Evidence map›Paper›PMID 35450082›Full record

ArticleOpen forum infectious diseases2022

Environmental Factors for Epstein-Barr Virus Reactivation in a High-Risk Area of Nasopharyngeal Carcinoma: A Population-Based Study.

Yufeng Chen, Ellen T Chang, Qing Liu, Yonglin Cai, Zhe Zhang, Guomin Chen, Qi-Hong Huang, Shang-Hang Xie, Su-Mei Cao, Wei-Hua Jia and 8 more

Open access · goldAbstract read
In one paragraph

Article in Open forum infectious diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. mOncogene · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 8 institutions in 4 countries.

Yufeng ChenDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Ellen T ChangExponent, Inc., Center for Health Sciences, Menlo Park, California, USA.ORCID https://orcid.org/0000-0002-7169-157X
Qing LiuDepartment of Cancer Prevention Center, Sun Yat-sen University Cancer Center, Guangzhou, China.
Yonglin CaiDepartment of Clinical Laboratory, Wuzhou Red Cross Hospital, Wuzhou, China.
Zhe ZhangDepartment of Otolaryngology-Head & Neck Surgery, First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Guomin ChenState Key Laboratory for Infectious Diseases Prevention and Control, Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China.
Qi-Hong HuangSihui Cancer Institute, Sihui, China.
Shang-Hang XieDepartment of Cancer Prevention Center, Sun Yat-sen University Cancer Center, Guangzhou, China.
Su-Mei CaoDepartment of Cancer Prevention Center, Sun Yat-sen University Cancer Center, Guangzhou, China.
Wei-Hua JiaState Key Laboratory of Oncology in South China & Collaborative Innovation Center for Cancer Medicine & Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Guangzhou, China.ORCID https://orcid.org/0000-0002-0528-8715
Yuming ZhengDepartment of Clinical Laboratory, Wuzhou Red Cross Hospital, Wuzhou, China.
Yancheng LiCangwu Institute for Nasopharyngeal Carcinoma Control and Prevention, Wuzhou, China.
Longde LinKey Laboratory of High-Incidence-Tumor Prevention & Treatment (Guangxi Medical University), Ministry of Education, Nanning, China.
Ingemar ErnbergDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0001-6518-1648
Guangwu HuangDepartment of Otolaryngology-Head & Neck Surgery, First Affiliated Hospital of Guangxi Medical University, Nanning, China.ORCID https://orcid.org/0000-0002-7376-5691
Yi-Xin ZengState Key Laboratory of Oncology in South China & Collaborative Innovation Center for Cancer Medicine & Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Guangzhou, China.
Hans-Olov AdamiDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Weimin YeDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Sun Yat-sen University · CNGuangxi Medical University · CNKarolinska Institutet · SEWuzhou University · CNExponent (United States) · USFujian Medical University · CNTumor Hospital of Guangxi Medical University · CNUniversity of Oslo · NO

Funding

Gene-environment EBV Interactions in the Etiology of Nasopharyngeal Carcinoma (NPR01CA115873 · NCI · HARVARD SCHOOL OF PUBLIC HEALTH · PI ADAMI, HANS-OLOV · 2008 to 2013
$2.4M
NCI NIH HHS R01 CA115873
6 · The paper itself

Abstract

Background: Epstein-Barr virus (EBV) reactivation from latent to lytic infection has been considered as a key step in nasopharyngeal carcinoma oncogenesis. However, epidemiological evidence regarding environmental risk factors for EBV reactivation on a population level remains largely lacking. Methods: We enrolled 1916 randomly selected adults from the general population of Guangdong and Guangxi, China, from 2010 to 2014. Information on environmental factors was collected via a structured interview. Serum immunoglobulin A antibodies against EBV viral capsid antigen and nuclear antigen 1 were measured by enzyme-linked immunosorbent assay to evaluate EBV reactivation status. We used logistic regression to calculate odds ratios (ORs) with 95% confidence intervals (CIs) for the associations of EBV reactivation with various environmental factors. Results: No associations were observed between EBV reactivation and extensive environmental factors, including alcohol or tea drinking, a history of chronic ear/nose/throat diseases, use of medications or herbs, consumption of salted fish or preserved foods, oral hygiene, sibship structure, and various residential and occupational exposures. Only cigarette smoking was associated with EBV reactivation (current smokers vs never smokers; OR = 1.37; 95% CI = 1.02-1.83), with positive exposure-response trends with increasing intensity, duration, and pack-years of smoking. Conclusions: Consistent with previous studies, we found an association between cigarette smoking and EBV reactivation. Other examined exposures were not associated with EBV reactivation. These null results could suggest either more complex interactions between exposures and EBV reactivation or a predominant role of host and/or viral genetic variation.

Indexed as

EBV reactivationenvironmental factorsEpstein-Barr virusnasopharyngeal carcinomarisk factorserology

Identifiers

PMID35450082
PMCPMC9017372
OpenAlexW4220833816

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.