Elke Mühlberger, Ph.D.
Professor of Microbiology
Director, Integrated Science Services
National Emerging Infectious Diseases Laboratories (NEIDL)
620 Albany Street
Office: NEIDL 4; 617-358-9153
Lab: NEIDL 4; 617-638-0337
Ph.D. Philipps University, Marburg, Germany
I have a long-standing research interest in studying highly pathogenic hemorrhagic fever viruses, including Ebola and Marburg viruses which belong to the filovirus family. Filoviruses cause a severe disease in humans with high case fatality rates. Due to the high pathogenicity of these viruses, they are classified as biosafety level 4 (BSL-4) pathogens. My lab studies different aspects of the filovirus infection cycle. One focus of our work is to dissect the mechanisms of filovirus genome replication and transcription with the goal to identify determinants of virulence. This includes work on Lloviu virus, a new member of the filovirus family, whose pathogenicity in humans is not known. Tools we use for this work include minigenome systems and recombinant viruses.
Another focus of our research is centered around the host response to filovirus infection. To mimic the events in infected patients, we mainly use human primary cells for our infection studies. This includes macrophages and monocyte-derived dendritic cells isolated from blood, as well as human immune and liver cells generated from induced pluripotent stem cells (iPSC). The iPSC-derived infection platforms are developed in collaboration with tissue engineers at BU’s Center for Regenerative Medicine (CReM). We use these platforms to analyze the host response to filovirus infection, including inflammatory signatures, cell damage and antiviral defense mechanisms. The information we obtain from these studies will help us to determine virulence factors and identify targets for antiviral therapeutics.
Based on our experience in studying emerging viral diseases, the Mühlberger lab recently joined the efforts to control the COVID-19 pandemic by providing virology service to members of the research community who do not have access to high containment space. We are currently performing SARS-CoV-2 infection studies in the NEIDL high containment facility for more than 20 investigators with highly diverse research interests, including antiviral drug screening, tissue engineering, molecular imaging, droplet stability, omics studies, and host response mechanisms.
- Hume, A. J. and Mühlberger, E. 2019. Distinct genome replication and transcription strategies within the growing filovirus family. J. Mol. Biol. 431(21): 4290-4320. PMID: 31260690
- Deflubé, L. R.*, Cressey, T. N.*, Hume, A. J.*, Olejnik, J., Haddock, E., Feldmann, F., Ebihara, H., Fearns, R.#, and Mühlberger, E.# 2019. Ebolavirus polymerase uses an unconventional genome replication mechanism. Proc. Natl. Acad. Sci. USA 116(17): 8535-8543. PMID: 30962389. *, # equal contribution.
- Olejnik, J., Hume, A. J. and Mühlberger, E. 2018. Toll-like receptor 4 in acute viral infection: too much of a good thing. PloS Pathog. 14(12):e1007390. PMID: 30571771.
- Manhart, W. A.*, Pacheco, J. R.*, Hume, A. J., Cressey, T. N., Deflubé, L. R., and Mühlberger, E. 2018. A chimeric Lloviu virus minigenome system reveals that the bat-derived filovirus replicates more similarly to ebolaviruses than marburgviruses. Cell Reports 24: 2573-2580. PMID: 30184492. * equal contribution.
- Hume, A. and Mühlberger, E. 2018. Marburg virus VP35 inhibits PKR activation in a cell-type specific manner. J Infect Dis. 218 (suppl_5): S403-S408. PMID: 30165526.
- Pavlovich, S. S., Lovett, S. P., Koroleva, G., Guito, J. C., Arnold, C. E., Nagle, E. R., Kulcsar, K., Lee, A., Thibaud-Nissen, F., Hume, A. J., Mühlberger, E., Uebelhoer, L. S., Towner, J. S., Rabadan, R., Sanchez-Lockhart, M., Kepler, T. B., and Palacios, G. 2018. The Egyptian rousette genome reveals unexpected features of bat antiviral immunity. Cell 173(5): 1098-1110.e18. PMID 29706541.
- Nelson, E. V.*, Pacheco, J. R.*, Hume, A. J.*, Cressey, T. N., Deflubé, L. R., Ruedas, J. B. Connor, J. H., Ebihara, H., and Mühlberger, E. 2017. An RNA polymerase II-driven Ebola virus minigenome system as an advanced tool for antiviral drug screening. Antiviral Res. 146: 21-27. PMID: 28807685. * equal contribution. Selected as Highlighted article – August 2017.
- Olejnik, J., Forero, A., Deflubé, L. R., Hume, A. J., Manhart, W. A., Nishida, A., Marzi, A., Katze, M. G., Ebihara, H., Rasmussen, A. L., and Mühlberger, E. 2017. Ebolavirus species associated with differential pathogenicity induce distinct host responses in human macrophages. J. Virol. 91: e00179-17. PMID: 28331091. Selected as Spotlight Article of Significant Interest.
- Nelson, E. V., Schmidt, K. M., Deflubé, L. R., Doganay, S., Banadyga, L., Olejnik, J., Hume, A. J., Ryabchikova, E., Ebihara, H., Kedersha, N., Ha, T., and Mühlberger, E. 2016. Ebola virus does not induce stress granule formation during infection and sequesters stress granule proteins within viral inclusions. J. Virol. 90: 7268-7284. PMID: 27252530. Cover page, JVI 90, issue 10.
- Brauburger, K., Boehmann, Y, Krähling, V., and Mühlberger, E. 2015. Transcriptional regulation in Ebola virus: effects of gene border structure and regulatory elements on gene expression and polymerase scanning behavior. J. Virol. 90: 1898-1909. PMID: 26656691
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