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Article: SARS-CoV-2 Portrayed against HIV: Contrary Viral Strategies in Similar Disguise.

Duerr, Ralf / Crosse, Keaton M / Valero-Jimenez, Ana M / Dittmann, Meike

2021 Volume 9, Issue 7

Abstract: SARS-CoV-2 and HIV are zoonotic viruses that rapidly reached pandemic scale, causing global losses and fear. The COVID-19 and AIDS pandemics ignited massive efforts worldwide to develop antiviral strategies and characterize viral architectures, ... ...

Abstract	SARS-CoV-2 and HIV are zoonotic viruses that rapidly reached pandemic scale, causing global losses and fear. The COVID-19 and AIDS pandemics ignited massive efforts worldwide to develop antiviral strategies and characterize viral architectures, biological and immunological properties, and clinical outcomes. Although both viruses have a comparable appearance as enveloped viruses with positive-stranded RNA and envelope spikes mediating cellular entry, the entry process, downstream biological and immunological pathways, clinical outcomes, and disease courses are strikingly different. This review provides a systemic comparison of both viruses' structural and functional characteristics, delineating their distinct strategies for efficient spread.
Language	English
Publishing date	2021-06-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms9071389
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: SARS-CoV-2 Portrayed against HIV: Contrary Viral Strategies in Similar Disguise

Duerr, Ralf / Crosse, Keaton M. / Valero-Jimenez, Ana M. / Dittmann, Meike

Microorganisms. 2021 June 27, v. 9, no. 7

2021

Abstract	SARS-CoV-2 and HIV are zoonotic viruses that rapidly reached pandemic scale, causing global losses and fear. The COVID-19 and AIDS pandemics ignited massive efforts worldwide to develop antiviral strategies and characterize viral architectures, biological and immunological properties, and clinical outcomes. Although both viruses have a comparable appearance as enveloped viruses with positive-stranded RNA and envelope spikes mediating cellular entry, the entry process, downstream biological and immunological pathways, clinical outcomes, and disease courses are strikingly different. This review provides a systemic comparison of both viruses’ structural and functional characteristics, delineating their distinct strategies for efficient spread.
Keywords	COVID-19 infection ; RNA ; Severe acute respiratory syndrome coronavirus 2 ; fearfulness ; pandemic
Language	English
Dates of publication	2021-0627
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms9071389
Database	NAL-Catalogue (AGRICOLA)

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Article: Type I interferon susceptibility distinguishes SARS-CoV-2 from SARS-CoV.

Lokugamage, Kumari G / Hage, Adam / de Vries, Maren / Valero-Jimenez, Ana M / Schindewolf, Craig / Dittmann, Meike / Rajsbaum, Ricardo / Menachery, Vineet D

bioRxiv : the preprint server for biology

2020

Abstract: SARS-CoV-2, a novel coronavirus (CoV) that causes COVID-19, has recently emerged causing an ongoing outbreak of viral pneumonia around the world. While distinct from SARS-CoV, both group 2B CoVs share similar genome organization, origins to bat CoVs, and ...

Abstract	SARS-CoV-2, a novel coronavirus (CoV) that causes COVID-19, has recently emerged causing an ongoing outbreak of viral pneumonia around the world. While distinct from SARS-CoV, both group 2B CoVs share similar genome organization, origins to bat CoVs, and an arsenal of immune antagonists. In this report, we evaluate type-I interferon (IFN-I) sensitivity of SARS-CoV-2 relative to the original SARS-CoV. Our results indicate that while SARS-CoV-2 maintains similar viral replication to SARS-CoV, the novel CoV is much more sensitive to IFN-I. In Vero and in Calu3 cells, SARS-CoV-2 is substantially attenuated in the context of IFN-I pretreatment, while SARS-CoV is not. In line with these findings, SARS-CoV-2 fails to counteract phosphorylation of STAT1 and expression of ISG proteins, while SARS-CoV is able to suppress both. Comparing SARS-CoV-2 and influenza A virus in human airway epithelial cultures (HAEC), we observe the absence of IFN-I stimulation by SARS-CoV-2 alone, but detect failure to counteract STAT1 phosphorylation upon IFN-I pretreatment resulting in near ablation of SARS-CoV-2 infection. Next, we evaluated IFN-I treatment post infection and found SARS-CoV-2 was sensitive even after establishing infection. Finally, we examined homology between SARS-CoV and SARS-CoV-2 in viral proteins shown to be interferon antagonists. The absence of an equivalent open reading frame (ORF) 3b and changes to ORF6 suggest the two key IFN-I antagonists may not maintain equivalent function in SARS-CoV-2. Together, the results identify key differences in susceptibility to IFN-I responses between SARS-CoV and SARS-CoV-2 that may help inform disease progression, treatment options, and animal model development.
Keywords	covid19
Language	English
Publishing date	2020-07-13
Publishing country	United States
Document type	Preprint
DOI	10.1101/2020.03.07.982264
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Article ; Online: Type I Interferon Susceptibility Distinguishes SARS-CoV-2 from SARS-CoV.

Lokugamage, Kumari G / Hage, Adam / de Vries, Maren / Valero-Jimenez, Ana M / Schindewolf, Craig / Dittmann, Meike / Rajsbaum, Ricardo / Menachery, Vineet D

Journal of virology

2020 Volume 94, Issue 23

Abstract	SARS-CoV-2, a novel coronavirus (CoV) that causes COVID-19, has recently emerged causing an ongoing outbreak of viral pneumonia around the world. While distinct from SARS-CoV, both group 2B CoVs share similar genome organization, origins to bat CoVs, and an arsenal of immune antagonists. In this report, we evaluate type I interferon (IFN-I) sensitivity of SARS-CoV-2 relative to the original SARS-CoV. Our results indicate that while SARS-CoV-2 maintains similar viral replication to SARS-CoV, the novel CoV is much more sensitive to IFN-I. In Vero E6 and in Calu3 cells, SARS-CoV-2 is substantially attenuated in the context of IFN-I pretreatment, whereas SARS-CoV is not. In line with these findings, SARS-CoV-2 fails to counteract phosphorylation of STAT1 and expression of ISG proteins, while SARS-CoV is able to suppress both. Comparing SARS-CoV-2 and influenza A virus in human airway epithelial cultures, we observe the absence of IFN-I stimulation by SARS-CoV-2 alone but detect the failure to counteract STAT1 phosphorylation upon IFN-I pretreatment, resulting in near ablation of SARS-CoV-2 infection. Next, we evaluated IFN-I treatment postinfection and found that SARS-CoV-2 was sensitive even after establishing infection. Finally, we examined homology between SARS-CoV and SARS-CoV-2 in viral proteins shown to be interferon antagonists. The absence of an equivalent open reading frame 3b (ORF3b) and genetic differences versus ORF6 suggest that the two key IFN-I antagonists may not maintain equivalent function in SARS-CoV-2. Together, the results identify key differences in susceptibility to IFN-I responses between SARS-CoV and SARS-CoV-2 that may help inform disease progression, treatment options, and animal model development.
MeSH term(s)	Animals ; Antiviral Agents/antagonists & inhibitors ; Antiviral Agents/metabolism ; Antiviral Agents/pharmacology ; Betacoronavirus/drug effects ; Betacoronavirus/immunology ; Betacoronavirus/physiology ; Cell Line ; Cell Line, Tumor ; Chlorocebus aethiops ; Humans ; Interferon Type I/antagonists & inhibitors ; Interferon Type I/immunology ; Interferon Type I/metabolism ; Interferon Type I/pharmacology ; Interferon-alpha/antagonists & inhibitors ; Interferon-alpha/immunology ; Interferon-alpha/metabolism ; Interferon-alpha/pharmacology ; Phosphorylation ; Recombinant Proteins/pharmacology ; Severe acute respiratory syndrome-related coronavirus/drug effects ; Severe acute respiratory syndrome-related coronavirus/immunology ; Severe acute respiratory syndrome-related coronavirus/physiology ; SARS-CoV-2 ; STAT1 Transcription Factor/metabolism ; Signal Transduction ; Vero Cells ; Viral Proteins/chemistry ; Viral Proteins/genetics ; Viral Proteins/metabolism ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; Interferon Type I ; Interferon-alpha ; Recombinant Proteins ; STAT1 Transcription Factor ; Viral Proteins
Keywords	covid19
Language	English
Publishing date	2020-11-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01410-20
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Article ; Online: A neonatal mouse model characterizes transmissibility of SARS-CoV-2 variants and reveals a role for ORF8.

Rodriguez-Rodriguez, Bruno A / Ciabattoni, Grace O / Duerr, Ralf / Valero-Jimenez, Ana M / Yeung, Stephen T / Crosse, Keaton M / Schinlever, Austin R / Bernard-Raichon, Lucie / Rodriguez Galvan, Joaquin / McGrath, Marisa E / Vashee, Sanjay / Xue, Yong / Loomis, Cynthia A / Khanna, Kamal M / Cadwell, Ken / Desvignes, Ludovic / Frieman, Matthew B / Ortigoza, Mila B / Dittmann, Meike

Nature communications

2023 Volume 14, Issue 1, Page(s) 3026

Abstract: Small animal models have been a challenge for the study of SARS-CoV-2 transmission, with most investigators using golden hamsters or ferrets. Mice have the advantages of low cost, wide availability, less regulatory and husbandry challenges, and the ... ...

Abstract	Small animal models have been a challenge for the study of SARS-CoV-2 transmission, with most investigators using golden hamsters or ferrets. Mice have the advantages of low cost, wide availability, less regulatory and husbandry challenges, and the existence of a versatile reagent and genetic toolbox. However, adult mice do not robustly transmit SARS-CoV-2. Here we establish a model based on neonatal mice that allows for transmission of clinical SARS-CoV-2 isolates. We characterize tropism, respiratory tract replication and transmission of ancestral WA-1 compared to variants Alpha (B.1.1.7), Beta (B.1.351), Gamma (P.1), Delta (B.1.617.2), Omicron BA.1 and Omicron BQ.1.1. We identify inter-variant differences in timing and magnitude of infectious particle shedding from index mice, both of which shape transmission to contact mice. Furthermore, we characterize two recombinant SARS-CoV-2 lacking either the ORF6 or ORF8 host antagonists. The removal of ORF8 shifts viral replication towards the lower respiratory tract, resulting in significantly delayed and reduced transmission in our model. Our results demonstrate the potential of our neonatal mouse model to characterize viral and host determinants of SARS-CoV-2 transmission, while revealing a role for an accessory protein in this context.
MeSH term(s)	Cricetinae ; Animals ; Humans ; Mice ; SARS-CoV-2/genetics ; Animals, Newborn ; COVID-19 ; Ferrets ; Disease Models, Animal ; Mesocricetus
Language	English
Publishing date	2023-05-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-38783-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: A neonatal mouse model characterizes transmissibility of SARS-CoV-2 variants and reveals a role for ORF8.

Rodriguez-Rodriguez, Bruno A / Ciabattoni, Grace O / Duerr, Ralf / Valero-Jimenez, Ana M / Yeung, Stephen T / Crosse, Keaton M / Schinlever, Austin R / Bernard-Raichon, Lucie / Rodriguez-Galvan, Joaquin J / McGrath, Marisa E / Vashee, Sanjay / Xue, Yong / Loomis, Cynthia / Khanna, Kamal M / Cadwell, Kenneth / Desvignes, Ludovic / Frieman, Matthew F / Ortigoza, Mila B / Dittmann, Meike

bioRxiv : the preprint server for biology

2023

Abstract: Small animal models have been a challenge for the study of SARS-CoV-2 transmission, with most investigators using golden hamsters or ... ...

Abstract	Small animal models have been a challenge for the study of SARS-CoV-2 transmission, with most investigators using golden hamsters or ferrets
Language	English
Publishing date	2023-03-24
Publishing country	United States
Document type	Preprint
DOI	10.1101/2022.10.04.510658
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A neonatal mouse model characterizes transmissibility of SARS-CoV-2 variants and reveals a role for ORF8

Rodriguez-Rodriguez, Bruno A / Ciabattoni, Grace / Valero-Jimenez, Ana M / Crosse, Keaton M / Schinlever, Austin / Rodriguez-Galvan, Joaquin J / Duerr, Ralf / McGrath, Marisa / Desvignes, Ludovic / Frieman, Matthew / Ortigoza, Mila B / Dittmann, Meike

bioRxiv

Abstract	Small animal models have been a challenge for the study of SARS-CoV-2 transmission, with most investigators using golden hamsters or ferrets. Mice have the advantages of low cost, wide availability, less regulatory and husbandry challenges, and a versatile reagent and genetic toolbox. However, adult mice do not transmit SARS-CoV-2. Here we establish a model based on neonatal mice that allows for transmission of clinical SARS-CoV-2 isolates. We characterize tropism, respiratory tract replication and transmission of ancestral WA-1 compared to variants alpha (B.1.1.7), beta (B.1.351), gamma (P.1), delta (B.1.617.2) and omicron (B.1.1.529). We found that an index shedding threshold is a key determinant for viral transmissibility. Furthermore, we characterize two recombinant SARS-CoV-2 lacking either the ORF6 or ORF8 host antagonists. The removal of ORF8 shifts viral replication towards the lower respiratory tract, resulting in delayed and reduced transmission. Our results demonstrate the potential of our neonatal mouse model to characterize viral and host determinants of SARS-CoV-2 transmission, while revealing for the first time a role for an accessory protein this context. We now have a tractable small animal model to help us decipher and counteract some of the most decisive aspects of SARS-CoV-2 continued spread in the human population.
Keywords	covid19
Language	English
Publishing date	2022-10-04
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2022.10.04.510658
Database	COVID19

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Article: Type I Interferon Susceptibility Distinguishes SARS-CoV-2 from SARS-CoV

Lokugamage, Kumari G / Hage, Adam / de Vries, Maren / Valero-Jimenez, Ana M / Schindewolf, Craig / Dittmann, Meike / Rajsbaum, Ricardo / Menachery, Vineet D

J. virol

Abstract	SARS-CoV-2, a novel coronavirus (CoV) that causes COVID-19, has recently emerged causing an ongoing outbreak of viral pneumonia around the world. While distinct from SARS-CoV, both group 2B CoVs share similar genome organization, origins to bat CoVs, and an arsenal of immune antagonists. In this report, we evaluate type I interferon (IFN-I) sensitivity of SARS-CoV-2 relative to the original SARS-CoV. Our results indicate that while SARS-CoV-2 maintains similar viral replication to SARS-CoV, the novel CoV is much more sensitive to IFN-I. In Vero E6 and in Calu3 cells, SARS-CoV-2 is substantially attenuated in the context of IFN-I pretreatment, whereas SARS-CoV is not. In line with these findings, SARS-CoV-2 fails to counteract phosphorylation of STAT1 and expression of ISG proteins, while SARS-CoV is able to suppress both. Comparing SARS-CoV-2 and influenza A virus in human airway epithelial cultures, we observe the absence of IFN-I stimulation by SARS-CoV-2 alone but detect the failure to counteract STAT1 phosphorylation upon IFN-I pretreatment, resulting in near ablation of SARS-CoV-2 infection. Next, we evaluated IFN-I treatment postinfection and found that SARS-CoV-2 was sensitive even after establishing infection. Finally, we examined homology between SARS-CoV and SARS-CoV-2 in viral proteins shown to be interferon antagonists. The absence of an equivalent open reading frame 3b (ORF3b) and genetic differences versus ORF6 suggest that the two key IFN-I antagonists may not maintain equivalent function in SARS-CoV-2. Together, the results identify key differences in susceptibility to IFN-I responses between SARS-CoV and SARS-CoV-2 that may help inform disease progression, treatment options, and animal model development.IMPORTANCE With the ongoing outbreak of COVID-19, differences between SARS-CoV-2 and the original SARS-CoV could be leveraged to inform disease progression and eventual treatment options. In addition, these findings could have key implications for animal model development as well as further research into how SARS-CoV-2 modulates the type I IFN response early during infection.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #772280
Database	COVID19

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Article ; Online: Type I interferon susceptibility distinguishes SARS-CoV-2 from SARS-CoV.

Lokugamage, Kumari G. / Hage, Adam / de Vries, Maren / Valero-Jimenez, Ana M. / Schindewolf, Craig / Dittmann, Meike / Rajsbaum, Ricardo / Menachery, Vineet D.

Journal of Virology ; ISSN 0022-538X 1098-5514

2020

Abstract	SARS-CoV-2, a novel coronavirus (CoV) that causes COVID-19, has recently emerged causing an ongoing outbreak of viral pneumonia around the world. While distinct from SARS-CoV, both group 2B CoVs share similar genome organization, origins to bat CoVs, and an arsenal of immune antagonists. In this report, we evaluate type-I interferon (IFN-I) sensitivity of SARS-CoV-2 relative to the original SARS-CoV. Our results indicate that while SARS-CoV-2 maintains similar viral replication to SARS-CoV, the novel CoV is much more sensitive to IFN-I. In Vero E6 and in Calu3 cells, SARS-CoV-2 is substantially attenuated in the context of IFN-I pretreatment, while SARS-CoV is not. In line with these findings, SARS-CoV-2 fails to counteract phosphorylation of STAT1 and expression of ISG proteins, while SARS-CoV is able to suppress both. Comparing SARS-CoV-2 and influenza A virus in human airway epithelial cultures (HAEC), we observe the absence of IFN-I stimulation by SARS-CoV-2 alone, but detect failure to counteract STAT1 phosphorylation upon IFN-I pretreatment resulting in near ablation of SARS-CoV-2 infection. Next, we evaluated IFN-I treatment post infection and found SARS-CoV-2 was sensitive even after establishing infection. Finally, we examined homology between SARS-CoV and SARS-CoV-2 in viral proteins shown to be interferon antagonists. The absence of an equivalent open reading frame (ORF) 3b and genetic differences to ORF6 suggest the two key IFN-I antagonists may not maintain equivalent function in SARS-CoV-2. Together, the results identify key differences in susceptibility to IFN-I responses between SARS-CoV and SARS-CoV-2 that may help inform disease progression, treatment options, and animal model development. IMPORTANCE With the ongoing outbreak of COVID-19, differences between SARS-CoV-2 and the original SARS-CoV could be leveraged to inform disease progression and eventual treatment options. In addition, these findings could have key implications for animal model development as well as further research into how SARS-CoV-2 modulates the type I IFN response early during infection.
Keywords	Immunology ; Insect Science ; Microbiology ; Virology ; covid19
Language	English
Publisher	American Society for Microbiology
Publishing country	us
Document type	Article ; Online
DOI	10.1128/jvi.01410-20
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A comparative analysis of SARS-CoV-2 antivirals characterizes 3CL

de Vries, Maren / Mohamed, Adil S / Prescott, Rachel A / Valero-Jimenez, Ana M / Desvignes, Ludovic / O'Connor, Rebecca / Steppan, Claire / Devlin, Joseph C / Ivanova, Ellie / Herrera, Alberto / Schinlever, Austin / Loose, Paige / Ruggles, Kelly / Koralov, Sergei B / Anderson, Annaliesa S / Binder, Joseph / Dittmann, Meike

Journal of virology

2021 Volume 95, Issue 7

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of Coronavirus Disease 2019 (COVID-19). There is a dire need for novel effective antivirals to treat COVID-19, as the only approved direct-acting antiviral to date is ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of Coronavirus Disease 2019 (COVID-19). There is a dire need for novel effective antivirals to treat COVID-19, as the only approved direct-acting antiviral to date is remdesivir, targeting the viral polymerase complex. A potential alternate target in the viral life cycle is the main SARS-CoV-2 protease 3CL
Language	English
Publishing date	2021-02-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01819-20
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 609: Show issues

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ab Jg. 2022: Lesesaal (EG)

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