Abstract
HIV-positive people showed a high oral prevalence of HPV-DNA and have a greater incidence of head and neck carcinomas compared to general population. We performed a molecular survey evaluating the presence of HPV-DNA in saliva of HIV-positive and HIV-negative subjects in order to quantify the risk represented by HIV-positivity. The sample was made up by 102 subjects: 40 HIV-positive, 32 HIV-negative with sexual risk behaviors (SRB) and 30 HIV-negative without risk factors. DNA was extracted from cellular pellets and HPV detection and genotyping were performed by PCR assays. In the HIV-positive group (of which 58.3% declared SRB) 33.33% of the sample were HPV-positive (33.33% to high-risk genotypes, 25.0% to low-risk genotypes and 41.66% to other genotypes). In the HIV-negative SRB group, HPV-positive subjects were 37.04% (60.0% to high risk genotypes, 20.0% to low risk genotypes, and 20.0% to other genotypes). Finally, in the control group, the HPV-positive subjects were 7.14% (50% to high-risk genotypes and 50% to low-risk genotypes). In the HIV group, concerning the HPV positivity, there was no significant difference between subjects with and without SRBs. In summary, we found a high oral HPV-DNA detection in HIV+ group, showing a strong relationship between HIV and HPV.
Highlights
Published: 26 August 2021Human Papilloma Viruses (HPV) and Human Immunodeficiency Virus (HIV) are both sexually transmitted viruses causing chronic infections with a significant burden worldwide [1,2,3] and characterised by a high negative impact on public health and individual social life [4,5,6]
The specimens were collected from 36 HIV-positive subjects (HIV+ group), aged between 22 and 59 years old (39.95 ± 10.86), of which 58.33% with
The higher prevalence of HPV infection that we found in HIV+ subjects with detectable viral load underlines a direct role of HIV, as confirmed by several studies [59,69,70,71,72,73,74,75] showing that the viral proteins gp120 and tat and the HIV-associated activation of inflammatory processes in the mucosal epithelium, can lead to the disruption of epithelial junctions, which may promote the penetration and/or dissemination of other viruses, including herpesviruses (HSV) and HPV
Summary
Published: 26 August 2021Human Papilloma Viruses (HPV) and Human Immunodeficiency Virus (HIV) are both sexually transmitted viruses causing chronic infections with a significant burden worldwide [1,2,3] and characterised by a high negative impact on public health and individual social life [4,5,6]. There are more than 100 different HPV-genotypes, grouped according their capacity to cause benign or malignant lesions in “low-risk HPV”. (Lr-HPV), including types 6, 11, 42, 43 and 44, and “high-risk HPV” (Hr-HPV), including the genotypes 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66 and 68 [9,10]. These viruses are characterized by a wide body distribution but they have been detected especially in cervical, ano-genital and oral lesions [11]. Based on GLOBOCAN data, about 2,2 million cancer cases (13% of global cancer incidence) are attributable to infections and HPV contributes for 690,000 new cases worldwide, including ano-genital cancers [13,14,15,16,17,18,19,20]
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