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Susan R. Weiss, Ph.D.
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Professor of Microbiology
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Department: Microbiology
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Graduate Group Affiliations
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- Cell and Molecular Biology 64
- Neuroscience 5c
- Immunology e
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Contact information
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203A Johnson Pavilion
3a 3610 Hamilton Walk
Philadelphia, PA 19104-6076
26
3a 3610 Hamilton Walk
Philadelphia, PA 19104-6076
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Office: (215) 898-8013
34 Fax: (215) 573-4858
32 Lab: 215-898-3551
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34 Fax: (215) 573-4858
32 Lab: 215-898-3551
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Publications
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Education:
21 9 B.A. 14 (Biology) c
2c Brandeis University, 1971.
21 a Ph.D. 30 (Microbiology and Molecular Genetics) c
2b Harvard University, 1975.
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21 9 B.A. 14 (Biology) c
2c Brandeis University, 1971.
21 a Ph.D. 30 (Microbiology and Molecular Genetics) c
2b Harvard University, 1975.
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Links
11d Search PubMed for articles
69 Primary Work Website
43 Cell and Molecular Biology graduate group faculty webpage.
41 Immunology graduate group faculty webpage.
75 Office of biomedical postoctoral programs
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Permanent link11d Search PubMed for articles
69 Primary Work Website
43 Cell and Molecular Biology graduate group faculty webpage.
41 Immunology graduate group faculty webpage.
75 Office of biomedical postoctoral programs
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2 29
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1e
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51 - Murine coronavirus pathogenesis, central nervous system, liver and lung
7d - Pathogenesis of human coronaviruses including MERS-CoV, SARS-CoV-2 and other nonlethal human respiratory viruses
56 - Activation and antagonism of the OAS-RNase L pathway in human and bat cells
2f - Viral and cellular phosphodiesterases
4a - Interaction of viruses with dsRNA induced innate immune pathways
21 - Zika virus pathogenesis
30 - Endogenous dsRNA induced pathogenesis
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8
97 Key words: murine coronavirus, SARS-CoV MERS-CoV, human respiratory coronavirus, viral pathogenesis, interferon antagonist, OAS-RNase L.
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28 Description of Research
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1a Susan Weiss, Ph.D.
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91 Professor and vice Chair, Department of Microbiology; Co-Director, Penn Center for Research on Coronaviruses and Other Emerging Pathogens
8
17 Office Address:
35 University of Pennsylvania School of Medicine
1e 203 A Johnson Pavilion
1a 3610 Hamilton Walk
23 Philadelphia, PA 19104-6076
8
18 TEL 215-898-8013
18 LAB 215-898-3551
18 FAX 215-573-4858
26 weisssr@pennmedicine.upenn.edu
8
8
18 RESEARCH SUMMARY
8
43a Our lab studies murine and human coronavirus pathogenesis, including MHV, MERS-CoV and SARS-CoV. We use MHV infection of mice as a model system for the study of: 1) acute viral encephalitis; 2) chronic demyelinating diseases such as Multiple Sclerosis and 3) virus-induced hepatitis and 4) severe acute respiratory diseases. We have the important tools of a well-developed animal model system and reverse genetic systems with which to manipulate the viral genome. We also investigate pathogenesis of human coronaviruses both the lethal MERS-CoV and SARS-CoV-2 as well as the common cold viruses OC43 and 229E and NL63. We are investigating these both in epithelial cell lines and primary cells and in primary human nasal epitheli culutres gwon on air liquid interface. Much of our current work focuses on coronavirus-encoded antagonists of host innate responses. Other foci of the lab are on activation and antagonism of the OAS-RNase L pathway in human and bat cells, the pathogenic effects of endogenous host dsRNA and pathogenesis of Zika virus and other flaviviruses.
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18 ROTATION PROJECT
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1d6 1. Human coronaviruses. Investigate activation and antagonism of dsRNA induced antiviral pathways during infections with nonlethal human coronaviruses OC43, 229E and NL63. This includes infecting both cell lines and primary respiratory cells with with each of these viruses and assessing activation of type I and type III interferon as well as activist of OAS-RNase L and PKR, the data will be compared with ongoing studies on MERS-CoV-2 and SARS-CoV-2. and MHV.
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11c 2. Coronavirus EndoU proteins. Investigate the role of EndoU (MHV, MERS-CoV, SARS-CoV-2) in innate immune antagonism. This involves working with wild type and mutant viruses, and comparing both single stranded and double stranded RNA expression using FISH and immunostaining.
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3f 3. Human coroanvirus infections of primary nasal cells
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8
16 Lab personnel:
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40 Shree Nikhila (Nikki) Tanneti - Postdoctoral Researcher
2d Nicole Bracci-Postdoctoral Researcher
30 Helena Winstone- Postdoctoral Researcher
3a Clayton Otter- Graduate Student (combined MD, PhD)
2a Helen Stillwell- Graduate Student
31 Nicholas A Parenti - Research Specialist
27 Anant Patel- Research Specialist
26 29
27
Description of Research Expertise
2b Research Interests51 - Murine coronavirus pathogenesis, central nervous system, liver and lung
7d - Pathogenesis of human coronaviruses including MERS-CoV, SARS-CoV-2 and other nonlethal human respiratory viruses
56 - Activation and antagonism of the OAS-RNase L pathway in human and bat cells
2f - Viral and cellular phosphodiesterases
4a - Interaction of viruses with dsRNA induced innate immune pathways
21 - Zika virus pathogenesis
30 - Endogenous dsRNA induced pathogenesis
8
8
97 Key words: murine coronavirus, SARS-CoV MERS-CoV, human respiratory coronavirus, viral pathogenesis, interferon antagonist, OAS-RNase L.
8
28 Description of Research
8
1a Susan Weiss, Ph.D.
8
91 Professor and vice Chair, Department of Microbiology; Co-Director, Penn Center for Research on Coronaviruses and Other Emerging Pathogens
8
17 Office Address:
35 University of Pennsylvania School of Medicine
1e 203 A Johnson Pavilion
1a 3610 Hamilton Walk
23 Philadelphia, PA 19104-6076
8
18 TEL 215-898-8013
18 LAB 215-898-3551
18 FAX 215-573-4858
26 weisssr@pennmedicine.upenn.edu
8
8
18 RESEARCH SUMMARY
8
43a Our lab studies murine and human coronavirus pathogenesis, including MHV, MERS-CoV and SARS-CoV. We use MHV infection of mice as a model system for the study of: 1) acute viral encephalitis; 2) chronic demyelinating diseases such as Multiple Sclerosis and 3) virus-induced hepatitis and 4) severe acute respiratory diseases. We have the important tools of a well-developed animal model system and reverse genetic systems with which to manipulate the viral genome. We also investigate pathogenesis of human coronaviruses both the lethal MERS-CoV and SARS-CoV-2 as well as the common cold viruses OC43 and 229E and NL63. We are investigating these both in epithelial cell lines and primary cells and in primary human nasal epitheli culutres gwon on air liquid interface. Much of our current work focuses on coronavirus-encoded antagonists of host innate responses. Other foci of the lab are on activation and antagonism of the OAS-RNase L pathway in human and bat cells, the pathogenic effects of endogenous host dsRNA and pathogenesis of Zika virus and other flaviviruses.
8
8
8
18 ROTATION PROJECT
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1d6 1. Human coronaviruses. Investigate activation and antagonism of dsRNA induced antiviral pathways during infections with nonlethal human coronaviruses OC43, 229E and NL63. This includes infecting both cell lines and primary respiratory cells with with each of these viruses and assessing activation of type I and type III interferon as well as activist of OAS-RNase L and PKR, the data will be compared with ongoing studies on MERS-CoV-2 and SARS-CoV-2. and MHV.
9
11c 2. Coronavirus EndoU proteins. Investigate the role of EndoU (MHV, MERS-CoV, SARS-CoV-2) in innate immune antagonism. This involves working with wild type and mutant viruses, and comparing both single stranded and double stranded RNA expression using FISH and immunostaining.
8
3f 3. Human coroanvirus infections of primary nasal cells
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8
16 Lab personnel:
8
40 Shree Nikhila (Nikki) Tanneti - Postdoctoral Researcher
2d Nicole Bracci-Postdoctoral Researcher
30 Helena Winstone- Postdoctoral Researcher
3a Clayton Otter- Graduate Student (combined MD, PhD)
2a Helen Stillwell- Graduate Student
31 Nicholas A Parenti - Research Specialist
27 Anant Patel- Research Specialist
26 29
23
171 Comar CE, Otter CJ, Pfannenstiel J, Doerger E, Renner DM, Tan LH, Perlman S, Cohen NA, Fehr AR, Weiss SR.: MERS-CoV endoribonuclease and accessory proteins jointly evade host innate immunity during infection of lung and nasal epithelial cells. Proc Natl Acad Sci U S A 119: e2123208119, May 2022.
213 Nguyen LC, Renner DM, Silva D, Yang D, Parenti NA, Medina KM, Nicolaescu V, Gula H, Drayman N, Valdespino A, Mohamed A, Dann C, Wannemo K, Robinson-Mailman L, Gonzalez A, Stock L, Cao M, Qiao Z, Moellering RE, Tay S, Randall G, Beers MF, Rosner MR, Oakes SA, Weiss SR.: SARS-CoV-2 Diverges from Other Betacoronaviruses in Only Partially Activating the IRE1α/XBP1 Endoplasmic Reticulum Stress Pathway in Human Lung-Derived Cells. mBio 13: e0241522, Oct 2022.
1dd Li Y, Renner DM, Comar CE, Whelan JN, Reyes HM, Cardenas-Diaz FL, Truitt R, Tan LH, Dong B, Alysandratos KD, Huang J, Palmer JN, Adappa ND, Kohanski MA, Kotton DN, Silverman RH, Yang W, Morrisey EE, Cohen NA, Weiss SR.: SARS-CoV-2 induces double-stranded RNA-mediated innate immune responses in respiratory epithelial-derived cells and cardiomyocytes. Proc Natl Acad Sci U S A 118: e2022643118, Apr 2021.
97 Weiss SR.: Forty years with coronaviruses. J Exp Med 217: e20200537, May 2020.
112 Ancar R, Li Y, Kindler E, Cooper DA, Ransom M, Thiel V, Weiss SR, Hesselberth JR, Barton DJ.: Physiologic RNA targets and refined sequence specificity of coronavirus EndoU. RNA 26: 1976-1999, Dec 2020.
11c Comar CE, Goldstein SA, Li Y, Yount B, Baric RS, Weiss SR.: Antagonism of dsRNA-Induced Innate Immune Pathways by NS4a and NS4b Accessory Proteins during MERS Coronavirus Infection. mBio 10: e00319-19, Mar 2019.
11a Li Y, Dong B, Wei Z, Silverman RH, Weiss SR.: Activation of RNase L in Egyptian Rousette Bat-Derived RoNi/7 Cells Is Dependent Primarily on OAS3 and Independent of MAVS Signaling. mBio 10: e02414-19, Nov 2019.
12a Thornbrough JM, Jha BK, Yount B, Goldstein SA, Li Y, Elliott R, Sims AC, Baric RS, Silverman RH, Weiss SR.: Middle East Respiratory Syndrome Coronavirus NS4b Protein Inhibits Host RNase L Activation. mBio 7: e00258, Mar 2016.
156 Zhao L, Jha BK, Wu A, Elliott R, Ziebuhr J, Gorbalenya AE, Silverman RH, Weiss SR.: Antagonism of the interferon-induced OAS-RNase L pathway by murine coronavirus ns2 protein is required for virus replication and liver pathology. Cell Host Microbe 11: 607-16, Jun 2012.
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Selected Publications
123 Otter CJ, Fausto A, Tan LH, Khosla AS, Cohen NA, Weiss SR.: Infection of primary nasal epithelial cells differentiates among lethal and seasonal human coronaviruses. Proc Natl Acad Sci U S A 120: e2218083120, Apr 2023.171 Comar CE, Otter CJ, Pfannenstiel J, Doerger E, Renner DM, Tan LH, Perlman S, Cohen NA, Fehr AR, Weiss SR.: MERS-CoV endoribonuclease and accessory proteins jointly evade host innate immunity during infection of lung and nasal epithelial cells. Proc Natl Acad Sci U S A 119: e2123208119, May 2022.
213 Nguyen LC, Renner DM, Silva D, Yang D, Parenti NA, Medina KM, Nicolaescu V, Gula H, Drayman N, Valdespino A, Mohamed A, Dann C, Wannemo K, Robinson-Mailman L, Gonzalez A, Stock L, Cao M, Qiao Z, Moellering RE, Tay S, Randall G, Beers MF, Rosner MR, Oakes SA, Weiss SR.: SARS-CoV-2 Diverges from Other Betacoronaviruses in Only Partially Activating the IRE1α/XBP1 Endoplasmic Reticulum Stress Pathway in Human Lung-Derived Cells. mBio 13: e0241522, Oct 2022.
1dd Li Y, Renner DM, Comar CE, Whelan JN, Reyes HM, Cardenas-Diaz FL, Truitt R, Tan LH, Dong B, Alysandratos KD, Huang J, Palmer JN, Adappa ND, Kohanski MA, Kotton DN, Silverman RH, Yang W, Morrisey EE, Cohen NA, Weiss SR.: SARS-CoV-2 induces double-stranded RNA-mediated innate immune responses in respiratory epithelial-derived cells and cardiomyocytes. Proc Natl Acad Sci U S A 118: e2022643118, Apr 2021.
97 Weiss SR.: Forty years with coronaviruses. J Exp Med 217: e20200537, May 2020.
112 Ancar R, Li Y, Kindler E, Cooper DA, Ransom M, Thiel V, Weiss SR, Hesselberth JR, Barton DJ.: Physiologic RNA targets and refined sequence specificity of coronavirus EndoU. RNA 26: 1976-1999, Dec 2020.
11c Comar CE, Goldstein SA, Li Y, Yount B, Baric RS, Weiss SR.: Antagonism of dsRNA-Induced Innate Immune Pathways by NS4a and NS4b Accessory Proteins during MERS Coronavirus Infection. mBio 10: e00319-19, Mar 2019.
11a Li Y, Dong B, Wei Z, Silverman RH, Weiss SR.: Activation of RNase L in Egyptian Rousette Bat-Derived RoNi/7 Cells Is Dependent Primarily on OAS3 and Independent of MAVS Signaling. mBio 10: e02414-19, Nov 2019.
12a Thornbrough JM, Jha BK, Yount B, Goldstein SA, Li Y, Elliott R, Sims AC, Baric RS, Silverman RH, Weiss SR.: Middle East Respiratory Syndrome Coronavirus NS4b Protein Inhibits Host RNase L Activation. mBio 7: e00258, Mar 2016.
156 Zhao L, Jha BK, Wu A, Elliott R, Ziebuhr J, Gorbalenya AE, Silverman RH, Weiss SR.: Antagonism of the interferon-induced OAS-RNase L pathway by murine coronavirus ns2 protein is required for virus replication and liver pathology. Cell Host Microbe 11: 607-16, Jun 2012.
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