High prevalence of human papillomavirus and European variants of HPV 16 infecting concomitantly to cervix and oral cavity in HIV positive women

Abstract

Human papillomavirus (HPV) is the most common sexually transmitted infection worldwide, with a high prevalence and high transmissibility. High-risk HPV (hrHPV) infection is the primary cause of cervical cancer. The HPV variants present in the uterine cervix and oral cavity of HIV+ women have not been described. Objective Identify the prevalence of HPV infections in the uterine cervix and oral cavity and HPV16 variants in HIV+ women. Methods A total of 174 HIV+ women attended an HIV+ specialized clinic in Mexico City. Cells were obtained from the oral cavity and cervix to extract DNA. Polymerase chain reaction (PCR) was used to amplify the HPV sequence with generic primers. We detected specific HPV types using the INNO-LiPA HPV Genotyping Extra II Kit (INNOGENETICS). The

Cervical Squamous Intraepithelial Lesions are Associated with Changes in the Vaginal Microbiota of Mexican Women

“…However, these findings are not uniform across studied populations, because, despite the fact that Latin American countries have a high prevalence of HPV and cervical cancer are one of the main causes of death in women in these areas (3, 23–25), including Mexico (7, 9), most of the studies have been conducted in developed countries (26). Likewise, the projected demographic changes in Latin America imply that the current burden of new cervical cancer cases will increase in the next 20 years (2, 27).…”

“…Some of these changes are responsible for increasing the levels of mucin-degrading enzymes, which may play a role in the degradation of the mucous layer that covers the vaginal and cervical epithelium and endocervical mucus (20,21). There is evidence of HPV evasion or infection mechanisms that support that microorganisms such as Sneathia, Anaerococcus, Fusobacterium and Gardnerella are implicated with higher frequency and severity of disease, potentially resulting in pre-cancerous and cancerous cervical lesions (22) However, these findings are not uniform across studied populations, because, despite the fact that Latin American countries have a high prevalence of HPV and cervical cancer are one of the main causes of death in women in these areas (3,(23)(24)(25), including Mexico (7,9), most of the studies have been conducted in developed countries (26). Likewise, the projected demographic changes in Latin America imply that the current burden of new cervical cancer cases will increase in the next 20 years (2,27).…”

“…After HPV infection and persistency, squamous intraepithelial lesions (SIL) development may occur, which may heal or persist and evolve to cancer (1). Despite overwhelming evidence that certain subtypes of HPV are the main causative agents of SIL development and progression to cervical cancer, it is also well-established that HPV alone is not sufficient to induce cervical malignant transformation (4–7). Many factors have been associated with the appearance SIL such as, intermenstrual bleeding, multiparity, use of contraceptives, multiple sexual partners, and smoking (8).…”

“…Likewise, the projected demographic changes in Latin America imply that the current burden of new cervical cancer cases will increase in the next 20 years (2, 27). The evidence observed so far suggests that the ethnic and sociodemographic factors that influence difference in vaginal microbiome composition may also underlie dysbiotic patterns linked to HPV infection and cervical cancer across different Latin America women populations (3,7,9, 23–25). Therefore, there is a growing need for more evidence in Latin America to demonstrate the association between vaginal microbiota patterns and HPV infection and its relationship with the progression of SIL to cervical cancer.…”

E6/E7 Variants of Human Papillomavirus 16 Associated with Cervical Carcinoma in Women in Southern Mexico

“…In Mexico City, the variants E-G131 (A1) E-G350, E-C188, E-A176 (A2), NA1 (D1), AA-a, and AA-c (D2) were reported and among them the AA variants are more oncogenic than the E variants [ 17 ]. In other studies, only the E-G350 (A2) variant was reported [ 18 , 19 ]. In southeastern Mexico, E-Prototype (A1), E-G350 (A2), Af2 (C), and AA (D2) were reported in samples from women with CC [ 20 ].…”