Honors & Awards

  • NSF Graduate Research Fellowship (GRFP) Recipient, NSF (2019)

Education & Certifications

  • Bachelor of Arts, UC Berkeley, Molecular and Cell Biology: Immunology & Infectious Diseases, Gender and Women's Studies (2017)

Work Experience

  • Research Associate, Infectious Disease Initiative, Chan Zuckerberg Biohub (June 5, 2017 - August 16, 2019)


    San Francisco, CA

All Publications

  • Single mosquito metatranscriptomics identifies vectors, emerging pathogens and reservoirs in one assay. eLife Batson, J., Dudas, G., Haas-Stapleton, E., Kistler, A. L., Li, L. M., Logan, P., Ratnasiri, K., Retallack, H. 2021; 10


    Mosquitoes are major infectious disease-carrying vectors. Assessment of current and future risks associated with the mosquito population requires knowledge of the full repertoire of pathogens they carry, including novel viruses, as well as their blood meal sources. Unbiased metatranscriptomic sequencing of individual mosquitoes offers a straightforward, rapid and quantitative means to acquire this information. Here, we profile 148 diverse wild-caught mosquitoes collected in California and detect sequences from eukaryotes, prokaryotes, 24 known and 46 novel viral species. Importantly, sequencing individuals greatly enhanced the value of the biological information obtained. It allowed us to a) speciate host mosquito, b) compute the prevalence of each microbe and recognize a high frequency of viral co-infections, c) associate animal pathogens with specific blood meal sources, and d) apply simple co-occurrence methods to recover previously undetected components of highly prevalent segmented viruses. In the context of emerging diseases, where knowledge about vectors, pathogens, and reservoirs is lacking, the approaches described here can provide actionable information for public health surveillance and intervention decisions.

    View details for DOI 10.7554/eLife.68353

    View details for PubMedID 33904402

  • Upper airway gene expression reveals suppressed immune responses to SARS-CoV-2 compared with other respiratory viruses NATURE COMMUNICATIONS Mick, E., Kamm, J., Pisco, A., Ratnasiri, K., Babik, J. M., Castaneda, G., DeRisi, J. L., Detweiler, A. M., Hao, S. L., Kangelaris, K. N., Kumar, G., Li, L. M., Mann, S. A., Neff, N., Prasad, P. A., Serpa, P., Shah, S. J., Spottiswoode, N., Tan, M., Calfee, C. S., Christenson, S. A., Kistler, A., Langelier, C. 2020; 11 (1): 5854


    SARS-CoV-2 infection is characterized by peak viral load in the upper airway prior to or at the time of symptom onset, an unusual feature that has enabled widespread transmission of the virus and precipitated a global pandemic. How SARS-CoV-2 is able to achieve high titer in the absence of symptoms remains unclear. Here, we examine the upper airway host transcriptional response in patients with COVID-19 (n = 93), other viral (n = 41) or non-viral (n = 100) acute respiratory illnesses (ARIs). Compared with other viral ARIs, COVID-19 is characterized by a pronounced interferon response but attenuated activation of other innate immune pathways, including toll-like receptor, interleukin and chemokine signaling. The IL-1 and NLRP3 inflammasome pathways are markedly less responsive to SARS-CoV-2, commensurate with a signature of diminished neutrophil and macrophage recruitment. This pattern resembles previously described distinctions between symptomatic and asymptomatic viral infections and may partly explain the propensity for pre-symptomatic transmission in COVID-19. We further use machine learning to build 27-, 10- and 3-gene classifiers that differentiate COVID-19 from other ARIs with AUROCs of 0.981, 0.954 and 0.885, respectively. Classifier performance is stable across a wide range of viral load, suggesting utility in mitigating false positive or false negative results of direct SARS-CoV-2 tests.

    View details for DOI 10.1038/s41467-020-19587-y

    View details for Web of Science ID 000594731600005

    View details for PubMedID 33203890

    View details for PubMedCentralID PMC7673985

  • Clinical features, diagnostics, and outcomes of patients presenting with acute respiratory illness: A retrospective cohort study of patients with and without COVID-19. EClinicalMedicine Shah, S. J., Barish, P. N., Prasad, P. A., Kistler, A. n., Neff, N. n., Kamm, J. n., Li, L. M., Chiu, C. Y., Babik, J. M., Fang, M. C., Kangelaris, K. N., Langelier, C. n., Abe-Jones, Y. n., Alipanah, N. n., Alvarez, F. N., Botvinnik, O. B., Castaneda, G. n., Dadasovich, R. M., Davis, J. n., Deng, X. n., DeRisi, J. L., Detweiler, A. M., Federman, S. n., Haliburton, J. n., Hao, S. n., Kerkhoff, A. D., Kumar, G. R., Malcolm, K. B., Mann, S. A., Martinez, S. n., Mary, R. K., Mick, E. n., Mwakibete, L. n., Najafi, N. n., Peluso, M. J., Phelps, M. n., Pisco, A. O., Ratnasiri, K. n., Rubio, L. A., Sellas, A. n., Sherwood, K. D., Sheu, J. n., Spottiswoode, N. n., Tan, M. n., Yu, G. n. 2020: 100518


    Most data on the clinical presentation, diagnostics, and outcomes of patients with COVID-19 have been presented as case series without comparison to patients with other acute respiratory illnesses.We examined emergency department patients between February 3 and March 31, 2020 with an acute respiratory illness who were tested for SARS-CoV-2. We determined COVID-19 status by PCR and metagenomic next generation sequencing (mNGS). We compared clinical presentation, diagnostics, treatment, and outcomes.Among 316 patients, 33 tested positive for SARS-CoV-2; 31 without COVID-19 tested positive for another respiratory virus. Among patients with additional viral testing (27/33), no SARS-CoV-2 co-infections were identified. Compared to those who tested negative, patients with COVID-19 reported longer symptoms duration (median 7d vs. 3d, p < 0.001). Patients with COVID-19 were more often hospitalized (79% vs. 56%, p = 0.014). When hospitalized, patients with COVID-19 had longer hospitalizations (median 10.7d vs. 4.7d, p < 0.001) and more often developed ARDS (23% vs. 3%, p < 0.001). Most comorbidities, medications, symptoms, vital signs, laboratories, treatments, and outcomes did not differ by COVID-19 status.While we found differences in clinical features of COVID-19 compared to other acute respiratory illnesses, there was significant overlap in presentation and comorbidities. Patients with COVID-19 were more likely to be admitted to the hospital, have longer hospitalizations and develop ARDS, and were unlikely to have co-existent viral infections.National Center for Advancing Translational Sciences, National Heart Lung Blood Institute, National Institute of Allergy and Infectious Diseases, Chan Zuckerberg Biohub, Chan Zuckerberg Initiative.

    View details for DOI 10.1016/j.eclinm.2020.100518

    View details for PubMedID 32864588

    View details for PubMedCentralID PMC7447618

  • Flavivirus NS1 Triggers Tissue-Specific Vascular Endothelial Dysfunction Reflecting Disease Tropism CELL REPORTS Puerta-Guardo, H., Glasner, D. R., Espinosa, D. A., Biering, S. B., Patana, M., Ratnasiri, K., Wang, C., Beatty, P., Harris, E. 2019; 26 (6): 1598-+


    Flaviviruses cause systemic or neurotropic-encephalitic pathology in humans. The flavivirus nonstructural protein 1 (NS1) is a secreted glycoprotein involved in viral replication, immune evasion, and vascular leakage during dengue virus infection. However, the contribution of secreted NS1 from related flaviviruses to viral pathogenesis remains unknown. Here, we demonstrate that NS1 from dengue, Zika, West Nile, Japanese encephalitis, and yellow fever viruses selectively binds to and alters permeability of human endothelial cells from lung, dermis, umbilical vein, brain, and liver in vitro and causes tissue-specific vascular leakage in mice, reflecting the pathophysiology of each flavivirus. Mechanistically, each flavivirus NS1 leads to differential disruption of endothelial glycocalyx components, resulting in endothelial hyperpermeability. Our findings reveal the capacity of a secreted viral protein to modulate endothelial barrier function in a tissue-specific manner both in vitro and in vivo, potentially influencing virus dissemination and pathogenesis and providing targets for antiviral therapies and vaccine development.

    View details for DOI 10.1016/j.celrep.2019.01.036

    View details for Web of Science ID 000457709200019

    View details for PubMedID 30726741

  • Dengue virus NS1 cytokine-independent vascular leak is dependent on endothelial glycocalyx components PLOS PATHOGENS Glasner, D. R., Ratnasiri, K., Puerta-Guardo, H., Espinosa, D. A., Beatty, P., Harris, E. 2017; 13 (11): e1006673


    Dengue virus (DENV) is the most prevalent, medically important mosquito-borne virus. Disease ranges from uncomplicated dengue to life-threatening disease, characterized by endothelial dysfunction and vascular leakage. Previously, we demonstrated that DENV nonstructural protein 1 (NS1) induces endothelial hyperpermeability in a systemic mouse model and human pulmonary endothelial cells, where NS1 disrupts the endothelial glycocalyx-like layer. NS1 also triggers release of inflammatory cytokines from PBMCs via TLR4. Here, we examined the relative contributions of inflammatory mediators and endothelial cell-intrinsic pathways. In vivo, we demonstrated that DENV NS1 but not the closely-related West Nile virus NS1 triggers localized vascular leak in the dorsal dermis of wild-type C57BL/6 mice. In vitro, we showed that human dermal endothelial cells exposed to DENV NS1 do not produce inflammatory cytokines (TNF-α, IL-6, IL-8) and that blocking these cytokines does not affect DENV NS1-induced endothelial hyperpermeability. Further, we demonstrated that DENV NS1 induces vascular leak in TLR4- or TNF-α receptor-deficient mice at similar levels to wild-type animals. Finally, we blocked DENV NS1-induced vascular leak in vivo using inhibitors targeting molecules involved in glycocalyx disruption. Taken together, these data indicate that DENV NS1-induced endothelial cell-intrinsic vascular leak is independent of inflammatory cytokines but dependent on endothelial glycocalyx components.

    View details for DOI 10.1371/journal.ppat.1006673

    View details for Web of Science ID 000416888500010

    View details for PubMedID 29121099

    View details for PubMedCentralID PMC5679539