Mathematical Modeling of Rhesus Cytomegalovirus Transplacental Transmission in Seronegative Rhesus Macaques-Reference-Cited by-同舟云学术

Mathematical Modeling of Rhesus Cytomegalovirus Transplacental Transmission in Seronegative Rhesus Macaques

Published:2023-10-01 Issue:10 Volume:15 Page:2040
ISSN:1999-4915
Container-title:Viruses
language:en
Short-container-title:Viruses

Author:

Gong Yishu¹^ORCID,Moström Matilda²,Otero Claire³,Valencia Sarah⁴^ORCID,Tarantal Alice F.⁵,Kaur Amitinder²,Permar Sallie R.⁶^ORCID,Chan Cliburn⁷⁸

Affiliation:

1. Department of Mathematics, Duke University, Durham, NC 27710, USA

2. Department of Immunology, Tulane National Primate Research Center, Covington, LA 70433, USA

3. Department of Pathology, Duke University, Durham, NC 27710, USA

4. Duke Human Vaccine Institute, Duke University Medical Center, Durham, NC 27710, USA

5. Department of Pediatrics, School of Medicine, California National Primate Research Center, UC Davis, Davis, CA 95616, USA

6. Department of Pediatrics, Joan & Weill Cornell Medicine, New York City, NY 10065, USA

7. Department of Biostatistics and Bioinformatics, Duke University, Durham, NC 27710, USA

8. Center for Human Systems Immunology, Duke University, Durham, NC 27710, USA

Abstract

Approximately 0.7% of infants are born with congenital cytomegalovirus (CMV), making it the most common congenital infection. About 1 in 5 congenitally infected babies will suffer long-term sequelae, including sensorineural deafness, intellectual disability, and epilepsy. CMV infection is highly species-dependent, and the rhesus CMV (RhCMV) infection of rhesus monkey fetuses is the only animal model that replicates essential features of congenital CMV (cCMV) infection in humans, including placental transmission, fetal disease, and fetal loss. Using experimental data from RhCMV seronegative rhesus macaques inoculated with RhCMV in the late first to early second trimesters of pregnancy, we built and calibrated a mathematical model for the placental transmission of CMV. The model was then used to study the effect of the timing of inoculation, maternal immune suppression, and hyper-immune globulin infusion on the risk of placental transmission in the context of primary and reactivated chronic maternal CMV infection.

Publisher

MDPI AG

Subject

Virology,Infectious Diseases

Link

https://www.mdpi.com/1999-4915/15/10/2040/pdf

Reference34 articles.

1. New estimates of the prevalence of neurological and sensory sequelae and mortality associated with congenital cytomegalovirus infection;Dollard;Rev. Med. Virol.,2007

2. Lawrence, R.S., Durch, J.S., Stratton, K.R., and Committee to Study Priorities for Vaccine Development National Academies of Sciences, Engineering, and Medicine (2001). Vaccines for the 21st Century: A Tool for Decisionmaking, The National Academies Press.

3. Maternal CD4+ T cells protect against severe congenital cytomegalovirus disease in a novel nonhuman primate model of placental cytomegalovirus transmission;Bialas;Proc. Natl. Acad. Sci. USA,2015

4. Preexisting antibodies can protect against congenital cytomegalovirus infection in monkeys;Nelson;JCI Insight,2017

5. Antibody binding to native cytomegalovirus glycoprotein B predicts efficacy of the gB/MF59 vaccine in humans;Jenks;Sci. Transl. Med.,2020