Abstract
Human papillomavirus type 16 (HPV16) is the most prevalent HPV type causing cervical cancers. Herein, using 1597 full genomes, we systemically investigated the mutation profiles, surface protein glycosylation sites and the codon usage bias (CUB) of HPV16 from different lineages and sublineages. Multiple lineage- or sublineage-conserved mutation sites were identified. Glycosylation analysis showed that HPV16 lineage D contained the highest number of different glycosylation sites from lineage A in both L1 and L2 capsid proteins, which might lead to their antigenic distances between the two lineages. CUB analysis showed that the HPV16 open reading frames (ORFs) preferred codons ending with A/T. The CUB of HPV16 ORFs was mainly affected by natural selection except for E1, E5 and L2. HPV16 only shared some of the preferred codons with humans, which might help reduce competition in translational resources. These findings increase our understanding of the heterogeneity between HPV16 lineages and sublineages, and the adaptation mechanism of HPV in human cells. In summary, this study might facilitate HPV classification and improve vaccine development and application.
Highlights
We aimed to explore the genomic mutation profiles and the glycosylation site distribution for surface proteins in different Human papillomavirus type 16 (HPV16) sublineages
HPV16 was adapted in using the host preferred by HPV16. These results suggested that HPV16 was adapted in using the host translational machinery, but protein producproductranslational machinery, and avoided avoided over over competition competition with with cellular cellular protein tion to reduce stimulation of the host immune response, which would help its persistence tion to reduce stimulation of the host immune response, which would help its persistence in in humans
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Summary
Academic Editors: Lisa Mirabello and Meredith Yeager. Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Human papillomaviruses (HPVs) cause mucosal and cutaneous infections. More than 200 different HPV types have been identified According to their carcinogenicity, HPVs can be divided into high-risk and low-risk types. High-risk types include HPV16, 18, 31, 33, 34, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68 and 70 [1], which can cause cervical cancer. HPV16 is the dominant type and accounts for above 50% of cervical cancer cases [2,3]
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