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.

Condyloma acuminata (CA), or genital warts, are benign proliferative epidermal or mucous lesions that are caused by infection with human papillomavirus (HPV), mainly the low-risk types 6 and 11. HPV variants are defined as viral sequences that share identity in the nucleotide sequence of the L1 gene greater than 98%. Based on this criterion, HPV6 and 11 variant lineages have been studied, and there are ongoing attempts to correlate these genetic variants with different clinical findings of infection. Therefore, the aims of this study were to detect variants and nucleotide alterations present in the E6 regions of HPV types 6 and 11 found in CA samples, to correlate the HPV presence with the clinical-pathological data of the patients, and to determine phylogenetic relationships with variants from other places in the world. The E6 regions of 25 HPV6 samples and 7 HPV11 samples from CA were amplified using PCR with specific primers. The products were ligated to a cloning vector and five colonies of each sample were sequenced to observe the nucleotide alterations. Twelve samples were identified as the HPV6B3 variant, presenting the mutation (guanine) G474A (adenine), and one of them also showed the mutation (thymine) T369G. The other 13 patients were positive for HPV6B1 without nucleotide alterations. In the analysis of the HPV11 samples, all patients showed the mutations T137C and (cytosine) C380T. One patient also presented the nucleotide alteration T410C. None of the mutations found in the 32 analyzed samples resulted in amino acid changes. Patient age, local occurrence, and HIV infection did not show significant association with HPV infection. Besides, the data found in this study did not show a relationship with the geographical region of isolation when compared to other data from different regions of the world. In this way, despite the nucleotide alterations found, it was not possible to observe amino acid changes and variants grouping according to geographical region.