About

Matt Aliota is an Assistant Professor in the Department of Veterinary and Biomedical Sciences at the University of Minnesota. He is affiliated with the Department of Entomology and is based in Hodson Hall in St. Paul, Minnesota. His professional role involves research and teaching within the fields of veterinary and biomedical sciences, with a focus on entomology-related topics. Specific details about his research interests, background, or key contributions are not provided in the available page text.

Research topics

• Medicine
• Biology
• Genetics
• Virology
• Immunology
• Pathology
• Internal medicine
• Chemistry
• Pediatrics
• Anesthesia
• Neuroscience
• Audiology

Selected publications

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

  Nature Communications · 2026-01-29

  articleOpen access

  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 access

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  PublisherOA PDFDOI

• Metagenomic surveillance of undiagnosed febrile illness in Nigeria does not reveal the etiological agent for most patients

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-09

  articleOpen accessCorresponding

  Molecular and microscopy-based diagnostic capacity is often insufficient or unavailable in places where infectious disease burdens are highest, such as in West Africa. Rapid diagnostic testing (RDT) can provide quick and affordable diagnoses of common infections but is an imperfect solution due to limitations around detecting and dealing with false negative and false positive results. An alternative to RDT is unbiased metagenomic sequencing for pathogen surveillance. Here, we present data from unbiased metagenomic sequencing used to identify causes of undiagnosed febrile illness in Jos, Plateau State, Nigeria. Proof of concept for this approach has been demonstrated by several groups who have identified epidemic and endemic viral diseases like Lassa fever, yellow fever, and Chikungunya. Here, we show that unbiased deep sequencing and metagenomic analysis can be used to identify RNA viruses in clinical samples. We sequenced RNA from sera of patients (n = 343), many of whom were acutely febrile (76 %) in a survey of clinics in Jos. We detected five human-infecting viruses in 39 (11 %) specimens. Among these were hepatitis B virus, human pegivirus, and several anelloviruses. While most of the viruses identified are unlikely to cause clinical symptoms in the patients we sampled, their presence demonstrates the validity of our approach. Additionally, our sequencing data allowed us to identify genetic material from potentially pathogenic bacteria, another possible etiological agent of febrile illness.

  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

• Zika virus-induced fetal demise is driven by strain- and dose-specific RLR-driven activation of the interferon response in the decidua, placenta, and fetus in <i> Ifnar1 ^-/- </i> mice

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-13

  preprintOpen accessSenior authorCorresponding

  ABSTRACT Congenital Zika syndrome (CZS), the set of fetal and neonatal complications associated with Zika virus (ZIKV) infection in pregnancy, was first noted during the outbreak in the Americas in 2015-16. However, there was an unequal distribution of ZIKV cases and severe outcomes in all areas where ZIKV emerged in the Americas, demonstrating that the risk of CZS varied over space and time. Recently, we demonstrated that phenotypic heterogeneity existed between closely-related ZIKV strains. All ZIKV strains tested infected the placenta but varied in their capacity to cause overt fetal harm. Here, we further characterized the relative contributions of virus genotype and infecting dose of two phenotypically distinct ZIKV strains across multiple timepoints in gestation in pregnant mice that lack type-I interferon receptor function ( Ifnar1 -/- ). To better understand the underlying causes of adverse fetal outcomes, we used RNA sequencing to compare ZIKV-infected and uninfected tissues. We found that ZIKV infection triggers retinoic acid-inducible gene I (RIG-I)-like receptor-mediated activation of the interferon response at the maternal-fetal interface. However, modest chemical inhibition of RIG-I activation in the decidua and placenta did not protect against fetal demise. Instead, the fetal interferon response was significantly associated with fetal demise. Together, these findings suggest that the response to ZIKV at the maternal-fetal interface can vary depending on the infecting ZIKV genotype and dose, and that the fetal immune response is an important mediator of fetal harm. IMPORTANCE Previously, we used a mouse model of ZIKV infection during pregnancy to assess the pathogenic potential to the fetus of a panel of five, low-passage ZIKV strains representing the viral genetic diversity in the Americas. We found that phenotypic heterogeneity existed between these closely-related ZIKV strains. Here, we show that this heterogeneity is driven by retinoic acid-inducible gene I (RIG-I)-like receptor-mediated activation of the interferon response at the maternal-fetal interface. We used chemical inhibition of the RIG-I pathway and measured the transcriptional activity of interferon stimulated genes in fetuses to demonstrate that the fetal immune response may contribute to fetal demise.

  PublisherDOI

• A Zika Virus-Like Particle Vaccine Mitigates Early Pregnancy Loss In Rhesus Macaques

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-16

  preprintOpen access

  Abstract Zika virus (ZIKV) is an arthropod-borne Orthoflavivirus that caused a major outbreak in the Americas in 2015-16. In Brazil, up to 46% of ZIKV positive pregnancies resulted in congenital Zika syndrome (CZS). CZS is characterized by a wide range of neurologic birth defects and miscarriage in up to 7.6% of affected pregnancies. With no current licensed ZIKV vaccines, we sought to evaluate a Zika virus-like particle (VLP) vaccine candidate in a rhesus macaque (RM) pregnancy model. VLPs were produced in mammalian cells expressing the pre-membrane-envelope region of the Asian-lineage ZIKV strain PRVABC59, which belongs to the Asian ZIKV lineage that is associated with outbreaks of congenital disease. To evaluate vaccine protection against adverse pregnancy complications, two cohorts of female RM were vaccinated with ZIKV-VLP with adjuvant Alhydrogel (alum) or adjuvant alone prior to mating. At gestational day (GD) 30 (early first trimester), pregnant animals were challenged with ZIKV-DAK 41524, an African-lineage strain shown to induce 1st-trimester fetal demise in 78% (n=11/14 animals) of RM, making it an ideal and stringent model for evaluating ZIKV vaccines. Within the vaccinated cohort, 2 of 3 animals reached the study endpoint of GD 90 with no observed adverse pregnancy outcomes. The third animal experienced pregnancy loss at GD 49 (18 d post infection), although no infectious virus was detected in placental or fetal tissues. In the unvaccinated cohort, two animals had severe adverse events. One animal experienced preterm labor, and another developed early-onset hydrops fetalis with widespread ZIKV-RNA detected via RNAscope and extensive placental damage. These results confirm a significant risk for early pregnancy loss in RM infected with ZIKV-DAK 41524. This model can be further used to understand the complexities of placental immunological features underlying stillbirth and miscarriage following infection. Our findings indicate that this ZIKV-VLP vaccine candidate protected pregnant macaques against fetal demise associated with highly pathogenic ZIKV challenge. Author Summary Zika virus (ZIKV) infection during pregnancy is associated with pregnancy loss, severe birth defects, including microcephaly and developmental delays, and other subtle neurologic changes. Although vaccine development efforts have been ongoing since the 2015/2016 ZIKV outbreak, no approved vaccine is currently available. Many existing studies have tested vaccines in animal models using strains such as ZIKV-PR that cause mild or moderate pregnancy complications at similar rates to human cases. Using challenge strains that only cause mild, or moderate pregnancy complications makes it difficult to rigorously evaluate vaccine efficacy. In this study, we tested a virus-like particle (VLP) vaccine, a safe and effective method for use during pregnancy as it is replication-deficient and only contains viral structural antigens. We found that the VLP vaccine, when paired with an adjuvant (alum), induced strong antibody responses in mice and controlled viral dissemination following challenge in nonpregnant macaques. To evaluate the protective efficacy of the ZIKV-VLP vaccine against in utero infection and disease, we used a stringent model of ZIKV infection during early pregnancy in rhesus macaques that is associated with high rates of fetal demise. In pregnant macaques, the vaccine reduced maternal viremia, limited viral spread to fetal and placental tissues, and conferred protection against virus-mediated fetal demise and placental damage. This is the first study to evaluate a VLP-based vaccine in a consistent pregnancy loss model of ZIKV infection. These findings support the continued development of VLP vaccines as a safe and effective strategy for protecting pregnant individuals and their developing fetuses from ZIKV.

  PublisherOA PDFDOI

• Differential Virulence and Host-Specific Fitness of Regionally Distinct Human-Derived Powassan Virus Lineage 2 Strains

  American Journal of Tropical Medicine and Hygiene · 2025-05-13 · 2 citations

  articleOpen access

  Powassan virus (POWV; family Flaviviridae) is a tick-borne encephalitic virus endemic to Canada, the United States, and Russia. In the United States, POWV is transmitted by ixodid ticks, and transmission foci reflect the geographic range of these vectors, primarily Ixodes scapularis. Thus, northeastern and midwestern regions of the United States contain the highest human case burdens and prevalence of infected ticks. Notably, New York (NY) and Minnesota (MN) have a long history of POWV transmission to humans. Over time, genetic divergence has occurred in these regions, giving rise to distinct midwestern and northeastern clades. Despite the established circulation of POWV, increases in reported human cases, and documented genetic distinction, an understanding of strain-specific POWV virulence is limited because of the lack of human isolates. In 2020 and 2021, two POWV strains were isolated from fatal human cases from MN (deer tick virus [DTV] MN-PV320) and NY (DTV NY21-027). Here, we provide the first characterization of geographically distinct, contemporary, human POWV isolates. Comprehensive genetic characterization was completed and phenotypic variability was determined in vitro and in vivo . Although strain fitness was similar in I. scapularis, higher mortality rates were measured in a susceptible POWV mouse model after infection with DTV NY21-027 compared with DTV MN-PV320. Genetic analysis revealed several variable amino acid substitutions, including I2173L in DTV NY21-027, which was selected for in all strains after neurological infection. These data suggest that genetic divergence of POWV strains from regionally distinct transmission foci could contribute to strain-dependent pathogenic potential in humans.

  PublisherOA PDFDOI

• Zika virus-induced fetal demise is triggered by strain- and dose-specific RLR-driven activation of the interferon response in the decidua, placenta, and fetus in <i>Ifnar1</i> ^−/− mice

  Journal of Virology · 2025-05-22 · 3 citations

  articleOpen accessSenior author

  ABSTRACT Congenital Zika syndrome (CZS), the set of fetal and neonatal complications associated with Zika virus (ZIKV) infection in pregnancy, was first noted during the outbreak in the Americas in 2015–2016. However, there was an unequal distribution of ZIKV cases and severe outcomes in all areas where ZIKV emerged in the Americas, demonstrating that the risk of CZS varied over space and time. Recently, we demonstrated that phenotypic heterogeneity existed between closely related ZIKV strains. All ZIKV strains tested infected the placenta but varied in their capacity to cause overt fetal harm. Here, we further characterized the relative contributions of virus genotype and infecting dose of two phenotypically distinct ZIKV strains across multiple timepoints in gestation in pregnant mice that lack type-I interferon receptor function ( Ifnar1 −/− ). To better understand the underlying causes of adverse fetal outcomes, we used RNA sequencing to compare ZIKV-infected and uninfected tissues. We found that ZIKV infection triggers retinoic acid-inducible gene I (RIG-I)-like receptor-mediated activation of the interferon response at the maternal-fetal interface. However, modest chemical inhibition of RIG-I activation in the decidua and placenta did not protect against fetal demise. Instead, the fetal interferon response was significantly associated with fetal demise. Together, these findings suggest that the response to ZIKV at the maternal-fetal interface can vary, depending on the infecting ZIKV genotype and dose, and that the fetal immune response is an important mediator of fetal harm. IMPORTANCE Congenital Zika syndrome is a constellation of fetal abnormalities ranging from fetal demise and microcephaly to infants that are born apparently healthy only to develop neurocognitive impacts later. ZIKV is now endemic in many regions worldwide, but how ZIKV harms the developing fetus remains an outstanding question. Previously, we used a mouse model of ZIKV infection during pregnancy to assess the pathogenic potential to the fetus of a panel of five low-passage ZIKV strains representing the viral genetic diversity in the Americas. We found that phenotypic heterogeneity existed between these closely related ZIKV strains. Here, we show that this heterogeneity is driven by RIG-I-like receptor-mediated activation of the interferon response at the maternal-fetal interface. We used chemical inhibition of the RIG-I pathway and measured the transcriptional activity of interferon-stimulated genes in fetuses to demonstrate that the fetal immune response may contribute to fetal demise.

  PublisherDOI

• Author Correction: Metagenomic sequencing detects human respiratory and enteric viruses in air samples collected from congregate settings

  Scientific Reports · 2024-01-15 · 1 citations

  erratumOpen access

  COVID-19 pandemic, environmental surveillance strategies, including wastewater and air sampling,"

  PublisherOA PDFDOI

• Analysis of Powassan Virus Genome Sequences from Human Cases Reveals Substantial Genetic Diversity with Implications for Molecular Assay Development

  Viruses · 2024-10-23 · 6 citations

  articleOpen access

  Powassan virus (POWV) is an emerging tick-borne virus that causes severe meningoencephalitis in the United States, Canada, and Russia. Serology is generally the preferred diagnostic modality, but PCR on cerebrospinal fluid, blood, or urine has an important role, particularly in immunocompromised patients who are unable to mount a serologic response. Although the perceived poor sensitivity of PCR in the general population may be due to the biology of infection and health-seeking behavior (with short viremic periods that end before hospital presentation), limitations in assay design may also contribute. Genome sequences from clinical POWV cases are extremely scarce; PCR assay design has been informed by those available, but the numbers are limited. Larger numbers of genome sequences from tick-derived POWV are available, but it is not known if POWV genomes from human infections broadly mirror genomes from tick hosts, or if human infections are caused by a subset of more virulent strains. We obtained viral genomic data from 10 previously unpublished POWV human infections and showed that they broadly mirror the diversity of genome sequences seen in ticks, including all three major clades (lineage I, lineage II Northeast, and lineage II Midwest). These newly published clinical POWV genome sequences include the first confirmed lineage I infection in the United States, highlighting the relevance of all clades in human disease. An in silico analysis of published POWV PCR assays shows that many assays were optimized against a single clade and have mismatches that may affect their sensitivity when applied across clades. This analysis serves as a launching point for improved PCR design for clinical diagnostics and environmental surveillance.

  PublisherOA PDFDOI

Recent grants

• Admin-Core-001

  NIH · $20.4M · 2018–2025

• Previous exposure to dengue as a risk factor for Zika during pregnancy

  NIH · $2.8M · 2018–2024

• Zika virus evolutionary dynamics in host adaptation

  NIH · $422k · 2017–2021

• NIH Grant R56AI132563

  NIH · $753k · 2017

Frequent coauthors

• Thomas C. Friedrich

  University of Wisconsin–Madison

  78 shared

• Anna S. Jaeger

  California University of Pennsylvania

  56 shared

• David H. O’Connor

  University of Wisconsin–Madison

  55 shared

• Andrea M. Weiler

  University of Wisconsin–Madison

  54 shared

• Shelby L. O’Connor

  University of Wisconsin–Madison

  44 shared

• Emma L. Mohr

  University of Pittsburgh

  39 shared

• Christina M. Newman

  University of Wisconsin–Madison

  37 shared

• Heather A. Simmons

  University of Wisconsin–Madison

  37 shared

Labs

• Veterinary Clinical Pathology LaboratoryPI

  The Veterinary Clinical Pathology Laboratory is staffed by full-time veterinary clinical pathology faculty. All are certified by the American College of Veterinary Pathologists. They are available for consultation regarding experimental design and data interpretation and to assist you in preparing regulatory documents.

Education

• Ph.D.

  University of Wisconsin-Madison

  2010