Quantitative definition of neurobehavior, vision, hearing and brain volumes in macaques congenitally exposed to Zika virus

Koenig, Michelle R.; Razo, Elaina; Mitzey, Ann M.; Newman, Christina M.; Dudley, Dawn M.; Breitbach, Meghan E.; Semler, Matthew R.; Stewart, Laurel M.; Weiler, Andrea M.; Rybarczyk, Sierra; Bach, K; Mohns, Mariel S.; Simmons, Heather A.; Mejía, Andrés; Fritsch, Michael K.; Dennis, Maria; Teixeira, Leandro; Schotzko, Michele L; Nork, T. Michael; Rasmussen, Carol A.; Katz, Arnold E.; Nair, Veena A.; Hou, Jiancheng; Hartman, Amy; Hoeve, James Ver; Kim, Charlene; Schneider, Mary L.; Ausderau, Karla; Kohn, Sarah; Jaeger, Anna S.; Aliota, Matthew T.; Hayes, Jennifer; Schultz-Darken, Nancy; Eickhoff, Jens; Antony, Kathleen M.; Noguchi, Kevin K.; Zeng, Xiankun; Permar, Sallie R.; Prabhakaran, Vivek; Capuano, Saverio; Friedrich, Thomas C.; Golos, Thaddeus G.; O’Connor, David H.; Mohr, Emma L.

doi:10.1371/journal.pone.0235877

Cited by 17 publications

(24 citation statements)

References 60 publications

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“…Other than our own work, we were not able to find any studies designed to interrogate the neuropathogenesis of postnatal ZIKV infection and the resultant developmental consequences using NHP models, although two reports describe postnatal ZIKV susceptibility in NHPs that were also exposed prenatally to ZIKV [ 104 , 105 ]. The features of congenital ZIKV syndrome have been recapitulated after fetal exposure in NHPs, with visual, hearing, neurobehavioral, and brain changes having been observed [ 106 ]. Given the spectrum of clinical manifestations following postnatal ZIKV infection that have been described, and given that some, but not all, children develop neurological symptoms and impaired neurodevelopment, it is paramount that future research efforts be dedicated to the understanding of these disparate outcomes.…”

Section: Discussionmentioning

confidence: 99%

Clinical and Preclinical Evidence for Adverse Neurodevelopment after Postnatal Zika Virus Infection

Raper

Chahroudi

2021

TropicalMed

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Although the Zika virus (ZIKV) typically causes mild or no symptoms in adults, during the 2015−2016 outbreak, ZIKV infection in pregnancy resulted in a spectrum of diseases in infants, including birth defects and neurodevelopmental disorders identified in childhood. While intense clinical and basic science research has focused on the neurodevelopmental outcomes of prenatal ZIKV infection, less is known about the consequences of infection during early life. Considering the neurotropism of ZIKV and the rapidly-developing postnatal brain, it is important to understand how infection during infancy may disrupt neurodevelopment. This paper reviews the current knowledge regarding early postnatal ZIKV infection. Emerging clinical evidence supports the hypothesis that ZIKV infection during infancy can result in negative neurologic consequences. However, clinical data regarding postnatal ZIKV infection in children are limited; as such, animal models play an important role in understanding the potential complications of ZIKV infection related to the vulnerable developing brain. Preclinical data provide insight into the potential behavioral, cognitive, and motor domains that clinical studies should examine in pediatric populations exposed to ZIKV during infancy.

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Section: Discussionmentioning

confidence: 99%

Clinical and Preclinical Evidence for Adverse Neurodevelopment after Postnatal Zika Virus Infection

Raper

Chahroudi

2021

TropicalMed

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“…Placental tissues from all dams and tissues for the fetus from dam 049-101 were assessed as described previously in Koenig et al. ( 44 ).…”

Section: Methodsmentioning

confidence: 99%

Early Embryonic Loss Following Intravaginal Zika Virus Challenge in Rhesus Macaques

et al. 2021

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Zika virus (ZIKV) is an arthropod-borne virus (arbovirus) and is primarily transmitted by Aedes species mosquitoes; however, ZIKV can also be sexually transmitted. During the initial epidemic and in places where ZIKV is now considered endemic, it is difficult to disentangle the risks and contributions of sexual versus vector-borne transmission to adverse pregnancy outcomes. To examine the potential impact of sexual transmission of ZIKV on pregnancy outcome, we challenged three rhesus macaques (Macaca mulatta) three times intravaginally with 1 x 107 PFU of a low passage, African lineage ZIKV isolate (ZIKV-DAK) in the first trimester (~30 days gestational age). Samples were collected from all animals initially on days 3 through 10 post challenge, followed by twice, and then once weekly sample collection; ultrasound examinations were performed every 3-4 days then weekly as pregnancies progressed. All three dams had ZIKV RNA detectable in plasma on day 3 post-ZIKV challenge. At approximately 45 days gestation (17-18 days post-challenge), two of the three dams were found with nonviable embryos by ultrasound. Viral RNA was detected in recovered tissues and at the maternal-fetal interface (MFI) in both cases. The remaining viable pregnancy proceeded to near term (~155 days gestational age) and ZIKV RNA was detected at the MFI but not in fetal tissues. These results suggest that sexual transmission of ZIKV may represent an underappreciated risk of pregnancy loss during early gestation.

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“…Non-human primate models of ZIKV vertical transmission have provided important insights into the complex nature of maternal–fetal infections with this virus (reviewed in ref. 156 ) and have also enabled studies that investigate neonatal and infant sequelae 157 . However, even these models have yet to elucidate the precise mechanisms by which the virus traverses the placental barrier.…”

Section: Torch Pathogensmentioning

confidence: 99%

Infections at the maternal–fetal interface: an overview of pathogenesis and defence

2021

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Infections are a major threat to human reproductive health, and infections in pregnancy can cause prematurity or stillbirth, or can be vertically transmitted to the fetus leading to congenital infection and severe disease. The acronym ‘TORCH’ ( Toxoplasma gondii , other, rubella virus, cytomegalovirus, herpes simplex virus) refers to pathogens directly associated with the development of congenital disease and includes diverse bacteria, viruses and parasites. The placenta restricts vertical transmission during pregnancy and has evolved robust mechanisms of microbial defence. However, microorganisms that cause congenital disease have likely evolved diverse mechanisms to bypass these defences. In this Review, we discuss how TORCH pathogens access the intra-amniotic space and overcome the placental defences that protect against microbial vertical transmission.

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Quantitative definition of neurobehavior, vision, hearing and brain volumes in macaques congenitally exposed to Zika virus

Cited by 17 publications

References 60 publications

Clinical and Preclinical Evidence for Adverse Neurodevelopment after Postnatal Zika Virus Infection

Clinical and Preclinical Evidence for Adverse Neurodevelopment after Postnatal Zika Virus Infection

Early Embryonic Loss Following Intravaginal Zika Virus Challenge in Rhesus Macaques

Infections at the maternal–fetal interface: an overview of pathogenesis and defence

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