Sandra Ciesek

Dr. Sandra Ciesek

Director of the Institute of Medical Virology, University Hospital Frankfurt, Paul-Ehrlich-Str. 40, D-60590 Frankfurt, Germany
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Research Focus & Metrics

Academic Career Length

18Years (2009-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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29 July 2020 in Nature
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DSDonghyuk Shin
Donghyuk Shin
RMRukmini Mukherjee
Rukmini Mukherjee
DGDiana Grewe
Diana Grewe
DBDenisa Bojkova
Denisa Bojkova
KBKheewoong Baek
Kheewoong Baek
IDIvan Dikic
Ivan Dikic

14 May 2020 in Nature
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DBDenisa Bojkova
Denisa Bojkova
KKKevin Klann
Kevin Klann
BKBenjamin Koch
Benjamin Koch
MWMarek Widera
Marek Widera
DKDavid Krause
David Krause
CMChristian Münch
Christian Münch

26 March 2020 in New England Journal of Medicine
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SHSebastian Hoehl
Sebastian Hoehl
HRHolger Rabenau
Holger Rabenau
ABAnnemarie Berger
Annemarie Berger
MKMarhild Kortenbusch
Marhild Kortenbusch
JCJindrich Cinatl
Jindrich Cinatl
SCSandra Ciesek
Sandra Ciesek
As the number of cases of infection with the novel coronavirus (SARS-CoV-2) has continued to increase, many countries have established restrictions regarding travelers who have recently visited China.1 With lockdown measures imposed in Hubei Province, China,2 and a public health emergency of international concern declared by the World Health Organization,3 foreign nationals have sought to return to their home countries from China, and public health authorities are racing to contain the spread of Covid-19 (the disease caused by SARS-CoV-2 infection) around the world. This process is complicated by epidemiologic uncertainty regarding possible transmission of the virus by asymptomatically or subclinically symptomatic infected persons. It is unclear whether persons who show no signs or symptoms of respiratory infection shed SARS-CoV-2.

1 January 2021 in Science of The Total Environment
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Journal Article
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SWSandra Westhaus
Sandra Westhaus
FWFrank-Andreas Weber
Frank-Andreas Weber
SSSabrina Schiwy
Sabrina Schiwy
VLVolker Linnemann
Volker Linnemann
MBMarkus Brinkmann
Markus Brinkmann
SCSandra Ciesek
Sandra Ciesek

2 December 2010 in Hepatology
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SCSandra Ciesek
Sandra Ciesek
THThomas von Hahn
Thomas von Hahn
CCChe Colpitts
Che Colpitts
LSLuis Schang
Luis Schang
MFMartina Friesland
Martina Friesland
ESEike Steinmann
Eike Steinmann
Hepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Current antiviral therapy fails to clear infection in a substantial proportion of cases. Drug development is focused on nonstructural proteins required for RNA replication. Individuals undergoing orthotopic liver transplantation face rapid, universal reinfection of the graft. Therefore, antiviral strategies targeting the early stages of infection are urgently needed for the prevention of HCV infection. In this study, we identified the polyphenol, epigallocatechin-3-gallate (EGCG), as an inhibitor of HCV entry. Green tea catechins, such as EGCG and its derivatives, epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC), have been previously found to exert antiviral and antioncogenic properties. EGCG had no effect on HCV RNA replication, assembly, or release of progeny virions. However, it potently inhibited Cell-culture–derived HCV (HCVcc) entry into hepatoma cell lines as well as primary human hepatocytes. The effect was independent of the HCV genotype, and both infection of cells by extracellular virions and cell-to-cell spread were blocked. Pretreatment of cells with EGCG before HCV inoculation did not reduce HCV infection, whereas the application of EGCG during inoculation strongly inhibited HCV infectivity. Moreover, treatment with EGCG directly during inoculation strongly inhibited HCV infectivity. Expression levels of all known HCV (co-)receptors were unaltered by EGCG. Finally, we showed that EGCG inhibits viral attachment to the cell, thus disrupting the initial step of HCV cell entry. Conclusion: The green tea molecule, EGCG, potently inhibits HCV entry and could be part of an antiviral strategy aimed at the prevention of HCV reinfection after liver transplantation. (Hepatology 2011)

11 July 2022 in EBioMedicine
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Journal Article
Open access
AWAlexander Wilhelm
Alexander Wilhelm
MWMarek Widera
Marek Widera
KGKatharina Grikscheit
Katharina Grikscheit
TTTuna Toptan
Tuna Toptan
BSBarbara Schenk
Barbara Schenk
SCSandra Ciesek
Sandra Ciesek
In recent months, Omicron variants of SARS-CoV-2 have become dominant in many regions of the world, and case numbers with Omicron subvariants BA.1 and BA.2 continue to increase. Due to numerous mutations in the spike protein, the efficacy of currently available vaccines, which are based on Wuhan-Hu 1 isolate of SARS-CoV-2, is reduced, leading to breakthrough infections. Efficacy of monoclonal antibody therapy is also likely impaired. In our in vitro study using A549-AT cells constitutively expressing ACE2 and TMPRSS2, we determined and compared the neutralizing capacity of vaccine-elicited sera, convalescent sera and monoclonal antibodies against authentic SARS-CoV-2 Omicron BA.1 and BA.2 compared with Delta. Almost no neutralisation of Omicron BA.1 and BA.2 was observed using sera from individuals vaccinated with two doses 6 months earlier, regardless of the type of vaccine taken. Shortly after the booster dose, most sera from triple BNT162b2-vaccinated individuals were able to neutralise both Omicron variants. In line with waning antibody levels three months after the booster, only weak residual neutralisation was observed for BA.1 (26%, n = 34, 0 median NT50) and BA.2 (44%, n = 34, 0 median NT50). In addition, BA.1 but not BA.2 was resistant to the neutralising monoclonal antibodies casirivimab/imdevimab, while BA.2 exhibited almost a complete evasion from the neutralisation induced by sotrovimab. Both SARS-CoV-2 Omicron subvariants BA.1 and BA.2 escape antibody-mediated neutralisation elicited by vaccination, previous infection with SARS-CoV-2, and monoclonal antibodies. Waning immunity renders the majority of tested sera obtained three months after booster vaccination negative in BA.1 and BA.2 neutralisation. Omicron subvariant specific resistance to the monoclonal antibodies casirivimab/imdevimab and sotrovimab emphasizes the importance of genotype-surveillance and guided application. This study was supported in part by the Goethe-Corona-Fund of the Goethe University Frankfurt (M.W.) and the Federal Ministry of Education and Research (COVIDready; grant 02WRS1621C (M.W.).