Detection and genotyping of human papillomavirus (HPV) in HIV-infected women and its relationship with HPV/HIV co-infection

• Published in: Medicine (Baltimore) Vol. 97; no. 14; p. e9545
• Main Authors: Badial, Rodolfo Miglioli, Dias, Marina Carrara, Stuqui, Bruna, Melli, Patrícia Pereira dos Santos, Quintana, Silvana Maria, Bonfim, Caroline Measso do, Cordeiro, José Antônio, Rabachini, Tatiana, Calmon, Marilia de Freitas, Provazzi, Paola Jocelan Scarin, Rahal, Paula
• Format: Journal Article
• Language: English
• Published: United States The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved 01-04-2018; Wolters Kluwer Health
• Subjects: Adult; Cervix Uteri - virology; Coinfection - epidemiology; Coinfection - virology; Female; Genotype; HIV Infections - epidemiology; HIV Infections - virology; Human papillomavirus 16 - genetics; Humans; Middle Aged; Observational Study; Papillomaviridae - genetics; Papillomaviridae - growth & development; Papillomavirus Infections - epidemiology; Papillomavirus Infections - virology; Prevalence; Prospective Studies; Risk Factors; Uterine Cervical Neoplasms - virology; Viral Load
• ISSN: 0025-7974; 1536-5964
• DOI: 10.1097/MD.0000000000009545

HPV have been identified as high-risk and low-risk, depending on their association with the development of cancer. HPV infections can be facilitated by co-infection with HIV. Here, we investigated HPV prevalence and genotypes and the risk factors affecting HPV/HIV co-infection. Forty HIV-positive patients had 80 cervical swab samples collected in 2 consecutive years. Polymerase chain reaction and DNA direct sequencing were used to perform HPV genotyping. Statistical analyses were performed regarding risk factors for HPV/HIV co-infection and the occurrence of cervical lesions. HPV DNA was detected in 59 samples (73.75%), and high-risk HPVs were predominant (59.3%). The most prevalent type was HPV56 (17%), followed by HPV16 (15.3%). Patient age did not affect the risk of cervical cancer (P = .84) or HPV prevalence in different years (P = .25/P = .63). CD4 count also did not affect the risk for cervical lesions in the tested samples (P = .15/P = .28). Although the HIV viral load was not correlated with an increase in cervical lesion detection in the first group of analyzed samples (P = .12), it did affect cervical cancer risk in the group of samples analyzed in the following year (P = .045). HIV-infected patients presented a high prevalence of HPV co-infection, and HPV16 and HPV56 were the most prevalent genotypes. Considering this, it is possible that immunodeficiency can contribute to increased susceptibility to HPV56 infection in HIV-infected patients. The association between HIV viral load and the lesions also confirmed the importance of monitoring HIV/HPV co-infected patients with high HIV viral loads.