Mutation Profiles, Glycosylation Site Distribution and Codon Usage Bias of Human Papillomavirus Type 16

Liu, Wei; Li, Junhua; Du, Hongli; Ou, Zhihua

doi:10.3390/v13071281

Cited by 6 publications

(6 citation statements)

References 64 publications

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“…Conversely, yeast glycans tend to be larger high mannosylated structures 73,74 . However, while L1 is traditionally thought to be pauci-glycosylated 75 , emerging data suggest that alterations in n-linked glycosylation may represent a key HPV diversification 76 . Thus, the use of glycosylated HPV in this study may be important to capture antibody responses to this evasive biology.…”

Section: Discussionmentioning

confidence: 99%

Differences in HPV-specific antibody Fc-effector functions following Gardasil® and Cervarix® vaccination

et al. 2023

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Gardasil® (Merck) and Cervarix® (GlaxoSmithKline) both provide protection against infection with Human Papillomavirus 16 (HPV16) and Human Papillomavirus 18 (HPV18), that account for around 70% of cervical cancers. Both vaccines have been shown to induce high levels of neutralizing antibodies and are known to protect against progression beyond cervical intraepithelial neoplasia grade 2 (CIN2+), although Cervarix® has been linked to enhanced protection from progression. However, beyond the transmission-blocking activity of neutralizing antibodies against HPV, no clear correlate of protection has been defined that may explain persistent control and clearance elicited by HPV vaccines. Beyond blocking, antibodies contribute to antiviral activity via the recruitment of the cytotoxic and opsonophagocytic power of the immune system. Thus, here, we used systems serology to comprehensively profile Gardasil®- and Cervarix®- induced antibody subclass, isotype, Fc-receptor binding, and Fc-effector functions against the HPV16 and HPV18 major capsid protein (L1). Overall, both vaccines induced robust functional humoral immune responses against both HPV16 and HPV18. However, Cervarix® elicited higher IgG3 and antibody-dependent complement activating responses, and an overall more coordinated response between HPV16 and 18 compared to Gardasil®, potentially related to the distinct adjuvants delivered with the vaccines. Thus, these data point to robust Fc-effector functions induced by both Gardasil® and Cervarix®, albeit with enhanced coordination observed with Cervarix®, potentially underlying immunological correlates of post-infection control of HPV.

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Section: Discussionmentioning

confidence: 99%

Differences in HPV-specific antibody Fc-effector functions following Gardasil® and Cervarix® vaccination

et al. 2023

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“…A study analyzing numerous HPV 16 L1 sequences indicated that the A1 sublineage had the largest number of potential glycosylation sites. Some glycosylation sites were lineage‐specific with 27 glycosylation sites observed only in lineage A 127 . However, the relationship between glycosylation and HPV vaccine escape is not definite yet.…”

Section: Hpvmentioning

confidence: 97%

“…Some glycosylation sites were lineage-specific with 27 glycosylation sites observed only in lineage A. 127 However, the relationship between glycosylation and HPV vaccine escape is not definite yet. In addition, a mutation in connected regions of two loops could also induce structural changes since these antigenic epitopes of HPV are discontinuous.…”

Section: Limited Evidence and Mechanism Research Of Hpv Vaccine Escapementioning

confidence: 99%

Vaccine escape challenges virus prevention: The example of two vaccine‐preventable oncogenic viruses

Qu,

Sui,

2023

Journal of Medical Virology

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Over the years, the pace of developing vaccines for HBV and HPV has never stopped. After more than 30 years of application, the HBV vaccine has reduced 80% of hepatocellular carcinoma (HCC). However, vaccine escape variants occur under selective pressure induced by widespread vaccination and antiviral therapy, which results in fulminant infection and horizontal transmission. Several mechanisms have been studied to explain HBV vaccine escape, including vaccine escape mutations (VEMs) in the major hydrophilic region, which leads to a decrease in the binding ability to neutralize antibodies and is the primary escape mechanism, protein conformational and N‐linked glycosylation sites changes caused by VEMs, differences in genotype distribution, gene recombination, and some temporarily unknown reasons. However, effective solutions are still being explored. The HPV vaccine has also been proven to prevent 70%–90% of cervical cancer worldwide. Cases of HPV infection after being vaccinated have been observed in clinical practice. However, few researchers have paid attention to the mechanism of HPV vaccine escape. Thus, we reviewed the literature on vaccine escape of both HBV and HPV to discuss the mechanism of the virus escaping from vaccine protection and possible solutions to this problem. We analyzed the gap between studies of HPV and HBV and made prospects for further research in HPV vaccine escape.

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“…Within many developing nations, cervical cancer emerges as a prevalent malignancy in women, with around 99.7% of affected individuals concurrently harboring HPV [4]. The classification of HPV is determined by its level of pathogenicity, categorizing it into high-risk and low-risk types [5]. Continual infection by high-risk human papillomavirus (HR-HPV) is strongly linked to the initiation and advancement of cervical cancer [6].…”

Section: Introductionmentioning

confidence: 99%

Codon usage bias of human papillomavirus type 33 and 58: A comprehensive analysis

Tan,

Xie,

Jiang

et al. 2024

J Basic Microbiol

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Cervical cancer is closely linked to specific strains of human papillomavirus (HPV), notably HPV‐33 and HPV‐58, which exhibit a significant prevalence among women in China. Nevertheless, the codon usage bias in HPV‐33 and HPV‐58 is not well comprehended. The objective of this research is to analyze the codon usage patterns HPV‐33 and HPV‐58, pinpoint the primary factors that influence codon preference. The overall preference for codon usage in two HPV genotypes is not significant. Both HPV genotypes exhibit a preference for codons that end with A/U. The GC3 content for HPV‐33 is 25.43% ± 0.35%, and for HPV‐58, it is 29.44% ± 0.57%. Out of the 26 favored codons in HPV‐33 and HPV‐58 (relative synonymous codon usage (RSCU) > 1), 25 conclude with A/U. Principal component analysis (PCA) shows a tight clustering of the entire genome sequences of HPV‐33 and HPV‐58, suggesting a similarity in their RSCU preferences. Moreover, an examination of dinucleotide abundance indicated that translation selection influenced the development of a distinctive dinucleotide usage pattern in HPV‐33 and HPV‐58. Additionally, a combined analysis involving an effective number of codons plot, parity rule 2, and neutrality analysis demonstrated that, for HPV‐33 and HPV‐58, the primary determinant influencing codon usage preference is natural selection. HPV‐33 and HPV‐58 exhibit a restricted set of favored codons in common with humans, potentially mitigating competition for translation resources. Our discoveries could provide valuable perspectives on the evolutionary patterns and codon usage preferences of HPV‐33 and HPV‐58 viruses, contributing to the development and application of relevant HPV subtype vaccines.

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Mutation Profiles, Glycosylation Site Distribution and Codon Usage Bias of Human Papillomavirus Type 16

Cited by 6 publications

References 64 publications

Differences in HPV-specific antibody Fc-effector functions following Gardasil® and Cervarix® vaccination

Differences in HPV-specific antibody Fc-effector functions following Gardasil® and Cervarix® vaccination

Vaccine escape challenges virus prevention: The example of two vaccine‐preventable oncogenic viruses

Codon usage bias of human papillomavirus type 33 and 58: A comprehensive analysis

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