About

Dr. Eva Harris is a professor at UC Berkeley, working within the Division of Infectious Disease & Vaccinology at the UC Berkeley School of Public Health. Her research focuses on virus research, particularly in the context of dengue and Zika viruses. She aims to make scientific life easier for her colleagues, enjoy great science, and contribute to the understanding of viral infections. Her background includes extensive experience in virology and immunology, with a focus on virus-host interactions, immune responses, and vaccine development. She has a history of working in structural virology, immunology, and epidemiology, and is involved in projects related to immune profiling of natural dengue virus infections. Dr. Harris also serves as the scientific coordinator of the 'Immune profiling of natural dengue virus infections' project of the Dengue Human Immunology Project Consortium (DHIPC). Her work is dedicated to advancing global public health through virus research and immunological studies.

Research topics

• Immunology
• Virology
• Medicine
• Biology
• Internal medicine
• Environmental health
• Pathology
• Genetics
• Political Science
• Demography
• Molecular biology
• Physics
• Chromatography
• Intensive care medicine
• Biochemistry
• Chemistry

Selected publications

• The contribution of viral toxins to infection and pathogenesis

  mBio · 2026-03-13

  articleOpen accessSenior author

  ABSTRACT The process by which viruses cause disease, viral pathogenesis, is the result of both infection of cells and the host immune response. A less studied but equally important contributor to viral pathogenesis is viral dissemination, the capacity of a virus to move from the primary site of infection, traverse physiological barriers, and gain access to secondary sites of infection. This dictates viral tropism and pathogenesis, but the mechanisms governing barrier crossing are incompletely understood. While the presence of viral receptors on cells is a major determinant of viral tropism and a prerequisite for infection, it does not completely explain the capacity of viruses to enter a tissue. Our recent work has begun to characterize the contribution of soluble viral proteins, acting as “viral toxins,” to viral dissemination, tissue tropism, and overall pathogenesis within an infected host. In this review, we discuss the characteristics of these viral toxins, which are soluble or surface-exposed viral proteins that can interact with endothelial and/or epithelial barriers, as well as immune cells, to trigger signaling pathways, resulting in the transient breakdown of cellular structures maintaining barrier integrity. The disruption of these barriers induces vascular leak and facilitates virus dissemination, influencing viral tropism and pathogenesis. Importantly, blocking this process prevents leak, viral dissemination, and severe disease during infection, highlighting the value of therapeutic intervention against viral toxin activity. Here, we summarize our current understanding of recently discovered viral toxins from the Flaviviridae, Coronaviridae, Nairoviridae, and Filoviridae .

  PublisherDOI

• Perturbed pediatric circulating metabolome in mild and severe dengue disease

  Journal of Virology · 2025-10-29 · 1 citations

  articleOpen access

  Four billion people are at risk of infection with dengue viruses (DENV), and this burden is rapidly increasing due to geographic expansion of the mosquito vector. Infection with any of the four serotypes of DENV can result in a self-limiting but debilitating febrile illness (DF), and some infections progress to severe disease with hemorrhagic manifestations and shock (dengue hemorrhagic fever/dengue shock syndrome [DHF/DSS]). DENV infection drives the metabolic state of host cells for viral benefit and induces a host-immune response with metabolic implications that link to disease. Here, a dynamic metabolic response to DENV infection and disease was measured in 535 pediatric patients from Nicaragua using liquid chromatography-tandem mass spectrometry. Metabolomic analyses revealed profound disruptions of critical biochemical pathways and metabolites within the circulating metabolome, especially in those with more severe manifestations of dengue disease. A biomarker panel of 28 metabolites was utilized to classify DF versus DHF/DSS with high sensitivity and specificity, equating to a balanced accuracy of 96.88%. Identified metabolites belonged to biochemical pathways of omega-3 and omega-6 fatty acids, sphingolipids, dipeptides, purines, and tryptophan metabolism. Dipeptides emerged as the most critical molecules for severe disease classification. Additionally, a previously reported trend between serotonin and platelets in DHF patients was expanded upon here, revealing a major depletion of serotonin, but not platelets, in DSS patients. In this study, the perturbed metabolome was used for disease state classification and exploration of the biochemistry of severe dengue disease pathology.IMPORTANCEThe international burden of dengue is intensifying, as the number of reported cases in only the first 5 months of 2025 exceeded that of the previous annual high in 2023. The occurrence of deadly severe manifestations of dengue disease will escalate as the total cases rise, and pediatric patients are at greater risk of developing the rapidly progressing severe dengue diseases than adults. Suboptimal vaccines, lack of clinically approved therapeutics, and no methodologies for prognosis of severe disease exacerbate the difficulty of preventative and supportive care. Because human metabolism is rapidly altered due to infection, perturbations in patients' circulating metabolome can be attributed to dengue disease and correlated to severity. This study contributes metabolic biomarkers of dengue disease in pediatric patients from Nicaragua, indicating that metabolic biomarkers are conserved across patients of different ages and geographic and genetic backgrounds. With validation across many cohorts, there is potential to improve diagnostics.

  PublisherDOI

• Correction: Interferon receptor-deficient mice are susceptible to eschar-associated rickettsiosis

  eLife · 2025-12-19

  erratumOpen access
  PublisherDOI

• Zika virus: advancing a priority research agenda for preparedness and response

  The Lancet Infectious Diseases · 2025-02-27 · 20 citations

  reviewOpen access
  PublisherOA PDFDOI

• Multiple roads lead to Rome: B cell imprinting in distinct sequential flavivirus infections reveals different pathways to acquiring virus-neutralizing antibodies 4434

  The Journal of Immunology · 2025-11-01

  articleOpen accessSenior author

  Abstract Description People experience multiple infections of the 4 related dengue virus serotypes (DENV1-4) and Zika (ZIKV) before acquiring protection, which is thought to be due to broadly neutralizing antibodies. Oddly, a primary ZIKV infection is a greater risk for subsequent severe dengue than primary DENV. To study underlying immune mechanisms, we conducted single cell sequencing on peripheral blood mononuclear cells from acute DENV2 cases in our cohort study in Nicaragua with no prior exposure (n = 1), prior DENV1 (n = 2), or prior ZIKV (n = 3), and analyzed ∼1,380 B cells/child. We found fewer acute antibody-secreting B cells (ASCs) in the ZIKV-DENV2 than the DENV1-DENV2 group, suggesting fewer precursors. ASCs of the ZIKV-DENV2 group revealed a transcriptional program of T-independent B cell responses, while DENV1-DENV2 ASCs showed use of memory and T-dependent regulation. Surprisingly, a single clone (18_VH3-23_V?1-39) dominated the ASC repertoire (33-50%) in all 3 ZIKV-DENV2 cases. Within this clone, we found a trajectory of evolution where the major constituent mAbs neutralized only ZIKV, but a minor constituent neutralized the infecting DENV2 virus. ASCs from DENV1-DENV2 showed clonal diversity and broader neutralization of DENV than the ZIKV-DENV2 clone. Thus, prior DENV1 infection led to diverse clones, whereas prior ZIKV led to selection and hypermutation of a single clone to achieve new specificity. This shows how populations may acquire immunity differently based on prior exposures. Funding Sources • HHMI Hanna H. Gray Fellowship to TS • U01 DHIPC 0255-C147-4609 to E.H. and S.W • P01 AI106695 and U01AI153416 to E.H. Topic Categories Viral Immunology (VIR)

  PublisherOA PDFDOI

• Longitudinal antibody profiling after dengue reveals distinct dynamics by antibody specificity over 18 months

  medRxiv · 2025-08-13

  preprintOpen accessSenior authorCorresponding

  The four dengue virus serotypes (DENV1-4) co-circulate worldwide, posing major challenges for vaccine development. One key issue is that certain levels and subsets of cross-reactive antibodies can enhance disease during subsequent infection with a different DENV serotype. We defined the magnitude and kinetics of 84 antiviral antibody subsets (by isotype, subclass, antigen, and cross-reactivity) after primary versus secondary dengue, using longitudinal samples collected <1, 3, 6 and 18 months post-symptom onset from a pediatric hospital study in Nicaragua. Interestingly, we found that post-primary infection, cross-reactive IgG antibodies against the envelope protein rise, not wane, over time. Antibody kinetics varied by specificity as measured by infecting serotype versus cross-reactive subsets, viral antigen, and subdomain of a single antigen. Further, substantial seropositivity of IgA, IgM, and IgG3 at 18 months post-infection was observed. These findings highlight several novel conceptual insights into flavivirus immunity and disease risk and have implications for vaccine design and serodiagnosis.

  PublisherOA PDFDOI

• Frequency of dengue virus–specific T cells is related to infection outcome in endemic settings

  JCI Insight · 2025-02-23 · 15 citations

  articleOpen access

  Dengue is widespread in tropical and subtropical regions globally and imposes a considerable disease burden. Annually, dengue virus (DENV) causes up to 400 million infections, of which approximately 25% present with clinical manifestations ranging from mild to fatal. Despite its significance as a growing public health concern, developing effective DENV vaccines has been challenging. One reason is the lack of comprehensive understanding of the influence exerted by prior DENV infections and immune responses with cross-reactive properties. To investigate this, we collected samples from a pediatric cohort study in dengue-endemic Managua, Nicaragua. We characterized T cell responses in 71 healthy children who had previously experienced 1 or more natural DENV infections and who, within 1 year after sample collection, had a subsequent DENV infection that was either symptomatic or inapparent. Our study investigated the effect of preexisting DENV-specific T cell responses on clinical outcomes of subsequent DENV infection. We assessed DENV-specific T cell responses using an activation-induced marker assay. Children with only 1 prior DENV infection displayed heterogeneous DENV-specific CD4+ and CD8+ T cell frequencies. In contrast, children with 2 or more prior DENV infections showed significantly higher DENV-specific CD4+ and CD8+ T cell frequencies associated with inapparent rather than symptomatic outcomes in subsequent infection. These findings demonstrate the protective role of DENV-specific T cells against symptomatic DENV infection and advance efforts to identify protective immune correlates against dengue.

  PublisherDOI

• Antibodies targeting Crimean-Congo hemorrhagic fever virus GP38 limit vascular leak and viral spread

  Science Translational Medicine · 2025-02-19 · 10 citations

  articleOpen accessSenior authorCorresponding

  Crimean-Congo hemorrhagic fever virus (CCHFV) is a priority pathogen transmitted by tick bites, with no vaccines or specific therapeutics approved to date. Severe disease manifestations include hemorrhage, endothelial dysfunction, and multiorgan failure. Infected cells release the viral glycoprotein GP38, whose extracellular function is presently unknown. GP38 is considered an important target for vaccine and therapeutic design because GP38-specific antibodies can protect against severe disease in animal models, albeit through an unknown mechanism of action. Here, we showed that GP38 induces endothelial barrier dysfunction in vitro by disrupting the endothelial glycocalyx layer and triggering hyperpermeability. We also demonstrated that GP38 alone can cause vascular leak in a mouse model. We found that CCHFV infection leads to vascular leak in vivo, which was exacerbated by exogenous administration of GP38, facilitating dissemination of CCHFV into target tissues such as the liver. Protective antibodies that recognized specific antigenic sites on GP38, but not a protective neutralizing antibody binding the structural protein Gc, potently inhibited endothelial hyperpermeability in vitro and vascular leak in vivo during CCHFV infection. This work uncovers a function of the circulating viral protein GP38 as a viral toxin in CCHFV pathogenesis and elucidates a potential mode of action of nonneutralizing yet protective GP38-specific antibodies.

  PublisherOA PDFDOI

• Meeting Report on an Integrated Research Agenda for Mosquito-Borne Arboviruses

  Open Forum Infectious Diseases · 2025-06-30 · 1 citations

  articleOpen access

  The emergence and re-emergence of mosquito-borne arbovirus (MBV) diseases pose a rapidly expanding global health threat fueled by the convergence of multiple ecologic, economic, and social factors, including climate change, land use, poverty, deficiencies of water storage and sanitation, and limitations of vector control programs. On December 6, 2023, the Wellcome Trust and the University of Minnesota's Center for Infectious Disease Research and Policy held a meeting titled "An integrated approach to mosquito-borne arboviruses: a priority research agenda." The meeting comprised presentations, panels, and facilitated discussions aimed at describing the state of the field, highlighting recent accomplishments, identifying novel strategies, and defining priority research goals and approaches for addressing MBV disease preparedness and response. This report summarizes meeting discussions in 3 key areas: the changing epidemiology of MBV disease, current and potential transmission- and disease-monitoring strategies, and evolutionary impacts on disease burden and transmission. It concludes with a list of priority strategies for research and investment in MBV disease prevention, preparedness, and control. To prepare for future epidemics of MBV diseases, research and policy will benefit from a multipathogen approach to MBVs. Building on existing knowledge and systems, these efforts must address social and ecological factors and connect with other global health agendas.

  PublisherOA PDFDOI

• Evaluación de la incidencia de la enfermedad del virus respiratorio sincitial en un estudio de Cohorte de Nacimiento Prospectivo en Managua, Nicaragua

  Translating the Americas · 2025-01-08

  articleOpen access

  This text is a Spanish translation of the following article: "Assessing the Incidence of Symptomatic Respiratory Syncytial Virus Illness Within a Prospective Birth Cohort in Managua, Nicaragua." It was published by Oxford University Press for the Infectious Diseases Society of America on July 29, 2019: https://doi.org/10.1093/cid/ciz585 Encontramos una carga sustancial de VSR en niños nicaragüenses menores de 2 años. Alrededor de 1/3 de las muertes por causas médicas en este estudio estaban asociadas a infecciones del VSR, lo cual sugiere que este agente es un importante impulsor de la mortalidad infantil en esta población, la cual ha sido vacunada en gran medida y padece poco de malaria o VIH.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R41AI062100

  NIH · $996k · 2007

• Core A - Administrative Core

  NIH · $83.5M · 2020–2023

• NIH Grant R21AI129508

  NIH · $435k · 2018

• NIH Grant R01AI052324

  NIH · $1.4M · 2010

• NIH Grant U01AI088654

  NIH · $3.2M · 2016

Frequent coauthors

• Ángel Balmaseda

  Sustainable Sciences Institute

  178 shared

• Aubree Gordon

  University of Michigan–Ann Arbor

  119 shared

• Ángel Balmaseda

  National Autonomous University of Nicaragua

  108 shared

• Guillermina Kuan

  Ministerio de Salud

  101 shared

• Guillermina Kuan

  Sustainable Sciences Institute

  95 shared

• Joséfina Coloma

  76 shared

• Lionel Gresh

  World Health Organization Regional Office for the Americas

  75 shared

• Sergio Ojeda

  Sustainable Sciences Institute

  70 shared

Labs

• Harris Research Program UC Berkeley TeamPI

Awards & honors

• MacArthur Award (1997)
• Sustainable Sciences Institute (SSI) founding (1998)