{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["McDonald JA"],"funding":["Herbert Irving Comprehensive Cancer Center","NIEHS NIH HHS","NIEHS Center for Environmental Health in Northern Manhattan","NCI NIH HHS","National Institutes of Health"],"pagination":["766-778"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8096486"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["190(5)"],"pubmed_abstract":["Earlier pubertal development is only partially explained by childhood body mass index; the role of other factors, such as childhood infections, is less understood. Using data from the LEGACY Girls Study (North America, 2011-2016), we prospectively examined the associations between childhood viral infections (cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV) 1, HSV2) and pubertal timing. We measured exposures based on seropositivity in premenarcheal girls (n = 490). Breast and pubic hair development were classified based on mother-reported Tanner Stage (TS) (TS2+ compared with TS1), adjusting for age, body mass index, and sociodemographic factors. The average age at first blood draw was 9.8 years (standard deviation, 1.9 years). The prevalences were 31% CMV+, 37% EBV+, 14% HSV1+, 0.4% HSV2+, and 16% for both CMV+/EBV+ coinfection. CMV+ infection without coinfection was associated with developing breasts an average of 7 months earlier (hazard ratio (HR) = 2.12, 95% confidence interval (CI): 1.32, 3.40). CMV infection without coinfection and HSV1 and/or HSV2 infection were associated with developing pubic hair 9 months later (HR = 0.41, 95% CI: 0.24, 0.71, and HR = 0.42, 95% CI: 0.22, 0.81, respectively). Infection was not associated with menarche. If replicated in larger cohorts with blood collection prior to any breast development, this study supports the hypothesis that childhood infections might play a role in altering pubertal timing."],"journal":["American journal of epidemiology"],"pubmed_title":["Common Childhood Viruses and Pubertal Timing: The LEGACY Girls Study."],"pmcid":["PMC8096486"],"funding_grant_id":["K01 CA186943","R01 CA138822","CA138819","R01 CA138844","CA186943","CA138638","CA138844","R01 CA138819","CA138822","P30 ES009089","P30 CA013696","R01 CA138638"],"pubmed_authors":["Santella RM","Knight JA","Schooling CM","Andrulis IL","Wei Y","Chung WK","Bradbury AR","Buys SS","Terry MB","Cherubin S","McDonald JA","Schwartz LA","Daly MB","Goldberg M","John EM"],"additional_accession":[]},"is_claimable":false,"name":"Common Childhood Viruses and Pubertal Timing: The LEGACY Girls Study.","description":"Earlier pubertal development is only partially explained by childhood body mass index; the role of other factors, such as childhood infections, is less understood. Using data from the LEGACY Girls Study (North America, 2011-2016), we prospectively examined the associations between childhood viral infections (cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV) 1, HSV2) and pubertal timing. We measured exposures based on seropositivity in premenarcheal girls (n = 490). Breast and pubic hair development were classified based on mother-reported Tanner Stage (TS) (TS2+ compared with TS1), adjusting for age, body mass index, and sociodemographic factors. The average age at first blood draw was 9.8 years (standard deviation, 1.9 years). The prevalences were 31% CMV+, 37% EBV+, 14% HSV1+, 0.4% HSV2+, and 16% for both CMV+/EBV+ coinfection. CMV+ infection without coinfection was associated with developing breasts an average of 7 months earlier (hazard ratio (HR) = 2.12, 95% confidence interval (CI): 1.32, 3.40). CMV infection without coinfection and HSV1 and/or HSV2 infection were associated with developing pubic hair 9 months later (HR = 0.41, 95% CI: 0.24, 0.71, and HR = 0.42, 95% CI: 0.22, 0.81, respectively). Infection was not associated with menarche. If replicated in larger cohorts with blood collection prior to any breast development, this study supports the hypothesis that childhood infections might play a role in altering pubertal timing.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 May","modification":"2025-04-04T11:00:45.923Z","creation":"2025-04-04T11:00:45.923Z"},"accession":"S-EPMC8096486","cross_references":{"pubmed":["33128063"],"doi":["10.1093/aje/kwaa240"]}}