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How Enhancing Immunity to Low-Risk HPV Could Cure Recurrent Respiratory Papillomatosis.

ABSTRACT: Recurrent respiratory papillomatosis (RRP) is currently treated with repeat surgical resection of papillomatous disease that does not address the fundamental underlying issue of chronic infection with low-risk human papillomavirus. Here, we review the biology and immunology of low-risk human papillomavirus (HPV) infections. Antiviral or antiangiogenic adjuvant treatments similarly address the papillomatous disease itself but do not activate HPV immunity. It is likely that only through immune-mediated clearance of low-risk HPV infection can patients with RRP be cured. In some patients, this occurs spontaneously. In others with more aggressive disease, adjuvant immunotherapy to activate immunity may be needed. Based on current understanding of antiviral immune responses, the only rational strategy to clear HPV-infected epithelial cells is through activation of the T-lymphocyte arm of the adaptive immune response. Translation of immunotherapies that are Food and Drug Administration-approved or under clinical study for cancer, such as immune checkpoint blockade or engineered therapeutic vaccines, may provide a path toward tolerable and efficacious adjuvant immunotherapy for RRP. LEVEL OF EVIDENCE: NA Laryngoscope, 131:2041-2047, 2021.

SUBMITTER: Bai K

PROVIDER: S-EPMC8363585 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:In this cohort study we examined whether gender, age at onset, observation time or human papillomavirus (HPV) genotype are risk factors for an aggressive clinical course in Recurrent Respiratory Papillomatosis (RRP). Clinical data from patient records comprised gender, age at onset, date of first endolaryngeal procedure with biopsy, date of last follow-up, total number of endolaryngeal procedures, and complications during the observation period. Disease was defined as juvenile (JoRRP) or adult onset (AoRRP) according to whether the disease was acquired before or after the age of 18. Aggressive disease was defined as distal spread, tracheostomy, four surgical operations annually or >10 surgeries in total. DNA was extracted from formalin-fixed paraffin-embedded tissue. HPV genotyping was performed by quantitative PCR assay identifying 15 HPV genotypes. The study included 224 patients. The majority were males (141/174 in AoRRPs and 31/50 in JoRRPs; p = 0.005). The median follow-up from initial diagnosis was 12.0 years (IQR 3.7-32.9) for JoRRPs and 4.0 years (IQR 0.8-11.7) for AoRRPs. The disease was more aggressive in juveniles than adults (p<0.001), a difference that disappeared after 10 years' observation. JoRRPs with aggressive disease were younger at onset (mean difference 4.6 years, 95%CI [2.4, 6.8], p = 0.009). HPV6 or -11 was present in all HPV-positive papillomas. HPV11 was more prevalent in aggressive disease, and HPV6 in non-aggressive disease (p<0.001). Multiple logistic regression revealed that only age at onset (OR = 0.69, 95% CI [0.53, 0.88], p = 0.003) was associated with aggressive disease in juveniles, while HPV11 (OR = 3.74, 95% CI [1.40, 9.97], p = 0.008) and observation time >10 years (OR = 13.41, 95% CI [5.46, 32.99[, p<001) were risk factors in adults. In conclusion, the only significant risk factor for developing aggressive disease in JoRRPs was age at onset, but both HPV11 and observation time >10 years were risk factors for an aggressive disease course in AoRRPs.

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How Enhancing Immunity to Low-Risk HPV Could Cure Recurrent Respiratory Papillomatosis.

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