Jaimie Z. Shing (United States of America)
National Cancer Institute
Division of Cancer Epidemiology and Genetics
Jaimie Z. Shing is a postdoctoral fellow at the United States National Cancer Institute's Infections and Immunoepidemiology Branch. Dr. Shing received a dual B.S. in health promotion and behavior/M.P.H. with a concentration in epidemiology in 2017 from the University of Georgia, where she was inducted into the Delta Omega Honorary Society in Public Health. In 2021, Dr. Shing earned her Ph.D. in epidemiology from Vanderbilt University, Nashville, Tennessee. Her doctoral research focused on assessing population-level human papillomavirus (HPV) vaccine impact and improving surveillance of cervical premalignant lesions using claims-based prediction models. At the National Cancer Institute, Dr. Shing's research focuses on 1) examining HPV vaccine impact, effectiveness, and efficacy on HPV-driven cancers, and 2) elucidating health disparities in infection-related cancers among marginalized communities, specifically among Asian American and Native Hawaiian and other Pacific Islander populations.

Moderator of 1 Session

 Conference Calendar

PUBLIC HEALTH ORAL: VACCINATION 1

Chair(s)
Session Type
Public Health
Date
Wed, Apr 19, 2023
Session Time
09:45 AM - 10:45 AM
Room
Ballroom C

Presenter of 3 Presentations

 Conference Calendar

PANEL DISCUSSION

Session Name
EARLY CAREER RESEARCHERS SESSION 2: PUBLISH OR PERISH: THE FUTURE OF ACADEMIC PUBLISHING
Session Type
Early Career Researchers
Date
Wed, Apr 19, 2023
Session Time
07:00 AM - 08:00 AM
Room
206
Presentation Type
ONSITE
Presenter
Lecture Time
07:05 AM - 08:00 AM

HPV VACCINATION TO PREVENT INVASIVE CERVICAL CANCER

Session Name
PUBLIC HEALTH WORKSHOP 01: HPV VACCINATION FOR PREVENTION OF CERVICAL CANCER
Session Type
Public Health
Date
Mon, Apr 17, 2023
Session Time
02:00 PM - 03:30 PM
Room
Ballroom C
Presentation Type
ONSITE
Presenter
Lecture Time
02:34 PM - 02:52 PM

DIFFERENTIAL HPV16/18 VACCINE EFFICACY AGAINST HPV31 BY VARIANTS IN THE L1 SEQUENCE UP TO 11-YEARS POST-VACCINATION IN THE COSTA RICA HPV VACCINE TRIAL

Session Name
PUBLIC HEALTH ORAL: VACCINATION 3
Session Type
Public Health
Date
Wed, Apr 19, 2023
Session Time
03:45 PM - 04:45 PM
Room
Ballroom C
Presentation Type
ONSITE
Presenter
Lecture Time
04:35 PM - 04:45 PM

Abstract

Introduction

The AS04-adjuvanted human papillomavirus (HPV)-16/18 vaccine (Cervarix®) induces partial cross-protection against phylogenetically-related HPV genotypes, which may be driven by variant-level [e.g., lineage and single nucleotide polymorphism (SNP)] heterogeneity. We examined vaccine efficacy (VE) across cross-protected genotype variants in the Costa Rica HPV Vaccine Trial.

Methods

We included 2846 HPV-vaccinated women (3-doses) and 5465 HPV-unvaccinated women [combined group of hepatitis-A-vaccinated women (3-doses) during the randomized study period (years 1-4) and all women in the screening-only, unvaccinated group during the observational study period (years 4-11)]. The analytical period started two-years post-vaccination (to ensure exclusion of infections present prior to vaccination) through 11-years. Outcomes were HPV31/33/35/45 detection among women HPV-negative for these types prior to the analytical period. Using viral whole genome sequencing, lineages were assigned based on the maximum likelihood tree topology. VEs and VE-ratios were evaluated by lineage and by SNPs in the L1 region.

Results

VE against HPV31 was 76.8% [95% confidence interval (95%CI)=67.5%-84.5%] overall. Compared to VE against HPV31-lineage-A (VE=90.0%; 95%CI=77.3%-98.0%), VE against HPV31-lineage-B (VE=61.6%; 95%CI=26.2%-83.1%) was significantly lower (VE-ratio=0.68; 95%CI=0.29-0.96), while VE against HPV31-lineages-B and-C were similar (VE-ratio=1.22; 95%CI=0.84-2.85) (Table 1). VE against HPV31 significantly differed at nucleotide positions 5921/6238/6367/6372/6772/6796 of L1 (all are lineage-defining positions). One of these SNPs was a nonsynonymous substitution at position 6372, and nucleotide A (defining lineages B/C) had significantly lower VE compared to nucleotide C (defining lineage A) (VE-ratio=0.79; 95%CI=0.65-0.94). Analyses for HPV33/35 were underpowered due to low prevalence of lineage-specific endpoints. VE against HPV45 was 83.0% (95%CI=73.8%-90.4%) overall and was similar between lineages and for L1 SNPs.

table 1.png

Conclusions

Cross-protection afforded by Cervarix against HPV31 may be driven by high VE against lineage-A compared to lower VE against lineages-B/C. An important SNP impacting HPV31 VE may be position 6372, located within the FG loop of L1, established to be important in neutralization.

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