rural residential area reflects poor socio-economic condition possibly related to lack of access to proper care which facilitates infection and persistence of HPV and an increasing risk of cancer development [41].”

• cites [41] Mitchell S, Sekikubo M, Biryabarema C, Byamugisha J, Steinberg M, Jeronimo J, et al. Factors associated with high-risk HPV positivity in a low-resource setting in sub-Saharan Africa. Am J Obstet Gynecol. 2014;210(1):81.e1–7. sourceNot checked — no full text of the source

Classified as probably not a substantial claim.

Estimating the attribution of cervical cancer cases to HPV types is confusing because multiple genotypes can be present in the same tumor.

“To know the impact of a vaccine, estimating the attribution of cases to HPV types is confusing due to multiple genotypes present in the same tumor.”

Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing).

In rural Odisha, where women's sexual behavior is conservative, men with multiple sexual partners might be a major source of HPV infection in women.

“In rural Odisha where sexual conception and behavior of women are conservative, men possessing multiple sexual partners might be a major source of HPV infection in a female.”