How Much Does HIV Positivity Affect the Presence of Oral HPV? A Molecular Epidemiology Survey

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.

Status and Determinants of Early Detection of Oral Premalignant and Malignant Lesions in India

“…Therefore, integrated testing and anti-retroviral treatment centres (ICTC/ART) are important oral cancer screening opportunities. 90 , 91 The health care providers trained for both the periodontal assessment for non-canonical pathologies and oral cancer screening along with appropriate referral and management will improve the screening coverage and outcomes.…”

A systematic review on the molecular and clinical association between Human Papillomavirus and Human Immunodeficiency Virus co‐infection in Head, Neck and Oral squamous cell carcinoma

“…Additionally, HIV/AIDS patients were diagnosed with HPV (HPV-16) DNA in the oral cavity. 4 Regardless of gender, HIV-HPV coinfection is diagnosed in both males and females. Some studies pointed out that it is prevalent among homosexuals and lifestyles.…”

“…It is widely known that HPV infection causes p53 and pRb to be degraded and rendered inactive, respectively, and this activity drives tumours' formation and development. 68,69 However, according to two studies, HPV pseudo-virions and virus-like particles (VLPs, also known as pseudo-virions), which lack the E6/E7 genes or their 4 The HIV PI (protease inhibitor) and HPV virus proteins both regulate the cyclin D which influences the transcription factor E2F which further triggers the downstream genes which are needed for the cell cycle to change from G1 phase to S phase. Therefore, pRb binding with E7 protein hinders the tumour repressor role it plays when it is in the hypo phosphorylated stage.…”

“…18 The poor management of HPV-associated risk or HPV infection in the oral region generally leads to the development of cancer in the oral region of the human body. 4,21 HPV interferes with many cellular pathways to cause several typical symptoms, which can lead to malignancy. Signalling pathways, immune pathways, cell cycle regulation, DNA repair, DNA methylation, and protein synthesis are some of the widely studied contributions to HPV-associated tumour formation.…”

“…It was divided based on the ability to cause benign or malignant tumours and skin lesions (warts). 4 The severity of HPV is classified as low-risk and high-risk HPV. High-risk variants are capable of causing malignancies among which HPV 16,18,31, and 56 are a few widely analysed genotypes.…”