About

Emma Mohr is an Assistant Professor on the tenure track in the Division of Infectious Diseases at the University of Wisconsin-Madison. She holds a BA from Gustavus Adolphus College, an MD from the University of Iowa Carver College of Medicine, and a PhD from the University of Iowa. Her training includes a residency in Pediatrics with an Integrated Research Pathway at Emory University and the Centers for Disease Control and Prevention, as well as a fellowship in Pediatric Infectious Disease at the University of Wisconsin-Madison. Dr. Mohr is dedicated to training the next generation of translational scientists, serving as the director of the Physician Scientist Training Pathway and participating in the Medical Scientist Training Program Admissions Committee. She also co-directs the Career Development Workshop and serves on the Research Affairs Committee for the Pediatric Infectious Diseases Society. Her clinical work focuses on pediatric infectious diseases, particularly caring for children with complicated infections and congenital infections. Her research aims to improve the health of children impacted by infections during pregnancy, with current studies on congenital Zika virus infection using a translational macaque model to define the infection’s pathogenesis and long-term neurodevelopment, ultimately seeking to identify novel therapeutic targets to improve health outcomes.

Research topics

• Biology
• Genetics
• Virology
• Immunology
• Medicine
• Neuroscience
• Pediatrics
• Audiology

Selected publications

• Prenatal Zika virus exposure disrupts social-emotional development and cortical visual function in infant macaques

  Nature Communications · 2026-01-29

  articleOpen accessSenior author

  Prenatal Zika virus (ZIKV) exposure can result in outcomes ranging from severe birth defects to subtle developmental delays, yet the underlying mechanisms remain unclear. Using a translational rhesus macaque model, we assess visual, auditory, and neurodevelopmental outcomes through 12 months of age following first-trimester ZIKV inoculation. Pregnant macaques, either flavivirus-naive or with prior dengue virus (DENV) exposure, are inoculated with Asian or African ZIKV lineages. Maternal viremia duration, placental viral burden, and neutralizing antibody titers vary but are not associated with developmental outcomes. At 12 months, ZIKV-exposed infants exhibit altered maternal attachment behaviors and reduced inhibition toward novel sensory stimuli. Visual evoked potentials are impaired at 3 months but normalize by 12 months; hearing loss is more frequent but not statistically significant. These outcomes are driven by ZIKV exposure itself, independent of maternal infection characteristics. Our findings highlight the limitations of maternal biomarkers in risk prediction and support incorporating infant-focused developmental outcomes in studies of maternal interventions. Prenatal Zika virus (ZIKV) exposure can lead to a spectrum of developmental issues, but the mechanisms remain unclear. Here the authors show that prenatal ZIKV exposure in macaques disrupts neurodevelopment, causing prolonged maternal attachment and visual deficits at 3 months that normalize by 12 months, independent of sensory function.

  PublisherDOI

• Author Correction: Prenatal Zika virus exposure disrupts social-emotional development and cortical visual function in infant macaques

  Nature Communications · 2026-04-13

  articleOpen accessSenior author

  vRNA-positive (%)."In the Fig. 1d legend,"The proportion of biopsies" originally appeared as "The percentageof biopsies...

  PublisherOA PDFDOI

• Role of non-human primate models in accelerating research and developing countermeasures against Zika virus infection

  The Lancet Microbe · 2025-02-27 · 12 citations

  reviewOpen access

  Zika virus, a mosquito-transmitted orthoflavivirus, has become a pathogen of global health concern ever since the virus caused an epidemic in Brazil in 2015 associated with approximately 700 000 laboratory-confirmed cases of congenital microcephaly. The subsequent spread of the epidemic in 2016 resulted in a wide spectrum of congenital neurological, ophthalmological, and developmental abnormalities across the Americas, Africa, and Asia. In this context, non-human primate models have become essential tools for Zika virus research to understand the pathogenesis of congenital brain injury and perinatal complications and for developing and testing medical countermeasures such as vaccines, diagnostics, and therapeutics. Fetal brain injury has been observed across various non-human primate species and is influenced by factors such as the Zika virus strain, gestational age at inoculation, and inoculation dose and route. Miscarriages are also seen as common outcomes of first trimester Zika virus infections. This Series paper reviews the diverse non-human primate models currently used for Zika virus research to mitigate the public health effects of future Zika virus epidemics.

  PublisherDOI

• Prenatal Zika Virus Exposure Disrupts Social-Emotional Development and Cortical Visual Function in Infant Macaques

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-09 · 1 citations

  preprintOpen accessSenior authorCorresponding

  Prenatal exposure to Zika virus (ZIKV) results in a spectrum of outcomes, ranging from severe birth defects and early childhood developmental delays to no apparent deficits. However, the mechanisms underlying these outcomes, particularly in the context of different maternal infection conditions, remain poorly defined. In this study, we employed a translational rhesus macaque model of prenatal ZIKV infection to evaluate longitudinal visual and auditory development from 1 to 12 months of age and characterize neurodevelopmental outcomes at 12 months. Pregnant macaques, either flavivirus-naive or with prior dengue virus (DENV) exposure, were inoculated in the first trimester (~30 or 45 gestational days) with an Asian or African lineage of ZIKV or received a saline injection as controls. Maternal plasma viremia duration, viral RNA burden at the maternal-fetal interface, and neutralizing antibody titers did not differ between inoculation cohorts or controls. At 12 months, ZIKV-exposed infants demonstrated altered maternal attachment behaviors and reduced inhibition when approaching sensory stimuli compared to controls. Visual pathway function, assessed by electrophysiology, was significantly impaired at 3 months but normalized by 12 months. Hearing loss was more common among ZIKV-exposed infants, although not statistically significant. Developmental outcomes were associated with prenatal ZIKV exposure itself, independent of viremia duration, neutralizing antibody titer, viral lineage, or maternal DENV immunity, and were not mediated by visual impairment or hearing loss. These findings highlight that any prenatal ZIKV exposure can disrupt early neurobehavioral development and visual function, underscoring the need for prevention strategies focused on maternal infection and early intervention.

  PublisherOA PDFDOI

• Clade IIb Mpox virus (MPXV) vertical transmission and fetal demise in a pregnant rhesus macaque model

  PLoS ONE · 2025-04-01 · 5 citations

  articleOpen accessSenior author

  Infection with clade I Mpox virus (MPXV) results in adverse pregnancy outcomes, yet the potential for vertical transmission resulting in fetal harm with clade IIb MPXV, the clade that is currently circulating in the Western Hemisphere, remains unknown. We sought to establish a pregnant rhesus macaque model of clade IIb MPXV infection with early gestation inoculation to understand if infection results in vertical transmission and adverse pregnancy outcomes. Three pregnant rhesus macaques were inoculated intradermally with 1.5 x 105 plaque forming units (PFU) of clade IIb MPXV near gestational day (GD) 30 and animals were monitored for viremia and maternal and fetal well-being. Animals were euthanized to collect tissues at 5, 14, or 25 days post-inoculation (dpi). Tissues were evaluated for viral DNA (vDNA) loads, infectious virus titers, histopathology, MPXV mRNA and protein localization, as well as MPXV protein co-localization with placental cells including, Hofbauer cells, mesenchymal stromal cells, endothelial cells, and trophoblasts. vDNA was detected in maternal blood and skin lesions by 5 dpi. Lack of fetal heartbeat was observed at 14 or 25 dpi for two dams indicating fetal demise; the third dam developed significant vaginal bleeding at 5 dpi and was deemed an impending miscarriage. vDNA was detected in placental and fetal tissue in both fetal demise cases. MPXV localized to placental villi by ISH and IHC. Clade IIb MPXV infection in pregnant rhesus macaques results in vertical transmission to the fetus and adverse pregnancy outcomes, like clade I MPXV. This suggests that clade IIb MPXV infection in human pregnancy poses a danger to maternal and fetal health as well. Further studies are needed to determine whether antiviral therapy with tecovirimat will prevent vertical transmission and improve pregnancy outcomes.

  PublisherDOI

• Macaque Models of Prenatal and Postnatal Zika Virus Exposure and Developmental Outcomes

  Journal of the Pediatric Infectious Diseases Society · 2025-03-10 · 2 citations

  reviewSenior author

  Prenatal and postnatal Zika virus (ZIKV) exposure can result in a constellation of developmental deficits in human infants that present during early childhood. Translational rhesus macaque models have been developed to interrogate these deficits. Here, we summarize and interpret the developmental findings from rhesus macaque studies of prenatal or postnatal ZIKV exposure. We looked for potential biomarkers that could be used to identify infants at risk for developmental deficits. Visual orientation and motor deficits were the most common developmental deficits across the studies. We identified a potential association between prolonged maternal RNAemia and worse infant developmental outcomes in prenatal exposure studies. Therefore, longitudinal screening of maternal blood for ZIKV RNA may help identify human infants at risk for visual orientation and motor deficits in early childhood; however, the diversity of research protocols across the groups made it challenging to make definitive associations.

  PublisherDOI

• Mpox virus (MPXV) vertical transmission and fetal demise in a pregnant rhesus macaque model

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-05-31 · 7 citations

  preprintOpen accessSenior authorCorresponding

  Infection with clade I Mpox virus (MPXV) results in adverse pregnancy outcomes, yet the potential for vertical transmission resulting in fetal harm with clade IIb MPXV, the clade that is currently circulating in the Western Hemisphere, remains unknown. We established a rhesus macaque model of vertical MPXV transmission with early gestation inoculation. Three pregnant rhesus macaques were inoculated intradermally with 1.5 × 10^5 plaque forming units (PFU) of clade IIb MPXV near gestational day (GD) 30 and animals were monitored for viremia and maternal and fetal well-being. Animals were euthanized to collect tissues at 5, 14, or 25 days post-inoculation (dpi). Tissues were evaluated for viral DNA (vDNA) loads, infectious virus titers, histopathology, MPXV mRNA and protein localization, as well as MPXV protein co-localization with placental cells including, Hofbauer cells, mesenchymal stromal cells, endothelial cells, and trophoblasts. vDNA was detected in maternal blood and skin lesions by 5 dpi. Lack of fetal heartbeat was observed at 14 or 25 dpi for two dams indicating fetal demise; the third dam developed significant vaginal bleeding at 5 dpi and was deemed an impending miscarriage. vDNA was detected in placental and fetal tissue in both fetal demise cases. MPXV localized to placental villi by ISH and IHC. Clade IIb MPXV infection in pregnant rhesus macaques results in vertical transmission to the fetus and adverse pregnancy outcomes, like clade I MPXV. Further studies are needed to determine whether antiviral therapy with tecovirimat will prevent vertical transmission and improve pregnancy outcomes. One Sentence Summary: Clade IIb Mpox virus infection of pregnant rhesus macaques results in vertical transmission from mother to fetus and adverse pregnancy outcomes.

  PublisherOA PDFDOI

• Sustained human outbreak of a new MPXV clade I lineage in eastern Democratic Republic of the Congo

  Nature Medicine · 2024 · 343 citations

  • Virology
  • Biology
  • Genetics

  Outbreaks of monkeypox (mpox) have historically resulted from zoonotic spillover of clade I monkeypox virus (MPXV) in Central Africa and clade II MPXV in West Africa. In 2022, subclade IIb caused a global epidemic linked to transmission through sexual contact. Here we describe the epidemiological and genomic features of an mpox outbreak in a mining region in eastern Democratic Republic of the Congo, caused by clade I MPXV. Surveillance data collected between September 2023 and January 2024 identified 241 suspected cases. Genomic analysis demonstrates a distinct clade I lineage divergent from previously circulating strains in the Democratic Republic of the Congo. Of the 108 polymerase chain reaction-confirmed mpox cases, the median age of individuals was 22 years, 51.9% were female and 29% were sex workers, suggesting a potential role for sexual transmission. The predominance of APOBEC3-type mutations and the estimated emergence time around mid-September 2023 imply recent sustained human-to-human transmission.

  PublisherOA PDFDOI

• Neurodevelopmental Screening Tests Outcomes of Children in Wisconsin With a Prenatal History of Travel to Zika Virus Endemic Regions During 2015-2018: A Retrospective Case-Control Study.

  PubMed · 2024-01-01

  articleSenior author

  BACKGROUND: Children with prenatal Zika virus exposure are at an increased risk of developing neurodevelopmental deficits in early childhood. Travel to Zika virus-endemic regions during pregnancy elevates the risk of offspring developing complications. This study examined developmental outcomes of children from Wisconsin with maternal or partner travel history to Zika virus-endemic regions during pregnancy compared to gestation and age-matched controls. METHODS: A retrospective chart review compared outcomes of cases (n = 181) with prenatal travel history to Zika virus-endemic regions to gestational and birth date-matched controls (n = 172) up to 7 years old. We reported Zika virus testing and travel, birth outcomes, standardized developmental screening tests, and specialist referral rates. RESULTS: = 0.059). One Zika virus-positive case was identified with complications surrounding birth, and 2.2% of children had documentation in their health records noting potential Zika virus exposure. Regardless of groups, limited referrals were made at 9 (0%), 18 (60%), and 24 (40%) months based on Ages and Stages Questionnaire-version 3 (ASQ-3) recommendations. CONCLUSIONS: This study found similar developmental screening outcomes and referral rates between groups. Longitudinal care of children whose mothers traveled to Zika virus-endemic regions could be improved with better documentation of prenatal Zika virus exposure in the child's medical record, use of standardized developmental screening tools at every recommended well-child visit, and referral when developmental screening test scores are low.

  Publisher

• Mpox virus (MPXV) vertical transmission and fetal demise in a pregnant rhesus macaque model

  Placenta · 2024-08-31

  articleOpen accessSenior author
  PublisherDOI

Recent grants

• Defining maternal and neonatal antibody responses in congenital Zika virus infection

  NIH · $1.0M · 2019–2024

Frequent coauthors

• David H. O’Connor

  University of Wisconsin–Madison

  49 shared

• Thomas C. Friedrich

  University of Wisconsin–Madison

  46 shared

• Andrea M. Weiler

  University of Wisconsin–Madison

  43 shared

• Dawn M. Dudley

  University of Wisconsin–Madison

  41 shared

• Matthew T. Aliota

  University of Minnesota

  39 shared

• Christina M. Newman

  University of Wisconsin–Madison

  38 shared

• Meghan E. Breitbach

  University of Wisconsin–Madison

  37 shared

• Thaddeus G. Golos

  University of Wisconsin–Madison

  37 shared

Education

• B.A.

  Gustavus Adolphus College

• M.D.

  University of Iowa Carver College of Medicine

• Ph.D.

  University of Iowa

• Other, Pediatrics with Integrated Research Pathway

  Emory University and Centers for Disease Control and Prevention

• Other, Pediatric Infectious Disease

  University of Wisconsin