Prevalence of anal infection due to high-risk human papillomavirus and analysis of E2 gene integrity among women with cervical abnormalities

González-Losa, Marı́a del Refugio; Puerto-Solı́s, Marylı́n; Ayora-Talavera, Guadalupe; Gómez-Carvallo, Jesús; Euán-López, Alejandra; Cisneros-Cutz, José I.; Rosado-López, Ariel; Salazar, Jesúa Echeverría; Conde-Ferráez, Laura

doi:10.1016/j.eimc.2016.11.010

Cited by 7 publications

(4 citation statements)

References 27 publications

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“…Discrepancies found in E6 splice patterns in diverse study models could be due to the presence of specific regulatory factors depending of the cell context or to differences in the physical state of the HPV genome during the progression of an HPV infection to cancer. The loss of E2 protein due to viral genome integration [ 122 ] could also affect the splicing process, since E2 is a mRNA binding protein which regulates E6 splicing [ 99 ]. Moreover, since HPV genome integration occurs at distinct sites in the host genome [ 75 ], it cannot be discarded that in some cases host genes involved in splicing regulation could be disrupted and therefore change the splicing patterns.…”

Section: Discussionmentioning

confidence: 99%

The Role of E6 Spliced Isoforms (E6*) in Human Papillomavirus-Induced Carcinogenesis

Olmedo-Nieva

Muñoz-Bello

Contreras‐Paredes

et al. 2018

Viruses

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Persistent infections with High Risk Human Papillomaviruses (HR-HPVs) are the main cause of cervical cancer development. The E6 and E7 oncoproteins of HR-HPVs are derived from a polycistronic pre-mRNA transcribed from an HPV early promoter. Through alternative splicing, this pre-mRNA produces a variety of E6 spliced transcripts termed E6*. In pre-malignant lesions and HPV-related cancers, different E6/E6* transcriptional patterns have been found, although they have not been clearly associated to cancer development. Moreover, there is a controversy about the participation of E6* proteins in cancer progression. This review addresses the regulation of E6 splicing and the different functions that have been found for E6* proteins, as well as their possible role in HPV-induced carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

The Role of E6 Spliced Isoforms (E6*) in Human Papillomavirus-Induced Carcinogenesis

Olmedo-Nieva

Muñoz-Bello

Contreras‐Paredes

et al. 2018

Viruses

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“…Women living with HIV and those with a history of cervical cancer are considered at a higher risk of developing anal pathologies; the anatomical proximity of the affected regions may play a role [ 27 ]. In a previous study from our research group involving 311 women with abnormal cervical cytology, HR-HPV (16, 18, 58, and 45) was found in 30.8% (96/311) of anal samples, and 11.25% had the same genotypes in both sites [ 28 ]. In the present study, 33.3% of our small group of HIV+ women had a HPV infection in both anatomical sites, with high agreement in terms of genotypes.…”

Section: Discussionmentioning

confidence: 99%

Human Papillomavirus Genotypes Infecting the Anal Canal and Cervix in HIV+ Men and Women, Anal Cytology, and Risk Factors for Anal Infection

et al. 2023

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The incidence of anal intraepithelial neoplasias associated with HPV is rising worldwide. In the general population, this pathology is rare, but individuals living with HIV/AIDS are at a significantly higher risk. We aimed to study HPV infection and performed cytological screening to study the epidemiological and behavioral determinants in a group of men and women living with HIV from a region in Mexico with high HIV incidence. This was a cross-sectional study including adults living with HIV/AIDS performed in Merida (Mexico). We invited patients of public HIV/STD clinics and those affiliated with social organizations of people living with HIV to participate in the study. Participants responded to an instrument to assess their risky behaviors and clinical history. Swabs from the anal canal and cervix and anal cytology specimens were obtained by medical staff from women and by self-sampling from men. For the 200 participants, 169 men and 31 women, anal HPV PCR tests resulted in 59.8% positivity (62.6% of men and 45.2% of women), and 17 genotypes were identified. The most frequent high-risk (HR) types for the anal canal were: HPV33 (35.3%), HPV58 (20.6%), HPV66 (18.6%), HPV45 (17.6%), and HPV16 (14.7%). Multiple genotypes were found in over 80% of the participants. Receptive anal intercourse in the previous 12 months, inconsistent condom use, and detectable HIV titers (≥50 cc/mL) were associated with HPV infection (p < 0.05). Cytology (smears and liquid-based) identified that 34.6% of the participants had low-grade squamous intraepithelial lesions (LSILs), and 3.5% had high-grade squamous intraepithelial lesions (HSILs). Neither HPV nor lesions were associated with low CD4+ counts (<200 cells/mm3, p > 0.05). Of the women, 60% were infected in the cervix and 45% in the anal canal, with an agreement of at least one genotype in 90%. The HR-HPV types associated with HSILs were HPV66, 33, 52, 51, 45, 18, and 68.

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“…It was also reported that the prevalence of anal cancer increases according to cervical lesion grade, with the occurrence of 15% in lowgrade squamous intraepithelial lesions (LSIL) and 55% in microinvasive carcinoma [109]. However, in another study, it was reported no significant association between LSIL vs. HSIL/CC to anal HPV infection [110]. This suggests that there are multiple risk factors associated with the progression of anal malignancies along with HPV infections, which need to be explored further.…”

Section: Anal Cancermentioning

confidence: 99%

Human Papilloma Virus: An Unraveled Enigma of Universal Burden of Malignancies

Khan

Harshithkumar

et al. 2023

Pathogens

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HPV, or Human Papilloma Virus, has been the primary causative agent of genital warts and cervical cancer worldwide. It is a sexually transmitted infection mainly affecting women of reproductive age group, also infecting men and high-risk group individuals globally, resulting in high mortality. In recent years, HPV has also been found to be the major culprit behind anogenital cancers in both gender and oropharyngeal and colorectal cancers. Few studies have reported the incidence of HPV in breast cancers as well. For a few decades, the burden of HPV-associated malignancies has been increasing at an alarming rate due to a lack of adequate awareness, famine vaccine coverage and hesitancy. The effectiveness of currently available vaccines has been limited to prophylactic efficacy and does not prevent malignancies associated with post-exposure persistent infection. This review focuses on the current burden of HPV-associated malignancies, their causes and strategies to combat the growing prevalence of the cancers. With the advent of new technologies associated with treatment pertaining to therapeutic interventions and employing effective vaccine coverage, the burden of this disease may be reduced in the population.

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Prevalence of anal infection due to high-risk human papillomavirus and analysis of E2 gene integrity among women with cervical abnormalities

Cited by 7 publications

References 27 publications

The Role of E6 Spliced Isoforms (E6*) in Human Papillomavirus-Induced Carcinogenesis

The Role of E6 Spliced Isoforms (E6*) in Human Papillomavirus-Induced Carcinogenesis

Human Papillomavirus Genotypes Infecting the Anal Canal and Cervix in HIV+ Men and Women, Anal Cytology, and Risk Factors for Anal Infection

Human Papilloma Virus: An Unraveled Enigma of Universal Burden of Malignancies

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