TY - JOUR
T1 - Congenital Cytomegalovirus and HIV Perinatal Transmission
AU - MPH for the NICHD HPTN 040 Study Team
AU - Adachi, Kristina
AU - Xu, Jiahong
AU - Ank, Bonnie
AU - Watts, D. Heather
AU - Camarca, Margaret
AU - Mofenson, Lynne M.
AU - Pilotto, Jose Henrique
AU - Joao, Esau
AU - Gray, Glenda
AU - Theron, Gerhard
AU - Santos, Breno
AU - Fonseca, Rosana
AU - Kreitchmann, Regis
AU - Pinto, Jorge
AU - Mussi-Pinhata, Marisa M.
AU - Machado, Daisy Maria
AU - Ceriotto, Mariana
AU - Morgado, Mariza G.
AU - Bryson, Yvonne J.
AU - Veloso, Valdilea G.
AU - Grinsztejn, Beatriz
AU - Mirochnick, Mark
AU - Moye, Jack
AU - Nielsen-Saines, Karin
AU - Szyld, Edgardo
AU - Marzo, Silvia
AU - Ferreira, Flavia Faleiro
AU - Kakehasi, Fabiana
AU - Lira, Rita
AU - de Fraga, Carla Franceschini
AU - Coelho, Debora Fernandes
AU - Sanseverino, Alberto
AU - Ribeiro, Luis Carlos
AU - Santos Cruz, M. Leticia
AU - Martins, Ezequias
AU - de Menezes, Jacqueline Anita
AU - Torres Salgado, Luisa Andrea
AU - Cordovil, Ana Valeria
AU - Gouveia, Andréa
AU - Mazzucanti, Priscila
AU - Ribeiro, Jorge Eurico
AU - Duarte, Geraldo
AU - Aparecida, Adriana
AU - Barbaro, Tiraboschi
AU - Vieira, Carolina Sales
AU - Succi, Regina
AU - Agwu, Allison
AU - Anderson, Jean
AU - Ellen, Jonathan
AU - Hutton, Nancy
N1 - Funding Information:
The NICHD HPTN 040 study was supported by NICHD Contract # HHSN267200800001C (NICHD Control # N01-HD-8-0001) and U01 AI047986 (Brazilian AIDS Prevention Trials International Network), NIAID/ NIH. Overall support for the International Maternal Pediatric Adolescent AIDS Clinical Trials Group (IMPAACT) was provided by the National Institute of Allergy and Infectious Diseases (NIAID) U01 AI068632, UM1AI068632 (IMPAACT LOC), UM1AI068616 (IMPAACT SDMC) and UM1AI106716 (IMPAACT LC), with co-funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the National Institute of Mental Health (NIMH) AI068632. The original parent study was supported in part by Boehringer Ingelheim Pharmaceuticals Inc. and GlaxoSmithKline, on behalf of ViiV Healthcare. Support was also provided by the UCLA Chil-dren’s Discovery and Innovation Institute through the Harry Winston Fel-lowship Award, the UCLA AIDS Institute, the UCLA Center for AIDS Research (CFAR) NIH/ NIAID AI02869 and AI28697, and the UCLA Pediatric AIDS Coalition.
Funding Information:
The NICHD HPTN 040 study was supported by NICHD Contract # HHSN267200800001C (NICHD Control # N01-HD-8-0001) and U01 AI047986 (Brazilian AIDS Prevention Trials International Network), NIAID/ NIH. Overall support for the International Maternal Pediatric Adolescent AIDS Clinical Trials Group (IMPAACT) was provided by the National Institute of Allergy and Infectious Diseases (NIAID) U01 AI068632, UM1AI068632 (IMPAACT LOC), UM1AI068616 (IMPAACT SDMC) and UM1AI106716 (IMPAACT LC), with co-funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the National Institute of Mental Health (NIMH) AI068632. The original parent study was supported in part by Boehringer Ingelheim Pharmaceuticals Inc. and GlaxoSmithKline, on behalf of ViiV Healthcare. Support was also provided by the UCLA Children?s Discovery and Innovation Institute through the Harry Winston Fellowship Award, the UCLA AIDS Institute, the UCLA Center for AIDS Research (CFAR) NIH/ NIAID AI02869 and AI28697, and the UCLA Pediatric AIDS Coalition.
Publisher Copyright:
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
PY - 2018/10/1
Y1 - 2018/10/1
N2 - Background: Congenital cytomegalovirus (CMV) infection (cCMV) is an important cause of hearing loss and cognitive impairment. Prior studies suggest that HIV-exposed children are at higher risk of acquiring cCMV. We assessed the presence, magnitude and risk factors associated with cCMV among infants born to HIV-infected women, who were not receiving antiretrovirals during pregnancy. Methods: cCMV and urinary CMV load were determined in a cohort of infants born to HIV-infected women not receiving antiretrovirals during pregnancy. Neonatal urines obtained at birth were tested for CMV DNA by qualitative and reflex quantitative real-time polymerase chain reaction. Results: Urine specimens were available for 992 (58.9%) of 1684 infants; 64 (6.5%) were CMV-positive. Mean CMV load (VL) was 470,276 copies/ ml (range: < 200–2,000,000 copies/ml). Among 89 HIV-infected infants, 16 (18%) had cCMV versus 42 (4.9%) of 858 HIV-exposed, uninfected infants (P < 0.0001). cCMV was present in 23.2% of infants with in utero and 9.1% infants with intrapartum HIV infection (P < 0.0001). Rates of cCMV among HIV-infected infants were 4-fold greater (adjusted OR, 4.4; 95% CI: 2.3–8.2) and 6-fold greater among HIV in utero–infected infants (adjusted OR, 6; 95% CI: 3–12.1) compared with HIV-exposed, uninfected infants. cCMV was not associated with mode of delivery, gestational age, Apgar scores, 6-month infant mortality, maternal age, race/ethnicity, HIV viral load or CD4 count. Primary cCMV risk factors included infant HIV-infection, particularly in utero infection. Conclusion: High rates of cCMV with high urinary CMV VL were observed in HIV-exposed infants. In utero HIV infection appears to be a major risk factor for cCMV in infants whose mothers have not received combination antiretroviral therapy in pregnancy.
AB - Background: Congenital cytomegalovirus (CMV) infection (cCMV) is an important cause of hearing loss and cognitive impairment. Prior studies suggest that HIV-exposed children are at higher risk of acquiring cCMV. We assessed the presence, magnitude and risk factors associated with cCMV among infants born to HIV-infected women, who were not receiving antiretrovirals during pregnancy. Methods: cCMV and urinary CMV load were determined in a cohort of infants born to HIV-infected women not receiving antiretrovirals during pregnancy. Neonatal urines obtained at birth were tested for CMV DNA by qualitative and reflex quantitative real-time polymerase chain reaction. Results: Urine specimens were available for 992 (58.9%) of 1684 infants; 64 (6.5%) were CMV-positive. Mean CMV load (VL) was 470,276 copies/ ml (range: < 200–2,000,000 copies/ml). Among 89 HIV-infected infants, 16 (18%) had cCMV versus 42 (4.9%) of 858 HIV-exposed, uninfected infants (P < 0.0001). cCMV was present in 23.2% of infants with in utero and 9.1% infants with intrapartum HIV infection (P < 0.0001). Rates of cCMV among HIV-infected infants were 4-fold greater (adjusted OR, 4.4; 95% CI: 2.3–8.2) and 6-fold greater among HIV in utero–infected infants (adjusted OR, 6; 95% CI: 3–12.1) compared with HIV-exposed, uninfected infants. cCMV was not associated with mode of delivery, gestational age, Apgar scores, 6-month infant mortality, maternal age, race/ethnicity, HIV viral load or CD4 count. Primary cCMV risk factors included infant HIV-infection, particularly in utero infection. Conclusion: High rates of cCMV with high urinary CMV VL were observed in HIV-exposed infants. In utero HIV infection appears to be a major risk factor for cCMV in infants whose mothers have not received combination antiretroviral therapy in pregnancy.
KW - Congenital CMV
KW - HIV MTCT
KW - HIV perinatal transmission
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U2 - 10.1097/INF.0000000000001975
DO - 10.1097/INF.0000000000001975
M3 - Article
C2 - 30216294
AN - SCOPUS:85050122040
SN - 0891-3668
VL - 37
SP - 1016
EP - 1021
JO - Pediatric Infectious Disease Journal
JF - Pediatric Infectious Disease Journal
IS - 10
ER -