TY - JOUR
T1 - Common childhood viruses and pubertal timing
T2 - The LEGACY girls study
AU - McDonald, Jasmine A.
AU - Cherubin, Sinaida
AU - Goldberg, Mandy
AU - Wei, Ying
AU - Chung, Wendy K.
AU - Schwartz, Lisa
AU - Knight, Julia A.
AU - Schooling, C. Mary
AU - Santella, Regina
AU - Bradbury, Angela
AU - Buys, Saundra S.
AU - Andrulis, Irene L.
AU - John, Esther M.
AU - Daly, Mary
AU - Terry, Mary Beth
N1 - © The Author(s) 2020. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: [email protected].
PY - 2021
Y1 - 2021
N2 - 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.
AB - 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.
KW - Adolescent
KW - Body Mass Index
KW - Child
KW - Coinfection
KW - Cytomegalovirus Infections/epidemiology
KW - Epstein-Barr Virus Infections/epidemiology
KW - Female
KW - Herpes Simplex/epidemiology
KW - Humans
KW - North America/epidemiology
KW - Prevalence
KW - Prospective Studies
KW - Puberty, Precocious/physiopathology
KW - Puberty/physiology
UR - http://www.scopus.com/inward/record.url?scp=85103949689&partnerID=8YFLogxK
U2 - 10.1093/aje/kwaa240
DO - 10.1093/aje/kwaa240
M3 - Article
C2 - 33128063
SN - 0002-9262
VL - 190
SP - 766
EP - 778
JO - American Journal of Epidemiology
JF - American Journal of Epidemiology
IS - 5
ER -