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Article ; Online: When good turns bad: how viruses exploit innate immunity factors.

Prelli Bozzo, Caterina / Kmiec, Dorota / Kirchhoff, Frank

2021 Volume 52, Page(s) 60–67

Abstract: Humans evolved numerous cell-intrinsic restriction factors as a first line of defense against viral pathogens. Typically, they inhibit efficient viral replication and thus prevent viral zoonoses and pandemics. However, viruses show enormous adaptability ... ...

Abstract	Humans evolved numerous cell-intrinsic restriction factors as a first line of defense against viral pathogens. Typically, they inhibit efficient viral replication and thus prevent viral zoonoses and pandemics. However, viruses show enormous adaptability and are well known for their ability to counteract antiviral mechanisms. Accumulating evidence shows that some viruses are even capable of exploiting antiviral factors for efficient infection. In addition, antiviral factors may exert enhancing effects under specific circumstances. While much progress has been made in understanding the antiviral mechanisms of restriction factors, their proviral effects are poorly defined. Here, we summarize current knowledge on how viral pathogens may exploit otherwise antiviral cellular factors for efficient infection and replication.
MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Humans ; Immunity, Innate ; Virus Replication ; Viruses/genetics
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2021-12-03
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2611378-8
ISSN	1879-6265 ; 1879-6257
ISSN (online)	1879-6265
ISSN	1879-6257
DOI	10.1016/j.coviro.2021.11.009
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: IFI16 knockdown in primary HIV-1 target cells

Matteo Bosso / Caterina Prelli Bozzo / Meta Volcic / Frank Kirchhoff

STAR Protocols, Vol 2, Iss 1, Pp 100236- (2021)

2021

Abstract: Summary: IFI16 is an important player of the host intrinsic immune response. Among others, it has been reported to sense intermediate products of HIV-1 reverse transcription in the cytosol and to sequester the transcription factor Sp1 in the nucleus to ... ...

Abstract	Summary: IFI16 is an important player of the host intrinsic immune response. Among others, it has been reported to sense intermediate products of HIV-1 reverse transcription in the cytosol and to sequester the transcription factor Sp1 in the nucleus to attenuate viral gene expression. Here, we present three different methods to reduce IFI16 protein expression levels in HIV-1 primary target cells. These techniques can be adapted for the investigation of other cellular factors in primary macrophages and CD4+ T lymphocytes.For complete details on the use and execution of this protocol, please refer to Hotter et al. (2019) and Bosso et al. (2020).
Keywords	Immunology ; Molecular Biology ; Science (General) ; Q1-390
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: IFI16 knockdown in primary HIV-1 target cells.

Bosso, Matteo / Bozzo, Caterina Prelli / Volcic, Meta / Kirchhoff, Frank

STAR protocols

2020 Volume 2, Issue 1, Page(s) 100236

Abstract: IFI16 is an important player of the host intrinsic immune response. Among others, it has been reported to sense intermediate products of HIV-1 reverse transcription in the cytosol and to sequester the transcription factor Sp1 in the nucleus to attenuate ... ...

Abstract	IFI16 is an important player of the host intrinsic immune response. Among others, it has been reported to sense intermediate products of HIV-1 reverse transcription in the cytosol and to sequester the transcription factor Sp1 in the nucleus to attenuate viral gene expression. Here, we present three different methods to reduce IFI16 protein expression levels in HIV-1 primary target cells. These techniques can be adapted for the investigation of other cellular factors in primary macrophages and CD4
MeSH term(s)	CD4-Positive T-Lymphocytes/metabolism ; CD4-Positive T-Lymphocytes/virology ; Gene Knockdown Techniques ; HIV Infections ; HIV-1/metabolism ; Humans ; Macrophages/metabolism ; Macrophages/virology ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phosphoproteins/genetics ; Phosphoproteins/metabolism
Chemical Substances	Nuclear Proteins ; Phosphoproteins ; IFI16 protein, human (148998-64-5)
Language	English
Publishing date	2020-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2020.100236
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Endogenous IFITMs boost SARS-coronavirus 1 and 2 replication whereas overexpression inhibits infection by relocalizing ACE2.

Xie, Qinya / Bozzo, Caterina Prelli / Eiben, Laura / Noettger, Sabrina / Kmiec, Dorota / Nchioua, Rayhane / Niemeyer, Daniela / Volcic, Meta / Lee, Jung-Hyun / Zech, Fabian / Sparrer, Konstantin M J / Drosten, Christian / Kirchhoff, Frank

iScience

2023 Volume 26, Issue 4, Page(s) 106395

Abstract: Opposing effects of interferon-induced transmembrane proteins (IFITMs 1, 2 and 3) on SARS-CoV-2 infection have been reported. The reasons for this are unclear and the role of IFITMs in infection of other human coronaviruses (hCoVs) remains poorly ... ...

Abstract	Opposing effects of interferon-induced transmembrane proteins (IFITMs 1, 2 and 3) on SARS-CoV-2 infection have been reported. The reasons for this are unclear and the role of IFITMs in infection of other human coronaviruses (hCoVs) remains poorly understood. Here, we demonstrate that endogenous expression of IFITM2 and/or IFITM3 is critical for efficient replication of SARS-CoV-1, SARS-CoV-2 and hCoV-OC43 but has little effect on MERS-, NL63-and 229E-hCoVs. In contrast, overexpression of IFITMs inhibits all these hCoVs, and the corresponding spike-containing pseudo-particles, except OC43, which is enhanced by IFITM3. We further demonstrate that overexpression of IFITMs impairs cell surface expression of ACE2 representing the entry receptor of SARS-CoVs and hCoV-NL63 but not hCoV-OC43. Our results explain the inhibitory effects of artificial IFITM overexpression on ACE2-tropic SARS-CoVs and show that three hCoVs, including major causative agents of severe respiratory disease, hijack IFITMs for efficient infection of human cells.
Language	English
Publishing date	2023-03-13
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106395
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Vpr attenuates antiviral immune responses and is critical for full pathogenicity of SIV

iScience

2023 Volume 26, Issue 12, Page(s) 108351

Abstract: The accessory viral protein R (Vpr) is encoded by all primate lentiviruses. Vpr counteracts DNA repair pathways, modulates viral immune sensing, and induces cell-cycle arrest in cell culture. However, its ... ...

Abstract	The accessory viral protein R (Vpr) is encoded by all primate lentiviruses. Vpr counteracts DNA repair pathways, modulates viral immune sensing, and induces cell-cycle arrest in cell culture. However, its impact
Language	English
Publishing date	2023-10-26
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108351
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: SARS-CoV-2 Variants of Concern Hijack IFITM2 for Efficient Replication in Human Lung Cells.

Nchioua, Rayhane / Schundner, Annika / Kmiec, Dorota / Prelli Bozzo, Caterina / Zech, Fabian / Koepke, Lennart / Graf, Alexander / Krebs, Stefan / Blum, Helmut / Frick, Manfred / Sparrer, Konstantin M J / Kirchhoff, Frank

Journal of virology

2022 Volume 96, Issue 11, Page(s) e0059422

Abstract: It has recently been shown that an early SARS-CoV-2 isolate (NL-02-2020) hijacks interferon-induced transmembrane proteins (IFITMs) for efficient replication in human lung cells, cardiomyocytes, and gut organoids. To date, several "variants of concern" ( ... ...

Abstract	It has recently been shown that an early SARS-CoV-2 isolate (NL-02-2020) hijacks interferon-induced transmembrane proteins (IFITMs) for efficient replication in human lung cells, cardiomyocytes, and gut organoids. To date, several "variants of concern" (VOCs) showing increased infectivity and resistance to neutralization have emerged and globally replaced the early viral strains. Here, we determined whether the five current SARS-CoV-2 VOCs (Alpha, Beta, Gamma, Delta, and Omicron) maintained the dependency on IFITM proteins for efficient replication. We found that depletion of IFITM2 strongly reduces viral RNA production by all VOCs in the human epithelial lung cancer cell line Calu-3. Silencing of IFITM1 had modest effects, while knockdown of IFITM3 resulted in an intermediate phenotype. Strikingly, depletion of IFITM2 generally reduced infectious virus production by more than 4 orders of magnitude. In addition, an antibody directed against the N terminus of IFITM2 inhibited SARS-CoV-2 VOC replication in induced pluripotent stem cell (iPSC)-derived alveolar epithelial type II cells, thought to represent major viral target cells in the lung. In conclusion, endogenously expressed IFITM proteins (especially IFITM2) are critical cofactors for efficient replication of genuine SARS-CoV-2 VOCs, including the currently dominant Omicron variant.
MeSH term(s)	COVID-19/virology ; Cell Line, Tumor ; Humans ; Lung/virology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; SARS-CoV-2/genetics ; SARS-CoV-2/physiology ; Virus Internalization ; Virus Replication
Chemical Substances	IFITM2 protein, human ; IFITM3 protein, human ; Membrane Proteins ; RNA-Binding Proteins
Language	English
Publishing date	2022-05-11
Publishing country	United States
Document type	Journal Article ; 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.00594-22
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 609: Show issues

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Article ; Online: Endogenous IFITMs boost SARS-coronavirus 1 and 2 replication whereas overexpression inhibits infection by relocalizing ACE2

Qinya Xie / Caterina Prelli Bozzo / Laura Eiben / Sabrina Noettger / Dorota Kmiec / Rayhane Nchioua / Daniela Niemeyer / Meta Volcic / Jung-Hyun Lee / Fabian Zech / Konstantin M.J. Sparrer / Christian Drosten / Frank Kirchhoff

iScience, Vol 26, Iss 4, Pp 106395- (2023)

2023

Abstract: Summary: Opposing effects of interferon-induced transmembrane proteins (IFITMs 1, 2 and 3) on SARS-CoV-2 infection have been reported. The reasons for this are unclear and the role of IFITMs in infection of other human coronaviruses (hCoVs) remains ... ...

Abstract	Summary: Opposing effects of interferon-induced transmembrane proteins (IFITMs 1, 2 and 3) on SARS-CoV-2 infection have been reported. The reasons for this are unclear and the role of IFITMs in infection of other human coronaviruses (hCoVs) remains poorly understood. Here, we demonstrate that endogenous expression of IFITM2 and/or IFITM3 is critical for efficient replication of SARS-CoV-1, SARS-CoV-2 and hCoV-OC43 but has little effect on MERS-, NL63-and 229E-hCoVs. In contrast, overexpression of IFITMs inhibits all these hCoVs, and the corresponding spike-containing pseudo-particles, except OC43, which is enhanced by IFITM3. We further demonstrate that overexpression of IFITMs impairs cell surface expression of ACE2 representing the entry receptor of SARS-CoVs and hCoV-NL63 but not hCoV-OC43. Our results explain the inhibitory effects of artificial IFITM overexpression on ACE2-tropic SARS-CoVs and show that three hCoVs, including major causative agents of severe respiratory disease, hijack IFITMs for efficient infection of human cells.
Keywords	Protein ; Immunity ; Virology ; Science ; Q
Subject code	570
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: IFITM dependency of SARS-CoV-2 variants of concern

Nchioua, Rayhane / Schundner, Annika / Kmiec, Dorota / Prelli Bozzo, Caterina / Zech, Fabian / Koepke, Lennart / Frick, Manfred / Sparrer, Konstantin MJ / Kirchhoff, Frank

bioRxiv

Abstract: We have recently shown that a SARS-CoV-2 strain isolated in the Netherlands in February 2020 (NL-02-2020) hijacks interferon-induced transmembrane proteins, especially IFITM2, as entry cofactors for efficient infection. Here, we examined whether SARS-CoV- ...

Abstract	We have recently shown that a SARS-CoV-2 strain isolated in the Netherlands in February 2020 (NL-02-2020) hijacks interferon-induced transmembrane proteins, especially IFITM2, as entry cofactors for efficient infection. Here, we examined whether SARS-CoV-2 9variants of concern9 (VOCs), including the currently dominating delta variant, maintained the dependency on IFITMs for efficient replication. Depletion of IFITM2 reduced viral RNA production from 31- (B.1.1.7) to 755-fold (P.1). In comparison, silencing of IFITM1 had little effect, while knock-down of IFITM3 resulted in an intermediate phenotype. Strikingly, silencing of IFITM2 generally reduced infectious virus production in Calu-3 cells to near background levels. An antibody directed against the N-terminus of IFITM2 inhibited SARS-CoV-2 VOC replication in iPSC-derived alveolar epithelial type II cells. In conclusion, endogenously expressed IFITM proteins (especially IFITM2) are important cofactors for replication of genuine SARS-CoV-2 VOCs, including the Delta variant.
Keywords	covid19
Language	English
Publishing date	2021-11-17
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2021.11.17.468942
Database	COVID19

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Article ; Online: Single-cell transcriptomics identifies prothymosin α restriction of HIV-1 in vivo.

Geretz, Aviva / Ehrenberg, Philip K / Clifford, Robert J / Laliberté, Alexandre / Prelli Bozzo, Caterina / Eiser, Daina / Kundu, Gautam / Yum, Lauren K / Apps, Richard / Creegan, Matthew / Gunady, Mohamed / Shangguan, Shida / Sanders-Buell, Eric / Sacdalan, Carlo / Phanuphak, Nittaya / Tovanabutra, Sodsai / Russell, Ronnie M / Bibollet-Ruche, Frederic / Robb, Merlin L /

Michael, Nelson L / Ake, Julie A / Vasan, Sandhya / Hsu, Denise C / Hahn, Beatrice H / Kirchhoff, Frank / Thomas, Rasmi

Science translational medicine

2023 Volume 15, Issue 707, Page(s) eadg0873

Abstract: Host restriction factors play key roles in innate antiviral defense, but it remains poorly understood which of them restricts HIV-1 in vivo. Here, we used single-cell transcriptomic analysis to identify host factors associated with HIV-1 control during ... ...

Abstract	Host restriction factors play key roles in innate antiviral defense, but it remains poorly understood which of them restricts HIV-1 in vivo. Here, we used single-cell transcriptomic analysis to identify host factors associated with HIV-1 control during acute infection by correlating host gene expression with viral RNA abundance within individual cells. Wide sequencing of cells from one participant with the highest plasma viral load revealed that intracellular viral RNA transcription correlates inversely with expression of the gene
MeSH term(s)	Humans ; HIV-1/genetics ; Transcriptome/genetics ; HIV Infections/genetics ; RNA, Viral
Chemical Substances	prothymosin alpha ; RNA, Viral
Language	English
Publishing date	2023-08-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.adg0873
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Vpr attenuates antiviral immune responses and is critical for full pathogenicity of SIVmac239 in rhesus macaques

iScience, Vol 26, Iss 12, Pp 108351- (2023)

2023

Abstract: Summary: The accessory viral protein R (Vpr) is encoded by all primate lentiviruses. Vpr counteracts DNA repair pathways, modulates viral immune sensing, and induces cell-cycle arrest in cell culture. However, its impact in vivo is controversial. Here, ... ...

Abstract	Summary: The accessory viral protein R (Vpr) is encoded by all primate lentiviruses. Vpr counteracts DNA repair pathways, modulates viral immune sensing, and induces cell-cycle arrest in cell culture. However, its impact in vivo is controversial. Here, we show that deletion of vpr is associated with delayed viral replication kinetics, rapid innate immune activation, development and maintenance of strong B and T cell responses, and increased neutralizing activity against SIVmac239 in rhesus macaques. All wild-type SIVmac239-infected animals maintained high viral loads, and five of six developed fatal immunodeficiency during ∼80 weeks of follow-up. Lack of Vpr was associated with better preservation of CD4+ T cells, lower viral loads, and an attenuated clinical course of infection in most animals. Our results show that Vpr contributes to efficient viral immune evasion and the full pathogenic potential of SIVmac in vivo. Inhibition of Vpr may improve humoral immune control of viral replication.
Keywords	Immunology ; Immunity ; Immune response ; Science ; Q
Subject code	570
Language	English
Publishing date	2023-12-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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