Computational Virology

RNA-Viren sind ubiquitär nachweisbar und gehören weltweit zu den am weitesten verbreiteten biologischen Organismen. Sie sind die Ursache für viele bestehende und neu auftretende Infektionskrankheiten wie zum Beispiel Hepatitis und COVID-19. Wir sind von der Vielfalt und Flexibilität der RNA-Viren fasziniert, und nutzen modernste Sequenzierungstechnologien und molekularbiologische Methoden um die Evolution und Virus-Wirt-Interaktion von RNA-Viren zu untersuchen. Obwohl wir uns derzeit auf hepatotrope Viren konzentrieren, haben wir in der Vergangenheit eine Vielzahl von Krankheitserregern, wie zum Beispiel SARS-CoV-2 untersucht. Ziel unserer Forschung ist es langfristig im Rahmen translationaler Kooperationen zur Entwicklung neuer antiviraler Strategien beizutragen.

CV_logo_Entwurf_v3_transparent

1. Evolution der RNA Viren
RNA-Viren verändern sich aufgrund zufällig auftretender Mutationen fortlaufend. Während einer Infektion können so in einem Patienten genetisch vielfältige Populationen, sogenannte Quasispezies, entstehen. Wir untersuchen, wie sich RNA-Viren während einer Infektion anpassen und verändern, um Varianten zu identifizieren, die mit viraler Persistenz oder Clearance verbunden sind (Gömer et al. 2022). Das hohe Mutationspotenzial der RNA-Viren erschwert zudem die erfolgreiche Entwicklung von Impfsoffen und antiviralen Medikamente, da resistente Mutationen oft innerhalb von Wochen oder Monaten nach Beginn einer Behandlung auftreten. Mittels Tiefensequenzierung konnten wir in Patienten so kürzlich erstmals zeigen, dass Ribavirin eine mutagene Wirkung auf das virale Genom des Hepatitis E Virus ausübt und so zur Bildung resistenter Varianten führt (Todt et al., 2016). In Zukunft wollen wir diese Technologie nutzen, um frühzeitig Patienten mit dem Risiko eines Therapieversagens zu identifizieren und personalisierte Behandlungsstrategien zu ermöglichen.

2. Virus-Wirt-Interaktionen
Der klinische Verlauf einer viralen Infektion wird sowohl vom viralen Erreger als auch von der Immunantwort des Wirts beeinflusst. Wir nutzen modernste RNA-Sequenzierungstechnologie um die Wirtsantwort auf einen viralen Erreger mit hoher Auflösung zu untersuchen und unser Verständnis viraler Pathogenese zu verbessern. Im Rahmen von RNA-Sequenzierungsstudien an HEV-infizierten primären menschlichen Hepatozyten konnten wir so eine zeitlich strukturierte transkriptionelle Abwehrreaktion gegen das Virus beobachten (Todt et al. 2020). Unser Ziel ist es, mit
Hilfe von Ansätzen des „maschinellen Lernens“ Transkriptomdaten zu analysieren und so Muster zu erkennen, welche den Verlauf einer Infektion maßgeblich bestimmen. Insbesondere wollen wir die unterschiedlichen Immunreaktionen bei Patienten mit chronischen oder akuten HEV-Infektionen verstehen.

3. Virale Fingerabdrücke
NGS Sequenzierungstechnologien erzeugen gewöhnlich riesige Datenmengen, von denen aufgrund ihrer Komplexität häufig jedoch nur Bruchteile systematisch analysiert und ausgewertet werden. Aus diesem Grund lassen sich oftmals auch aus bereits vorhandenen Datensätzen wichtige neue Erkenntnisse und Einblicke gewinnen. Im Rahmen translationaler Kooperationen entwickeln wir neue Analysepipelines, Algorithmen und bioinformatische work flows, um das volle Potenzial von klinisch gewonnenen Sequenzierdaten auszuschöpfen. Hierbei interessieren wir uns besonders für Datensätze aus verschiedeneren Patientenkohorten, um (Ko-)Infektionen mit mehreren Viren, Virusmutationen und Virusintegrationsstellen im Wirtsgenom zu erkennen und sie mit klinischen Merkmalen zu korrelieren.

Projekte:

Host-virus interaction and evolution of Hepaciviruses.

Unser Team:

Daniel Todt

Group leader
Passionate about virus sequencing, transcriptomics, translational medicine and emerging technologies.

Interested ?

This could be you !
Are you interested virology and programming. We are always welcome to new passionate bachelor and master students.

Richard Brown

Postdoc

André Gömer

Postdoc

Maximilian Nocke

PhD Student

Leyla Sirkinti

PhD Student

Saskia Janshoff

PhD Student

Maximilian Beikirch

Medical Doctoral Student

Hannah Sturm

Master Student

Ian Perez Medina

Bachelor Student
Github Linkedin

Key publications

[1]
D. Todt et al., “Robust hepatitis E virus infection and transcriptional response in human hepatocytes,” Proceedings of the National Academy of Sciences of the United States of America, vol. 117, Art. no. 201912307, 2020, doi: 10.1073/pnas.1912307117.
[2]
D. Todt et al., “In vivo evidence for ribavirin-induced mutagenesis of the hepatitis E virus genome,” Gut, vol. 65, no. 10, pp. 1733–1743, 2016, doi: 10.1136/gutjnl-2015-311000.
[3]
A. Gömer et al., “Intra-host analysis of Hepaciviral glycoprotein evolution reveals signatures associated with viral persistence and clearance,” Virus Evolution [ISSN: 2057-1577], Jan. 2022, Published, doi: 10.1093/ve/veac007.
[4]
A. Gömer et al., “Emergence of resistance-associated variants during sofosbuvir treatment in chronically infected hepatitis E patients,” Hepatology, Jun. 2023, Published, doi: 10.1097/hep.0000000000000514.
[5]
M. Wißing et al., “Genetic determinants of host- and virus-derived insertions for hepatitis E virus replication,” Nature communications, vol. 15, no. 1, Art. no. 4855, Jun. 2024, doi: 10.1038/s41467-024-49219-8.

Publications

2025

[1]
L. Pottkämper, M. Jagst, D. Todt, and E. Steinmann, “Stability and inactivation of hepatitis A virus on inanimate surfaces,” The Journal of hospital infection, vol. 2025, Mar. 2025, doi: 10.1016/j.jhin.2025.02.020.
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2024

[1]
A. Gömer et al., “Dynamic evolution of the sofosbuvir-associated variant A1343V in HEV-infected patients under concomitant sofosbuvir-ribavirin treatment,” JHEP reports, Art. no. 100989, Jan. 2024, Published, doi: 10.1016/j.jhepr.2023.100989.
[2]
F. Rau et al., “Monitoring of hepatitis E virus in wastewater can identify clinically relevant variants,” Liver international, Jan. 2024, Published, doi: 10.1111/liv.15842.
[3]
J. E. Konkol et al., “A comprehensive approach for evaluating the virucidal performance of domestic laundry detergents under practical conditions,” Journal of applied microbiology, vol. 135, no. 3, Art. no. lxae052, Mar. 2024, doi: 10.1093/jambio/lxae052.
[4]
N. Frericks et al., “Unraveling the dynamics of hepatitis C virus adaptive mutations and their impact on antiviral responses in primary human hepatocytes,” Journal of virology, vol. 98, no. 3, Art. no. e0192123, Feb. 2024, doi: 10.1128/jvi.01921-23.
[5]
M. Klöhn et al., “Targeting cellular cathepsins inhibits hepatitis E virus entry,” Hepatology, vol. 80, no. 5, pp. 1239–1251, May 2024, doi: 10.1097/hep.0000000000000912.
[6]
M. Klöhn et al., “The glutamate receptor antagonist ifenprodil inhibits hepatitis E virus infection,” Antimicrobial agents and chemotherapy, vol. 2024, Art. no. e01035-24, Oct. 2024, doi: 10.1128/aac.01035-24.
[7]
D. Kühn et al., “Divergent autoantibody and cytokine levels in COVID‐19 sepsis patients influence survival,” Journal of medical virology, vol. 96, no. 10, Art. no. e29935, Sep. 2024, doi: 10.1002/jmv.29935.
[8]
R. Khanal et al., “MicroRNAs modulate SARS-CoV-2 infection of primary human hepatocytes by regulating the entry factors ACE2 and TMPRSS2,” Liver international, vol. 44, no. 11, pp. 2983–2995, Aug. 2024, doi: 10.1111/liv.16079.
[9]
T. L. Meister et al., “Inactivation of yellow fever virus by WHO-recommended hand rub formulations and surface disinfectants,” PLoS neglected tropical diseases, vol. 18, no. 6, Art. no. e0012264, Jun. 2024, doi: 10.1371/journal.pntd.0012264.
[10]
B. Gisevius et al., “Propionic acid promotes neurite recovery in damaged multiple sclerosis neurons,” Brain communications , vol. 6, no. 3, Art. no. fcae182, Jun. 2024, doi: 10.1093/braincomms/fcae182.
[11]
R. Plümers et al., “Hepatitis E virus infections in German blood donors : results of 8 years of screening, 2015 to 2022,” Eurosurveillance, vol. 29, no. 24, Art. no. 2300665, Jun. 2024, doi: 10.2807/1560-7917.es.2024.29.24.2300665.
[12]
M. Schemmerer et al., “Proof of infectivity of hepatitis E virus particles from the ejaculate of chronically infected patients,” Journal of medical virology, vol. 96, no. 6, Art. no. e29735, Jun. 2024, doi: 10.1002/jmv.29735.
[13]
R. Plümers, J. P. Dreier, C. Knabbe, E. Steinmann, D. Todt, and T. Vollmer, “Kinetics of Hepatitis E Virus Infections in Asymptomatic Persons,” Emerging infectious diseases, vol. 30, no. 5, pp. 934–940, Apr. 2024, doi: 10.3201/eid3005.231764.
[14]
M. Jagst et al., “Modeling extrahepatic hepatitis E virus infection in induced human primary neurons,” Proceedings of the National Academy of Sciences of the United States of America, vol. 121, no. 47, Art. no. e2411434121, Nov. 2024, doi: 10.1073/pnas.2411434121.
[15]
J. A. Haase et al., “The tyrosine kinase Yes1 is a druggable host factor of HEV,” Hepatology communications, vol. 8, no. 11, Art. no. e0553, Oct. 2024, doi: 10.1097/hc9.0000000000000553.
[16]
X. Zhang et al., “A pan-genotypic hepatitis E virus replication inhibitor with high potency in a rat infection model,” Gastroenterology, vol. 2024, Nov. 2024, doi: 10.1053/j.gastro.2024.10.043.
[17]
X. Zhang et al., “A Pangenotypic Hepatitis E Virus Replication Inhibitor with High Potency in a Rat Infection Model,” Gastroenterology [ISSN: 0016-5085], Nov. 2024, Published, doi: 10.1053/j.gastro.2024.10.043.
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2023

[1]
T. L. Meister et al., “Efficient inactivation of monkeypox virus by World Health Organization-recommended hand rub formulations and alcohols,” Emerging infectious diseases, vol. 29, no. 1, pp. 189–192, 2023, doi: 10.3201/eid2901.221429.
[2]
J. A. Schrader et al., “Epidermal growth factor receptor modulates hepatitis e virus entry in human hepatocytes –HEP-22-1113,” Hepatology, vol. 77, no. 6, pp. 2104–2117, 2023, doi: 10.1097/hep.0000000000000308.
[3]
P. Biedermann et al., “Insertions and deletions in the hypervariable region of the hepatitis E virus genome in individuals with acute and chronic infection,” Liver international, vol. 43, no. 4, pp. 794–804, Jan. 2023, doi: 10.1111/liv.15517.
[4]
J.-E. Wißmann, Y. Brüggemann, D. Todt, J. Steinmann, and E. Steinmann, “Survival and inactivation of hepatitis E virus on inanimate surfaces,” The Journal of hospital infection, vol. 134, pp. 57–62, 2023, doi: 10.1016/j.jhin.2023.01.013.
[5]
M. Ruhlandt et al., “Impact of concentration, temperature and pH on the virucidal activity of alcohols against human adenovirus,” American journal of infection control, vol. 2023, Feb. 2023, doi: 10.1016/j.ajic.2023.01.014.
[6]
T. L. Meister et al., “Stability and inactivation of monkeypox virus on inanimate surfaces,” The journal of infectious diseases, vol. 2023, May 2023, doi: 10.1093/infdis/jiad127.
[7]
Y. Zhang et al., “Mouse liver-expressed shiftless is an evolutionarily conserved antiviral effector restricting human and murine hepaciviruses,” Microbiology spectrum, vol. 11, no. 4, Art. no. e01284-23, Jun. 2023, doi: 10.1128/spectrum.01284-23.
[8]
T. L. Meister et al., “Virucidal activity of oral, hand and surface disinfectants against respiratory syncytial virus,” The Journal of hospital infection, vol. 141, pp. 25–32, Aug. 2023, doi: 10.1016/j.jhin.2023.08.009.
[9]
V. Kinast et al., “Janus kinase-inhibition modulates hepatitis E virus infection,” Antiviral research, vol. 217, Art. no. 105690, Jul. 2023, doi: 10.1016/j.antiviral.2023.105690.
[10]
O. Bagato et al., “Spatiotemporal analysis of SARS-CoV-2 infection reveals an expansive wave of monocyte-derived macrophages associated with vascular damage and virus clearance in hamster lungs,” Microbiology spectrum, vol. 12, no. 1, Art. no. e02469, Nov. 2023, doi: 10.1128/spectrum.02469-23.
[11]
V. Kinast and D. Todt, “The relation of host genetics to symptomatic hepatitis E,” in Hepatology, vol. 79, no. 6, Hoboken. NJ: Wiley Interscience, 2023, pp. 1261–1263. doi: 10.1097/hep.0000000000000749.
[12]
N. Heinen et al., “Productive infection of primary human hepatocytes with SARS-CoV-2 induces antiviral and proinflammatory responses,” Gut, vol. 73, no. 10, Art. no. e14, Dec. 2023, doi: 10.1136/gutjnl-2023-330961.
[13]
T. L. Meister, L. Kirchhoff, Y. Brüggemann, D. Todt, J. Steinmann, and E. Steinmann, “Stability of pathogens on banknotes and coins: a narrative review,” Journal of medical virology, vol. 95, no. 12, Art. no. e29312, Dec. 2023, doi: 10.1002/jmv.29312.
[14]
N. Frericks et al., “Hepatitis C virus cell culture adaptive mutations enhance cell culture propagation by multiple mechanisms but boost antiviral responses in primary human hepatocytes,” Nov. 22, 2023.
Back to top

2022

[1]
P. Behrendt et al., “Hepatitis E virus is highly resistant to alcohol-based disinfectants,” Journal of hepatology, vol. 76, no. 5, pp. 1062–1069, 2022, doi: 10.1016/j.jhep.2022.01.006.
[2]
R. Bertram et al., “Risk stratification of SARS-CoV-2 breakthrough infections based on an outbreak at a student festive event,” Vaccines, vol. 10, no. 3, Art. no. 432, Mar. 2022, doi: 10.3390/vaccines10030432.
[3]
T. Burkard et al., “Viral interference of Hepatitis C and E virus replication in novel experimental co-infection systems,” Cells, vol. 11, no. 6, Art. no. 927, Mar. 2022, doi: 10.3390/cells11060927.
[4]
D. Praditya et al., “Identification of structurally re-engineered rocaglates as inhibitors against hepatitis E virus replication,” Antiviral research, vol. 204, Art. no. 105359, 2022, doi: 10.1016/j.antiviral.2022.105359.
[5]
J. Schuhenn et al., “Differential interferon-α subtype induced immune signatures are associated with suppression of SARS-CoV-2 infection,” Proceedings of the National Academy of Sciences of the United States of America, vol. 119, no. 8, Art. no. e2111600119, 2022, doi: 10.1073/pnas.2111600119.
[6]
T. L. Meister et al., “Low risk of Severe Acute Respiratory Syndrome Coronavirus 2 transmission by fomites: a clinical observational study in highly infectious COVID-19 patients,” The journal of infectious diseases, vol. 226, no. 9, pp. 1608–1615, May 2022, doi: 10.1093/infdis/jiac170.
[7]
J. F. Schijven, M. Wind, D. Todt, J. Howes, B. Tamele, and E. Steinmann, “Risk assessment of banknotes as a fomite of SARS‐CoV‐2 in cash payment transactions,” Risk analysis, vol. 43, no. 4, pp. 700–708, May 2022, doi: 10.1111/risa.13935.
[8]
T. L. Meister et al., “Virucidal activity of nasal sprays against severe acute respiratory syndrome coronavirus-2,” The Journal of hospital infection, vol. 120, pp. 9–13, 2022, doi: 10.1016/j.jhin.2021.10.019.
[9]
A. Ebenig et al., “Vaccine-associated enhanced respiratory pathology in COVID-19 hamsters after TH2-biased immunization,” Cell reports, vol. 40, no. 7, Art. no. 111214, Aug. 2022, doi: 10.1016/j.celrep.2022.111214.
[10]
T. L. Meister et al., “A ribavirin-induced ORF2 single-nucleotide variant produces defective hepatitis E virus particles with immune decoy function,” Proceedings of the National Academy of Sciences of the United States of America, vol. 119, no. 34, Art. no. e2202653119, 2022, doi: 10.1073/pnas.2202653119.
[11]
A. Gömer et al., “Dose-dependent hepacivirus infection reveals linkage between infectious dose and immune response,” Microbiology spectrum, vol. 10, no. 5, Art. no. e01686-22, Aug. 2022, doi: 10.1128/spectrum.01686-22.
[12]
Y. Brüggemann, M. Klöhn, and D. Todt, “The pivotal role of CD8+ T cells in hepatitis E virus infection,” Journal of hepatology, vol. 77, no. 4, pp. 909–911, 2022, doi: 10.1016/j.jhep.2022.08.002.
[13]
M. Badenhorst et al., “An equine model for vaccination against a hepacivirus : insights into host responses to E2 recombinant protein vaccination and subsequent equine hepacivirus inoculation,” Viruses, vol. 14, no. 7, Art. no. 1401, Jun. 2022, doi: 10.3390/v14071401.
[14]
A. Gömer et al., “Experimental cross-species infection of donkeys with equine hepacivirus and analysis of host immune signatures,” One health outlook, vol. 4, no. 1, Art. no. 9, May 2022, doi: 10.1186/s42522-022-00065-y.
[15]
T. L. Meister et al., “Mouthrinses against SARS-CoV-2 – High antiviral effectivity by membrane disruption in vitro translates to mild effects in a randomized placebo-controlled clinical trial,” Virus research, vol. 316, Art. no. 198791, May 2022, doi: 10.1016/j.virusres.2022.198791.
[16]
T. L. Meister, Y. Brüggemann, B. Tamele, J. Howes, E. Steinmann, and D. Todt, “A touch transfer assay to determine surface transmission of highly pathogenic viruses,” STAR Protocols, vol. 3, no. 2, Art. no. 101188, 2022, doi: 10.1016/j.xpro.2022.101188.
[17]
J. Steinmann et al., “Evaluation of the substitution of poliomyelitis virus for testing virucidal activities of instrument and surface disinfection,” The Journal of hospital infection, vol. 122, pp. 60–63, 2022, doi: 10.1016/j.jhin.2021.12.022.
[18]
N. Heinen et al., “In-depth analysis of T cell immunity and antibody responses in heterologous prime-boost-boost vaccine regimens against SARS-CoV-2 and Omicron variant,” Frontiers in immunology, vol. 13, Art. no. 1062210, Dec. 2022, doi: 10.3389/fimmu.2022.1062210.
[19]
V. Kinast, M. Klöhn, M. K. Nocke, D. Todt, and E. Steinmann, “Hepatitis E virus species barriers: seeking viral and host determinants,” Current opinion in virology, vol. 56, Art. no. 101274, 2022, doi: 10.1016/j.coviro.2022.101274.
[20]
U. Gravemann et al., “Hepatitis E virus is effectively inactivated by methylene blue plus light treatment,” Transfusion, vol. 62, no. 11, pp. 2200–2204, Sep. 2022, doi: 10.1111/trf.17108.
[21]
T. L. Meister et al., “Infection of young foals with Equine Parvovirus-Hepatitis following a fatal non-biologic case of Theiler’s disease,” Veterinary microbiology, vol. 274, Art. no. 109557, 2022, doi: 10.1016/j.vetmic.2022.109557.
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2021

[1]
Y. Du et al., “The impact of hepatitis B surface antigen on natural killer cells in patients with chronic hepatitis B infection,” Liver international, vol. 2021, Apr. 2021, doi: 10.1111/liv.14885.
[2]
B. Tegtmeyer et al., “Initial HCV infection of adult hepatocytes triggers a temporally structured transcriptional program containing diverse pro- and anti-viral elements,” Journal of virology, vol. 2021, pp. 1–36, Mar. 2021, doi: 10.1128/jvi.00245-21.
[3]
K. Steinhauer et al., “Comparison of the in vitro-efficacy of different mouthwash solutions targeting SARS-CoV-2 based on the European Standard EN 14476,” The Journal of hospital infection, vol. 111, pp. 180–183, 2021, doi: 10.1016/j.jhin.2021.01.031.
[4]
J. E. Wißmann, L. Kirchhoff, Y. Brüggemann, D. Todt, J. Steinmann, and E. Steinmann, “Persistence of pathogens on inanimate surfaces: a narrative review,” Microorganisms, vol. 9, no. 2, Art. no. 343, Feb. 2021, doi: 10.3390/microorganisms9020343.
[5]
T. Khera et al., “Long-lasting imprint in the Soluble inflammatory milieu despite early treatment of acute symptomatic Hepatitis C,” The journal of infectious diseases, vol. 2021, pp. 1–26, Jan. 2021, doi: 10.1093/infdis/jiab048.
[6]
T. Horvatits et al., “Hepatitis E virus persists in the ejaculate of chronically infected men,” Journal of hepatology, vol. 75, no. 1, pp. 55–63, Jul. 2021, doi: 10.1016/j.jhep.2020.12.030.
[7]
D. Bankwitz et al., “Hepatitis C reference viruses highlight potent antibody responses and diverse viral functional interactions with neutralising antibodies,” Gut, vol. 70, no. 9, pp. 1734–1745, Sep. 2021, doi: 10.1136/gutjnl-2020-321190.
[8]
C. Conzelmann et al., “Pasteurization inactivates SARS-CoV-2 spiked breast milk,” Pediatrics, vol. 147, no. 1, Art. no. e2020031690, Jan. 2021, doi: 10.1542/peds.2020-031690.
[9]
M. Wißing, Y. Brüggemann, E. Steinmann, and D. Todt, “Virus-host cell interplay during hepatitis E virus infection,” Trends in microbiology, vol. 29, no. 4, pp. 309–319, 2021, doi: 10.1016/j.tim.2020.07.002.
[10]
B. Reinecke et al., “Clinical course of infection and cross-species detection of equine parvovirus-hepatitis,” Viruses, vol. 13, no. 8, Art. no. 1454, Jul. 2021, doi: 10.3390/v13081454.
[11]
N. Heinen, T. L. Meister, M. Klöhn, E. Steinmann, D. Todt, and S. Pfänder, “Antiviral effect of budesonide against SARS-CoV-2,” Viruses, vol. 13, no. 7, Art. no. 1411, Jul. 2021, doi: 10.3390/v13071411.
[12]
D. Todt et al., “A realistic transfer method reveals low risk of SARS-CoV-2 transmission via contaminated euro coins and banknotes,” iScience, vol. 24, no. 8, Art. no. 102908, Aug. 2021, doi: 10.1016/j.isci.2021.102908.
[13]
J. Steinmann et al., “Virucidal efficacy of an ozone-generating system for automated room disinfection,” The Journal of hospital infection, vol. 116, pp. 16–20, Oct. 2021, doi: 10.1016/j.jhin.2021.06.004.
[14]
P. Wollschläger et al., “SARS-CoV-2 N gene dropout and N gene Ct value shift as indicator for the presence of B.1.1.7 lineage in a commercial multiplex PCR assay,” Clinical microbiology and infection, vol. 27, no. 9, p. 1353.e1-1353.e5, 2021, doi: 10.1016/j.cmi.2021.05.025.
[15]
T. L. Meister et al., “Comparable environmental stability and disinfection profiles of the currently circulating SARS-CoV-2 variants of concern B.1.1.7 and B.1.351,” The journal of infectious diseases, vol. 224, no. 3, pp. 420–424, May 2021, doi: 10.1093/infdis/jiab260.
[16]
K. Cirksena et al., “The C-mannosylome of human induced pluripotent stem cells implies a role for ADAMTS16 C-mannosylation in eye development,” Molecular & cellular proteomics, vol. 20, Art. no. 100092, May 2021, doi: 10.1016/j.mcpro.2021.100092.
[17]
T. P. Velavan et al., “Hepatitis E : An update on One Health and clinical medicine,” Liver international, vol. 41, no. 7, pp. 1462–1473, May 2021, doi: 10.1111/liv.14912.
[18]
L. van de Sand et al., “Glycyrrhizin effectively inhibits SARS-CoV-2 replication by inhibiting the viral main protease,” Viruses, vol. 13, no. 4, Art. no. 609, Apr. 2021, doi: 10.3390/v13040609.
[19]
Y. Du et al., “The impact of hepatitis B surface antigen on natural killer cells in patients with chronic hepatitis B virus infection,” Liver international, vol. 41, no. 9, pp. 2046–2058, Apr. 2021, doi: 10.1111/liv.14885.
[20]
K. Steinhauer et al., “Virucidal efficacy of different formulations for hand and surface disinfection targeting SARS CoV-2,” The Journal of hospital infection, vol. 112, pp. 27–30, 2021, doi: 10.1016/j.jhin.2021.03.015.
[21]
P. Behrendt et al., “Significant compartment‐specific impact of different RNA extraction methods and PCR assays on the sensitivity of hepatitis E virus detection,” Liver international, vol. 41, no. 8, pp. 1815–1823, Aug. 2021, doi: 10.1111/liv.14870.
[22]
B. Tegtmeyer et al., “Initial hepatitis C virus infection of adult hepatocytes triggers a temporally structured transcriptional program containing diverse pro- and antiviral elements,” Journal of virology, vol. 95, no. 10, Art. no. e00245-21, Apr. 2021, doi: 10.1128/jvi.00245-21.
[23]
T. L. Meister, Y. Brüggemann, D. Todt, S. Pfänder, and E. Steinmann, “Reply to Lamarca et al,” The journal of infectious diseases, vol. 223, no. 6, pp. 1114–1115, Mar. 2021, doi: 10.1093/infdis/jiaa795.
[24]
M. Klöhn, J. A. Schrader, Y. Brüggemann, D. Todt, and E. Steinmann, “Beyond the usual suspects: hepatitis E virus and its implications in hepatocellular carcinoma,” Cancers, vol. 13, no. 22, Art. no. 5867, Nov. 2021, doi: 10.3390/cancers13225867.
[25]
C. R. Torres Reyes et al., “Students in dormitories were not major drivers of the pandemic during winter term 2020/2021: a cohort study with RT-PCR and antibody surveillance in a German university city,” Covid, vol. 1, no. 1, pp. 345–356, Sep. 2021, doi: 10.3390/covid1010029.
[26]
A. Kratzel et al., “A genome-wide CRISPR screen identifies interactors of the autophagy pathway as conserved coronavirus targets,” PLoS biology, vol. 19, no. 12, Art. no. e3001490, Dec. 2021, doi: 10.1371/journal.pbio.3001490.
[27]
Y. Du et al., “Imprint of unconventional T‐cell response in acute hepatitis C persists despite successful early antiviral treatment,” European journal of immunology, vol. 52, no. 3, pp. 472–483, Nov. 2021, doi: 10.1002/eji.202149457.
[28]
J. Schuhenn et al., “Differential interferon-α subtype immune signatures suppress SARS-CoV-2 infection,” May 2021. doi: 10.1101/2021.05.20.444757.
[29]
D. Todt et al., “A realistic touch-transfer method reveals low risk of transmission for SARS-CoV-2 by contaminated coins and bank notes,” Apr. 2021. doi: 10.1101/2021.04.02.438182.
[30]
T. L. Meister et al., “Comparable environmental stability and disinfection profiles of the currently circulating SARS-CoV-2 variants of concern B.1.1.7 and B.1.351,” Apr. 08, 2021.
[31]
A. Kratzel et al., “A genome-wide CRISPR screen identifies interactors of the autophagy pathway as conserved coronavirus targets,” Feb. 2021. doi: 10.1101/2021.02.24.432634.
[32]
B. Tegtmeyer et al., “Initial HCV infection of adult hepatocytes triggers a temporally structured transcriptional program containing diverse pro- and anti-viral elements,” Feb. 2021. doi: 10.1101/2021.02.12.431054.
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B. Qu et al., “TMPRSS2-mediated SARS-CoV-2 uptake boosts innate immune activation, enhances cytopathology, and drives convergent virus evolution,” Proceedings of the National Academy of Sciences of the United States of America, vol. 121, no. 23, Art. no. e2407437121, 2021, doi: 10.1073/pnas.2407437121.
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2020

[1]
R. J. P. Brown et al., “Liver-expressed Cd302 and Cr1l limit hepatitis C virus cross-species transmission to mice,” Science advances, vol. 6, no. 45, Art. no. eabd3233, Nov. 2020, doi: 10.1126/sciadv.abd3233.
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S. R. Pallerla et al., “Hepatitis E virus infection: circulation, molecular epidemiology, and impact on global health,” Pathogens, vol. 9, no. 10, Art. no. 856, Oct. 2020, doi: 10.3390/pathogens9100856.
[3]
T. L. Meister et al., “Erratum to: Virucidal efficacy of different oral rinses against severe acute respiratory syndrome Coronavirus 2,” The journal of infectious diseases, vol. 2020, Oct. 2020, doi: 10.1093/infdis/jiaa539.
[4]
P. Behrendt et al., “Significant compartment-specific impact of the RNA extraction and quantification method on the sensitivity of hepatitis E virus detection: implications for clinical care?,” Journal of hepatology, vol. 73, p. S852, Sep. 2020, doi: 10.1016/s0168-8278(20)32147-4.
[5]
A. Wahid et al., “Clinical and molecular characterization of the human kidney as extrahepatic site of hepatitis E virus infection,” Journal of hepatology, vol. 73, pp. S833–S834, Sep. 2020, doi: 10.1016/s0168-8278(20)32109-7.
[6]
C. Conzelmann et al., “Holder pasteurization inactivates SARS-CoV-2 in human breast milk,” Aug. 04, 2020.
[7]
T. L. Meister et al., “Virucidal efficacy of different oral rinses against SARS-CoV-2,” The journal of infectious diseases, vol. 222, no. 8, pp. 1289–1292, Jul. 2020, doi: 10.1093/infdis/jiaa471.
[8]
C. Elsner et al., “Absence of cGAS-mediated type I IFN responses in HIV-1–infected T cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 117, no. 32, pp. 19475–19486, Jul. 2020, doi: 10.1073/pnas.2002481117.
[9]
S. Pfänder et al., “LY6E impairs coronavirus fusion and confers immune control of viral disease,” Nature microbiology, vol. 5, no. 11, pp. 1330–1339, Jul. 2020, doi: 10.1038/s41564-020-0769-y.
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F. Zettl et al., “Rapid quantification of SARS-CoV-2-neutralizing antibodies using propagation-defective vesicular stomatitis virus pseudotypes,” Vaccines, vol. 8, no. 3, Art. no. 386, Jul. 2020, doi: 10.3390/vaccines8030386.
[11]
M. Cornberg et al., “Sofosbuvir monotherapy fails to achieve HEV RNA elimination in patients with chronic hepatitis E: the HepNet SofE pilot study,” Journal of hepatology, vol. 73, no. 3, pp. 696–699, Jul. 2020, doi: 10.1016/j.jhep.2020.05.020.
[12]
T. L. Meister, M. Klöhn, E. Steinmann, and D. Todt, “A cell culture model for producing high titer hepatitis e virus stocks,” Journal of visualized experiments, no. 160, Art. no. e61373, Jun. 2020, doi: 10.3791/61373.
[13]
A. Kratzel et al., “Temperature-dependent surface stability of SARS-CoV-2,” Journal of infection, vol. 81, no. 3, pp. 452–482, 2020, doi: 10.1016/j.jinf.2020.05.074.
[14]
D. Praditya et al., “Hepatitis E virus is effectively inactivated in platelet concentrates by ultraviolet C light,” Vox sanguinis, vol. 2020, May 2020, doi: 10.1111/vox.12936.
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A. Kratzel et al., “Inactivation of severe acute respiratory syndrome coronavirus 2 by WHO-recommended hand rub formulations and alcohols,” Emerging infectious diseases, vol. 26, no. 7, pp. 1592–1595, Jul. 2020, doi: 10.3201/eid2607.200915.
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V. Kinast et al., “C19orf66 is an interferon-induced inhibitor of HCV replication that restricts formation of the viral replication organelle,” Journal of hepatology, vol. 73, no. 3, pp. 549–558, Apr. 2020, doi: 10.1016/j.jhep.2020.03.047.
[17]
G. Kampf, D. Todt, S. Pfänder, and E. Steinmann, “Persistence of coronaviruses on inanimate surfaces and its inactivation with biocidal agents,” The Journal of hospital infection, vol. 104, no. 3, pp. 246–251, 2020, doi: 10.1016/j.jhin.2020.01.022.
[18]
F. H. H. Brill et al., “Virucidal efficacy of glutaraldehyde for instrument disinfection,” GMS hygiene and infection control, vol. 15, pp. 1–5, 2020, doi: 10.3205/dgkh000369.
[19]
L. van de Sand et al., “Glycyrrhizin effectively neutralizes SARS-CoV-2 in vitro by inhibiting the viral main protease,” Dec. 2020. doi: 10.1101/2020.12.18.423104.
[20]
K. Steinhauer et al., “Virucidal efficacy of different formulations for hand and surface disinfection targeting SARS CoV-2,” Nov. 2020. doi: 10.1101/2020.11.08.373738.
[21]
K. Steinhauer et al., “Comparison of the in vitro-efficacy of different mouthwash solutions targeting SARS-CoV-2 based on the European Standard EN 14476,” Oct. 2020. doi: 10.1101/2020.10.25.354571.
[22]
C. Conzelmann et al., “Holder pasteurization inactivates SARS-CoV-2 in human breast milk,” Jun. 17, 2020.
[23]
A. Kratzel et al., “Efficient inactivation of SARS-CoV-2 by WHO-recommended hand rub formulations and alcohols,” Mar. 2020. doi: 10.1101/2020.03.10.986711.
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S. Pfaender et al., “LY6E impairs coronavirus fusion and confers immune control of viral disease,” Mar. 2020. doi: 10.1101/2020.03.05.979260.
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2019

[1]
T. L. Meister et al., “Characterization of equine parvovirus in thoroughbred breeding horses from Germany,” Viruses, vol. 11, no. 10, Art. no. 965, Oct. 2019, doi: 10.3390/v11100965.
[2]
V. Passos et al., “Characterization of endogenous SERINC5 protein as anti-HIV-1 factor,” Journal of virology, vol. 2019, pp. 1–35, Oct. 2019, doi: 10.1128/jvi.01221-19.
[3]
A. König et al., “High tolerance of hepatitis B virus to thermal disinfection,” Journal of hepatology, vol. 71, no. 6, pp. 1249–1251, Sep. 2019, doi: 10.1016/j.jhep.2019.08.022.
[4]
B. Schlevogt et al., “Chronic hepatitis E virus infection during lymphoplasmacytic lymphoma and Ibrutinib treatment,” Pathogens, vol. 8, no. 3, Art. no. 129, Aug. 2019, doi: 10.3390/pathogens8030129.
[5]
R. Stauf et al., “In vitro activity of active ingredients of disinfectants against drug-resistant fungi,” The Journal of hospital infection, vol. 103, no. 4, pp. 468–473, Jul. 2019, doi: 10.1016/j.jhin.2019.07.013.
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B. Becker et al., “Evaluation of the virucidal efficacy of disinfectant wipes with a test method simulating practical conditions,” Antimicrobial resistance and infection control, vol. 8, Art. no. 121, Jul. 2019, doi: 10.1186/s13756-019-0569-4.
[7]
B. Tegtmeyer et al., “Chronic equine hepacivirus infection in an adult gelding with severe hepatopathy,” Veterinary medicine and science, vol. 2019, Jul. 2019, doi: 10.1002/vms3.181.
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C. F. Soon et al., “Defining virus-specific CD8+ TCR repertoires for therapeutic regeneration of T cells against chronic hepatitis E,” Journal of hepatology, vol. 71, no. 4, pp. 673–684, Jun. 2019, doi: 10.1016/j.jhep.2019.06.005.
[9]
D. Bankwitz et al., “FRI-133-HCV neutralizing antibody responses in natural infections mapped by metric multi-dimensional scaling reveals new insights into HCV antigenicity and broadly neutralzing antibodies,” Journal of hepatology, vol. 70, no. 1, pp. e446–e446, Apr. 2019, doi: 10.1016/s0618-8278(19)30878-3.
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B. Schlevogt et al., “SAT-204-Hepatitis E virus antigen in urine as a useful diagnostic background and aims: for monitoring infection and detection of recent infection,” Journal of hepatology, vol. 70, no. 1. Amsterdam, Elsevier, p. e719, Apr. 16, 2019. doi: 10.1016/s0618-8278(19)31438-0.
[11]
P. Behrendt, J. Brüning, D. Todt, and E. Steinmann, “Influence of tattoo ink on hepatitis C virus infectiousness,” Open forum infectious diseases, vol. 6, Feb. 2019, doi: 10.1093/ofid/ofz047.
[12]
T. L. Meister, J. Brüning, D. Todt, and E. Steinmann, “Cell culture systems for the study of hepatitis E virus,” Antiviral research, vol. 163, pp. 34–49, Jan. 2019, doi: 10.1016/j.antiviral.2019.01.007.
[13]
T. T. Than et al., “High environmental stability of hepatitis B virus and inactivation requirements for chemical biocides,” The journal of infectious diseases, vol. 219, no. 7, pp. 1044–1048, 2019, doi: 10.1093/infdis/jiy620.
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O. E. Anastasiou et al., “Clinical outcome and viral genome variability of hepatitis B virus induced acute liver failure (HEP-18-0579),” Hepatology, vol. 69, no. 3, pp. 993–1003, 2019, doi: 10.1002/hep.30279.
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D. H. Banda et al., “A central hydrophobic E1 region controls the pH range of hepatitis C virus membrane fusion and susceptibility to fusion inhibitors,” Journal of hepatology, vol. 70, no. 6, pp. 1082–1092, 2019, doi: 10.1016/j.jhep.2019.01.033.
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T. Khera et al., “Functional and immunogenic characterization of diverse HCV glycoprotein E2 variants,” Journal of hepatology, vol. 70, no. 4, pp. 593–6002, 2019, doi: 10.1016/j.jhep.2018.11.003.
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R. Costa et al., “SEC14L2, a lipid-binding protein, regulates HCV replication in culture with inter- and intra- genotype variations,” Journal of hepatology, vol. 70, no. 4, pp. 603–614, 2019, doi: 10.1016/j.jhep.2018.11.012.
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T. L. Meister et al., “Equine parvovirus-hepatitis frequently detectable in commercial equine serum pools,” Viruses, vol. 11, no. 5, Art. no. 461, May 2019, doi: 10.3390/v11050461.
[19]
V. Kinast, T. Burkard, D. Todt, and E. Steinmann, “Hepatitis e virus drug development,” Viruses, vol. 11, no. 6, Art. no. 485, May 2019, doi: 10.3390/v11060485.
[20]
V. Kinast et al., “Identification of Keratin 23 as a Hepatitis C virus-induced host factor in the human liver,” Cells, vol. 8, no. 6, Art. no. 610, Jun. 2019, doi: 10.3390/cells8060610.
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2018

[1]
D. Todt, T. L. Meister, and E. Steinmann, “Hepatitis E virus treatment and ribavirin therapy: viral mechanisms of nonresponse,” Current opinion in virology, vol. 32, pp. 80–87, Oct. 2018, doi: 10.1016/j.coviro.2018.10.001.
[2]
O. García-Nicolás et al., “The small compound inhibitor K22 displays broad antiviral activity against different members of the family Flaviviridae and offers potential as pan-viral inhibitor,” Antimicrobial agents and chemotherapy, vol. 62, no. 11, pp. e01206-18, Sep. 2018, doi: 10.1128/aac.01206-18.
[3]
W. Koestner et al., “Interferon-beta expression and type I interferon receptor signaling of hepatocytes prevent hepatic necrosis and virus dissemination in Coxsackievirus B3-infected mice,” PLoS pathogens, vol. 14, no. 8, Art. no. e1007235, Aug. 2018, doi: 10.1371/journal.ppat.1007235.
[4]
M. Badenhorst et al., “First detection and frequent occurrence of Equine Hepacivirus in horses on the African continent,” Veterinary microbiology, vol. 223, pp. 51–58, Jul. 2018, doi: 10.1016/j.vetmic.2018.07.015.
[5]
D. Todt et al., “The natural compound silvestrol inhibits hepatitis E virus (HEV) replication in vitro and in vivo,” Antiviral research, vol. 157, pp. 151–158, Jul. 2018, doi: 10.1016/j.antiviral.2018.07.010.
[6]
S. Franz et al., “Susceptibility of Chikungunya virus to inactivation by heat and commercially and WHO-recommended biocides,” The journal of infectious diseases, vol. 218, no. 9, pp. 1507–1510, Jun. 2018, doi: 10.1093/infdis/jiy359.
[7]
L. Knegendorf et al., “Hepatitis E virus replication and interferon responses in human placental cells,” Hepatology communications, vol. 2, no. 2, pp. 173–187, Jan. 2018, doi: 10.1002/hep4.1138.
[8]
S. Pfaender et al., “Environmental stability and infectivity of hepatitis C virus (HCV) in different human body fluids,” Frontiers in microbiology, vol. 9, p. 504, 2018, doi: 10.3389/fmicb.2018.00504.
[9]
M. Olsowski et al., “Exophiala dermatitidis isolates from various sources: using alternative invertebrate host organisms (Caenorhabditis elegans and Galleria mellonella) to determine virulence,” Scientific reports, vol. 8, no. 1, Art. no. 12747, 2018, doi: 10.1038/s41598-018-30909-5.
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2017

[1]
R. Weller et al., “Hepatitis C virus strain-dependent usage of Apolipoprotein E modulates assembly efficiency and specific infectivity of secreted virions,” Journal of virology, vol. 91, no. 18, pp. e00422-17-1-e00422-17–17, Jun. 2017, doi: 10.1128/jvi.00422-17.
[2]
P. Behrendt et al., “Exacerbation d’infection par le virus de l’hépatite E au cours d’un traitement par anti-TNFα,” Revue du rhumatisme Edition française, vol. 84, no. 3, pp. 244–247, 2017, doi: 10.1016/j.rhum.2016.11.010.
[3]
D. Todt et al., “Successful retreatment of a patient with chronic hepatitis C genotype 2k/1b virus with ombitasvir/paritaprevir/ritonavir plus dasabuvir,” The journal of antimicrobial chemotherapy, vol. 75, no. 5, pp. 1541–1543, 2017, doi: 10.1093/jac/dkw572.
[4]
A. Siddharta et al., “Virucidal activity of world health organization-recommended formulations against enveloped viruses, including zika, ebola, and emerging coronaviruses,” The journal of infectious diseases, vol. 215, no. 6, pp. 902–906, 2017, doi: 10.1093/infdis/jix046.
[5]
P. Behrendt et al., “Exacerbation of hepatitis E virus infection during anti-TNFα treatment,” Joint bone spine, vol. 84, no. 2, pp. 217–219, 2017, doi: 10.1016/j.jbspin.2016.09.017.
[6]
B. Becker et al., “Virucidal efficacy of peracetic acid for instrument disinfection,” Antimicrobial resistance and infection control, vol. 6, no. 1, Art. no. 114, 2017, doi: 10.1186/s13756-017-0271-3.
[7]
S. Pfaender et al., “Immune protection against reinfection with nonprimate hepacivirus,” Proceedings of the National Academy of Sciences of the United States of America, vol. 114, no. 12, pp. E2430–E2439, 2017, doi: 10.1073/pnas.1619380114.
[8]
S. Walter et al., “Differential infection patterns and recent evolutionary origins of equine hepaciviruses in donkeys,” Journal of virology, vol. 91, no. 1, pp. e01711–e01716, 2017, doi: 10.1128/jvi.01711-16.
[9]
T. Khera et al., “Tracking HCV protease population diversity during transmission and susceptibility of founder populations to antiviral therapy,” Antiviral research, vol. 139, pp. 129–137, 2017, doi: 10.1016/j.antiviral.2017.01.001.
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2016

[1]
G. Ionidis et al., “Development and virucidal activity of a novel alcohol-based hand disinfectant supplemented with urea and citric acid,” BMC infectious diseases, vol. 16, Art. no. 77, 2016, doi: 10.1186/s12879-016-1410-9.
[2]
T. Gather et al., “Vertical transmission of hepatitis C virus-like non-primate hepacivirus in horses,” The journal of general virology, vol. 97, no. 10, pp. 2540–2551, 2016, doi: 10.1099/jgv.0.000561.
[3]
P. Behrendt et al., “Hepatitis E virus (HEV) ORF2 antigen levels differentiate between acute and chronic HEV infection,” The journal of infectious diseases, vol. 214, no. 3, pp. 361–368, 2016, doi: 10.1093/infdis/jiw161.
[4]
D. Todt, S. Walter, R. Brown, and E. Steinmann, “Mutagenic effects of ribavirin on hepatitis E virus-viral extinction versus selection of fitness-enhancing mutations,” Viruses, vol. 8, no. 10, Art. no. 283, 2016, doi: 10.3390/v8100283.
[5]
R. Weller et al., “Apolipoprotein E polymorphisms and their protective effect on hepatitis E virus replication,” Hepatology, vol. 64, no. 6, pp. 2274–2276, 2016, doi: 10.1002/hep.28788.
[6]
T. Gather et al., “Acute and chronic infections with nonprimate hepacivirus in young horses,” Veterinary research, vol. 47, no. 1, Art. no. 97, 2016, doi: 10.1186/s13567-016-0381-6.
[7]
M. Krull et al., “Emergence of linezolid- and vancomycin-resistant Enterococcus faecium in a department for hematologic stem cell transplantation,” Antimicrobial resistance and infection control, vol. 5, no. 1, Art. no. 31, 2016, doi: 10.1186/s13756-016-0131-6.
[8]
N. Anggakusuma et al., “Hepacivirus NS3/4A proteases interfere with MAVS signaling in both their cognate animal hosts and humans: implications for zoonotic transmission,” Journal of virology, vol. 90, no. 23, pp. 10670–10681, 2016, doi: 10.1128/jvi.01634-16.
[9]
D. Todt et al., “Antiviral activities of different interferon types and subtypes against hepatitis E virus replication,” Antimicrobial agents and chemotherapy, vol. 60, no. 4, pp. 2132–2139, 2016, doi: 10.1128/aac.02427-15.
[10]
S. A. Drave et al., “Extra-hepatic replication and infection of hepatitis E virus in neuronal-derived cells,” Journal of viral hepatitis, vol. 23, no. 7, pp. 512–521, 2016, doi: 10.1111/jvh.12515.
[11]
A. Siddharta et al., “Inactivation of HCV and HIV by microwave: a novel approach for prevention of virus transmission among people who inject drugs,” Scientific reports, vol. 6, no. 1, Art. no. 36619, 2016, doi: 10.1038/srep36619.
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2015

[1]
K. Hüging et al., “Several human liver cell expressed apolipoproteins complement HCV virus production with varying efficacy conferring differential specific infectivity to released viruses,” PLoS ONE, vol. 10, no. 7, Art. no. e0134529, Jul. 2015, doi: 10.1371/journal.pone.0134529.
[2]
S. Pfaender et al., “Assessment of cross-species transmission of hepatitis C virus-related non-primate hepacivirus in a population of humans at high risk of exposure,” The journal of general virology, vol. 96, no. 9, pp. 2636–2642, 2015, doi: 10.1099/vir.0.000208.
[3]
S. Pfaender et al., “Mechanisms of methods for hepatitis C virus inactivation,” Applied and environmental microbiology, vol. 81, no. 5, pp. 1616–1621, 2015, doi: 10.1128/aem.03580-14.
[4]
N. Anggakusuma et al., “Interferon-inducible cholesterol-25-hydroxylase restricts hepatitis C virus replication through blockage of membranous web formation,” Hepatology, vol. 62, no. 3, pp. 702–714, 2015, doi: 10.1002/hep.27913.
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