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Article ; Online: An inventory of adjuvants used for vaccination in horses: the past, the present and the future.

Carnet, Flora / Perrin-Cocon, Laure / Paillot, Romain / Lotteau, Vincent / Pronost, Stéphane / Vidalain, Pierre-Olivier

2023 Volume 54, Issue 1, Page(s) 18

Abstract: Vaccination is one of the most widely used strategies to protect horses against pathogens. However, available equine vaccines often have limitations, as they do not always provide effective, long-term protection and booster injections are often required. ...

Abstract	Vaccination is one of the most widely used strategies to protect horses against pathogens. However, available equine vaccines often have limitations, as they do not always provide effective, long-term protection and booster injections are often required. In addition, research efforts are needed to develop effective vaccines against emerging equine pathogens. In this review, we provide an inventory of approved adjuvants for equine vaccines worldwide, and discuss their composition and mode of action when available. A wide range of adjuvants are used in marketed vaccines for horses, the main families being aluminium salts, emulsions, polymers, saponins and ISCOMs. We also present veterinary adjuvants that are already used for vaccination in other species and are currently evaluated in horses to improve equine vaccination and to meet the expected level of protection against pathogens in the equine industry. Finally, we discuss new adjuvants such as liposomes, polylactic acid polymers, inulin, poly-ε-caprolactone nanoparticles and co-polymers that are in development. Our objective is to help professionals in the horse industry understand the composition of marketed equine vaccines in a context of mistrust towards vaccines. Besides, this review provides researchers with a list of adjuvants, either approved or at least evaluated in horses, that could be used either alone or in combination to develop new vaccines.
MeSH term(s)	Horses ; Animals ; Adjuvants, Immunologic/pharmacology ; Vaccination/veterinary ; Nanoparticles/therapeutic use ; Polymers
Chemical Substances	Adjuvants, Immunologic ; Polymers
Language	English
Publishing date	2023-03-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1146298-x
ISSN	1297-9716 ; 0928-4249
ISSN (online)	1297-9716
ISSN	0928-4249
DOI	10.1186/s13567-023-01151-3
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Article ; Online: What role for cellular metabolism in the control of hepatitis viruses?

Diaz, Olivier / Vidalain, Pierre-Olivier / Ramière, Christophe / Lotteau, Vincent / Perrin-Cocon, Laure

Frontiers in immunology

2022 Volume 13, Page(s) 1033314

Abstract: Hepatitis B, C and D viruses (HBV, HCV, HDV, respectively) specifically infect human hepatocytes and often establish chronic viral infections of the liver, thus escaping antiviral immunity for years. Like other viruses, hepatitis viruses rely on the ... ...

Abstract	Hepatitis B, C and D viruses (HBV, HCV, HDV, respectively) specifically infect human hepatocytes and often establish chronic viral infections of the liver, thus escaping antiviral immunity for years. Like other viruses, hepatitis viruses rely on the cellular machinery to meet their energy and metabolite requirements for replication. Although this was initially considered passive parasitism, studies have shown that hepatitis viruses actively rewire cellular metabolism through molecular interactions with specific enzymes such as glucokinase, the first rate-limiting enzyme of glycolysis. As part of research efforts in the field of immunometabolism, it has also been shown that metabolic changes induced by viruses could have a direct impact on the innate antiviral response. Conversely, detection of viral components by innate immunity receptors not only triggers the activation of the antiviral defense but also induces in-depth metabolic reprogramming that is essential to support immunological functions. Altogether, these complex triangular interactions between viral components, innate immunity and hepatocyte metabolism may explain why chronic hepatitis infections progressively lead to liver inflammation and progression to cirrhosis, fibrosis and hepatocellular carcinoma (HCC). In this manuscript, we first present a global overview of known connections between the innate antiviral response and cellular metabolism. We then report known molecular mechanisms by which hepatitis viruses interfere with cellular metabolism in hepatocytes and discuss potential consequences on the innate immune response. Finally, we present evidence that drugs targeting hepatocyte metabolism could be used as an innovative strategy not only to deprive viruses of key metabolites, but also to restore the innate antiviral response that is necessary to clear infection.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular ; Liver Neoplasms ; Hepatitis Viruses ; Hepatocytes ; Antiviral Agents/therapeutic use
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2022-11-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1033314
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Article ; Online: Rôle du métabolisme cellulaire dans le contrôle des hépatites virales chroniques.

Diaz, Olivier / Legrand, Anne-Flore / El-Orch, Walid / Jacolin, Florentine / Lotteau, Vincent / Ramière, Christophe / Vidalain, Pierre-Olivier / Perrin-Cocon, Laure

Medecine sciences : M/S

2023 Volume 39, Issue 10, Page(s) 754–762

Abstract: Hepatitis viruses modify the cellular metabolism of hepatocytes by interacting with specific enzymes such as glucokinase. The metabolic changes induced by viruses can have a direct impact on the innate antiviral response. The complex interactions between ...

Title translation	Role of cellular metabolism in the control of chronic viral hepatitis.
Abstract	Hepatitis viruses modify the cellular metabolism of hepatocytes by interacting with specific enzymes such as glucokinase. The metabolic changes induced by viruses can have a direct impact on the innate antiviral response. The complex interactions between viral components, innate immunity, and hepatocyte metabolism explain why chronic hepatitis infections lead to liver inflammation, progressing to cirrhosis, fibrosis, and hepatocellular carcinoma. Metabolic regulators could be used in innovative therapies to deprive viruses of key metabolites and induce an antiviral defense.
MeSH term(s)	Humans ; Hepatitis, Chronic ; Carcinoma, Hepatocellular ; Liver Neoplasms ; Hepatitis, Viral, Human ; Antiviral Agents/therapeutic use
Chemical Substances	Antiviral Agents
Language	French
Publishing date	2023-11-09
Publishing country	France
Document type	English Abstract ; Journal Article
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2023125
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Article ; Online: The PACS-2 protein and trafficking motifs in CCHFV Gn and Gc cytoplasmic tails govern CCHFV assembly.

Gautam, Anupriya / Lalande, Alexandre / Ritter, Maureen / Freitas, Natalia / Lerolle, Solène / Canus, Lola / Amirache, Fouzia / Lotteau, Vincent / Legros, Vincent / Cosset, François-Loïc / Mathieu, Cyrille / Boson, Bertrand

Emerging microbes & infections

2024 , Page(s) 2348508

Abstract: ... ...

Abstract	Abstract
Language	English
Publishing date	2024-04-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2681359-2
ISSN	2222-1751 ; 2222-1751
ISSN (online)	2222-1751
ISSN	2222-1751
DOI	10.1080/22221751.2024.2348508
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Article ; Online: Instability of the NS1 Glycoprotein from La Reunion 2018 Dengue 2 Virus (Cosmopolitan-1 Genotype) in Huh7 Cells Is Due to Lysine Residues on Positions 272 and 324.

Ogire, Eva / Diaz, Olivier / Vidalain, Pierre-Olivier / Lotteau, Vincent / Desprès, Philippe / Roche, Marjolaine

International journal of molecular sciences

2021 Volume 22, Issue 4

Abstract: La Reunion island in the South West Indian Ocean is now endemic for dengue following the introduction of dengue virus serotype 2 (DENV-2) cosmopolitan-I genotype in 2017. DENV-2 infection causes a wide spectrum of clinical manifestations ranging from flu- ...

Abstract	La Reunion island in the South West Indian Ocean is now endemic for dengue following the introduction of dengue virus serotype 2 (DENV-2) cosmopolitan-I genotype in 2017. DENV-2 infection causes a wide spectrum of clinical manifestations ranging from flu-like disease to severe dengue. The nonstructural glycoprotein 1 (NS1) has been identified as playing a key role in dengue disease severity. The intracellular NS1 exists as a homodimer, whereas a fraction is driven towards the plasma membrane or released as a soluble hexameric protein. Here, we characterized the NS1 glycoproteins from clinical isolates DES-14 and RUN-18 that were collected during the DENV-2 epidemics in Tanzania in 2014 and La Reunion island in 2018, respectively. In relation to hepatotropism of the DENV, expression of recombinant DES-14 NS1 and RUN-18 NS1 glycoproteins was compared in human hepatoma Huh7 cells. We observed that RUN-18 NS1 was poorly stable in Huh7 cells compared to DES-14 NS1. The instability of RUN-18 NS1 leading to a low level of NS1 secretion mostly relates to lysine residues on positions 272 and 324. Our data raise the issue of the consequences of a defect in NS1 stability in human hepatocytes in relation to the major role of NS1 in the pathogenesis of the DENV-2 infection.
MeSH term(s)	Amino Acid Substitution ; Antigens, Viral/chemistry ; Antigens, Viral/genetics ; Cell Line, Tumor ; Dengue/epidemiology ; Dengue/metabolism ; Dengue/virology ; Dengue Virus/metabolism ; Epidemics ; Genotype ; HEK293 Cells ; Hepatocytes/metabolism ; Hepatocytes/virology ; Humans ; Lysine/chemistry ; Protein Multimerization ; Protein Stability ; Recombinant Proteins/chemistry ; Reunion/epidemiology ; Serogroup ; Tanzania/epidemiology ; Transfection ; Viral Nonstructural Proteins/chemistry ; Viral Nonstructural Proteins/genetics
Chemical Substances	Antigens, Viral ; NS1 protein, Dengue virus type 2 ; Recombinant Proteins ; Viral Nonstructural Proteins ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2021-02-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22041951
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Article ; Online: Farnesoid X receptor alpha ligands inhibit HDV in vitro replication and virion infectivity.

Legrand, Anne-Flore / Lucifora, Julie / Lacombe, Benoît / Ménard, Camille / Michelet, Maud / Foca, Adrien / Abrial, Pauline / Salvetti, Anna / Rivoire, Michel / Lotteau, Vincent / Durantel, David / André, Patrice / Ramière, Christophe

Hepatology communications

2023 Volume 7, Issue 5

Abstract: Background and aims: HDV, a satellite of HBV, is responsible for the most severe form of human viral hepatitis, for which curative therapy is still awaited. Both HBV and HDV use the hepatic transporter of bile acids (ie, Na+-taurocholate cotransporting ... ...

Abstract	Background and aims: HDV, a satellite of HBV, is responsible for the most severe form of human viral hepatitis, for which curative therapy is still awaited. Both HBV and HDV use the hepatic transporter of bile acids (ie, Na+-taurocholate cotransporting polypeptide) to enter hepatocytes. We have previously shown that ligands of the farnesoid-X-receptor alpha (FXR), a master regulator of bile acids metabolism, inhibit HBV replication. Here we asked whether FXR ligands can also control HDV infection. Approach and results: In vitro HDV monoinfections or HDV/HBV coinfections and superinfections were performed in differentiated HepaRG cells (dHepaRG) and primary human hepatocytes. Following treatment with FXR ligands, HDV RNAs and antigens were analyzed by RT-qPCR, northern blot, immunofluorescence, and western blot. Virus secretion was studied by RNA quantification in supernatants, and the infectivity of secreted HDV particles was measured by reinfection of naive HuH7.5-Na+-taurocholate cotransporting polypeptide cells. In HDV/HBV superinfection models, a 10-day treatment with FXR ligand GW4064 decreased intracellular HDV RNAs by 60% and 40% in dHepaRG cells and primary human hepatocytes, respectively. Both HDV genomic and antigenomic RNAs were affected by treatment, which also reduced the amount of intracellular delta antigen. This antiviral effect was also observed in HDV monoinfected dHepaRG cells, abolished by FXR loss of function, and reproduced with other FXR ligands. In HBV/HDV coinfected dHepaRG cells, HDV secretion was decreased by 60% and virion-specific infectivity by >95%. Conclusions: FXR ligands both inhibit directly (ie, independently of anti-HBV activity) and indirectly (ie, dependently of anti-HBV activity) the replication, secretion, and infectivity of HDV. The overall anti-HDV activity was superior to that obtained with interferon-α, highlighting the therapeutic potential of FXR ligands in HDV-infected patients.
MeSH term(s)	Humans ; Hepatitis B virus/genetics ; Ligands ; Bile Acids and Salts ; Virion/metabolism ; Taurocholic Acid/metabolism ; Peptides
Chemical Substances	Ligands ; Bile Acids and Salts ; Taurocholic Acid (5E090O0G3Z) ; Peptides
Language	English
Publishing date	2023-04-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2471-254X
ISSN (online)	2471-254X
DOI	10.1097/HC9.0000000000000078
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Article: Hamster organotypic kidney culture model of early-stage SARS-CoV-2 infection highlights a two-step renal susceptibility.

Shyfrin, Sophie R / Ferren, Marion / Perrin-Cocon, Laure / Espi, Maxime / Charmetant, Xavier / Brailly, Manon / Decimo, Didier / Iampietro, Mathieu / Canus, Lola / Horvat, Branka / Lotteau, Vincent / Vidalain, Pierre-Olivier / Thaunat, Olivier / Mathieu, Cyrille

Journal of tissue engineering

2022 Volume 13, Page(s) 20417314221122130

Abstract: Kidney pathology is frequently reported in patients hospitalized with COVID-19, the pandemic disease caused by the Severe acute respiratory coronavirus 2 (SARS-CoV-2). However, due to a lack of suitable study models, the events occurring in the kidney ... ...

Abstract	Kidney pathology is frequently reported in patients hospitalized with COVID-19, the pandemic disease caused by the Severe acute respiratory coronavirus 2 (SARS-CoV-2). However, due to a lack of suitable study models, the events occurring in the kidney during the earliest stages of infection remain unknown. We have developed hamster organotypic kidney cultures (OKCs) to study the early stages of direct renal infection. OKCs maintained key renal structures in their native three-dimensional arrangement. SARS-CoV-2 productively replicated in hamster OKCs, initially targeting endothelial cells and later disseminating into proximal tubules. We observed a delayed interferon response, markers of necroptosis and pyroptosis, and an early repression of pro-inflammatory cytokines transcription followed by a strong later upregulation. While it remains an open question whether an active replication of SARS-CoV-2 takes place in the kidneys of COVID-19 patients with AKI, our model provides new insights into the kinetics of SARS-CoV-2 kidney infection and can serve as a powerful tool for studying kidney infection by other pathogens and testing the renal toxicity of drugs.
Language	English
Publishing date	2022-09-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2573915-3
ISSN	2041-7314
ISSN	2041-7314
DOI	10.1177/20417314221122130
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Article ; Online: Characterization and functional interrogation of the SARS-CoV-2 RNA interactome.

Labeau, Athéna / Fery-Simonian, Luc / Lefevre-Utile, Alain / Pourcelot, Marie / Bonnet-Madin, Lucie / Soumelis, Vassili / Lotteau, Vincent / Vidalain, Pierre-Olivier / Amara, Ali / Meertens, Laurent

Cell reports

2022 Volume 39, Issue 4, Page(s) 110744

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the COVID-19 pandemic, which has led to a devastating global health crisis. The emergence of variants that escape neutralizing responses emphasizes the urgent need to ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the COVID-19 pandemic, which has led to a devastating global health crisis. The emergence of variants that escape neutralizing responses emphasizes the urgent need to deepen our understanding of SARS-CoV-2 biology. Using a comprehensive identification of RNA-binding proteins (RBPs) by mass spectrometry (ChIRP-MS) approach, we identify 107 high-confidence cellular factors that interact with the SARS-CoV-2 genome during infection. By systematically knocking down their expression in human lung epithelial cells, we find that the majority of the identified RBPs are SARS-CoV-2 proviral factors. In particular, we show that HNRNPA2B1, ILF3, QKI, and SFPQ interact with the SARS-CoV-2 genome and promote viral RNA amplification. Our study provides valuable resources for future investigations into the mechanisms of SARS-CoV-2 replication and the identification of host-centered antiviral therapies.
MeSH term(s)	COVID-19/genetics ; Humans ; Pandemics ; RNA, Viral/genetics ; SARS-CoV-2/genetics ; Virus Replication/genetics
Chemical Substances	RNA, Viral
Language	English
Publishing date	2022-04-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110744
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Article ; Online: Domain 2 of Hepatitis C Virus Protein NS5A Activates Glucokinase and Induces Lipogenesis in Hepatocytes.

Perrin-Cocon, Laure / Kundlacz, Cindy / Jacquemin, Clémence / Hanoulle, Xavier / Aublin-Gex, Anne / Figl, Marianne / Manteca, Jeremy / André, Patrice / Vidalain, Pierre-Olivier / Lotteau, Vincent / Diaz, Olivier

International journal of molecular sciences

2022 Volume 23, Issue 2

Abstract: Hepatitis C virus (HCV) relies on cellular lipid metabolism for its replication, and actively modulates lipogenesis and lipid trafficking in infected hepatocytes. This translates into an intracellular accumulation of triglycerides leading to liver ... ...

Abstract	Hepatitis C virus (HCV) relies on cellular lipid metabolism for its replication, and actively modulates lipogenesis and lipid trafficking in infected hepatocytes. This translates into an intracellular accumulation of triglycerides leading to liver steatosis, cirrhosis and hepatocellular carcinoma, which are hallmarks of HCV pathogenesis. While the interaction of HCV with hepatocyte metabolic pathways is patent, how viral proteins are able to redirect central carbon metabolism towards lipogenesis is unclear. Here, we report that the HCV protein NS5A activates the glucokinase (GCK) isoenzyme of hexokinases through its D2 domain (NS5A-D2). GCK is the first rate-limiting enzyme of glycolysis in normal hepatocytes whose expression is replaced by the hexokinase 2 (HK2) isoenzyme in hepatocellular carcinoma cell lines. We took advantage of a unique cellular model specifically engineered to re-express GCK instead of HK2 in the Huh7 cell line to evaluate the consequences of NS5A-D2 expression on central carbon and lipid metabolism. NS5A-D2 increased glucose consumption but decreased glycogen storage. This was accompanied by an altered mitochondrial respiration, an accumulation of intracellular triglycerides and an increased production of very-low density lipoproteins. Altogether, our results show that NS5A-D2 can reprogram central carbon metabolism towards a more energetic and glycolytic phenotype compatible with HCV needs for replication.
MeSH term(s)	Cell Line, Tumor ; Gene Knockdown Techniques ; Glucokinase/metabolism ; Glycogen/metabolism ; Glycolysis ; Hepacivirus/physiology ; Hepatitis C/metabolism ; Hepatitis C/virology ; Hepatocytes/metabolism ; Hepatocytes/virology ; Host-Pathogen Interactions ; Humans ; Lipid Metabolism ; Lipogenesis ; Mitochondria/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; RNA-Dependent RNA Polymerase/chemistry ; RNA-Dependent RNA Polymerase/metabolism ; Viral Nonstructural Proteins/chemistry ; Viral Nonstructural Proteins/metabolism
Chemical Substances	Viral Nonstructural Proteins ; Glycogen (9005-79-2) ; Glucokinase (EC 2.7.1.2) ; NS-5 protein, hepatitis C virus (EC 2.7.7.48) ; RNA-Dependent RNA Polymerase (EC 2.7.7.48)
Language	English
Publishing date	2022-01-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23020919
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Article ; Online: The current landscape of coronavirus-host protein-protein interactions.

Perrin-Cocon, Laure / Diaz, Olivier / Jacquemin, Clémence / Barthel, Valentine / Ogire, Eva / Ramière, Christophe / André, Patrice / Lotteau, Vincent / Vidalain, Pierre-Olivier

Journal of translational medicine

2020 Volume 18, Issue 1, Page(s) 319

Abstract: In less than 20 years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat for ... ...

Abstract	In less than 20 years, three deadly coronaviruses, SARS-CoV, MERS-CoV and SARS-CoV-2, have emerged in human population causing hundreds to hundreds of thousands of deaths. Other coronaviruses are causing epizootic representing a significant threat for both domestic and wild animals. Members of this viral family have the longest genome of all RNA viruses, and express up to 29 proteins establishing complex interactions with the host proteome. Deciphering these interactions is essential to identify cellular pathways hijacked by these viruses to replicate and escape innate immunity. Virus-host interactions also provide key information to select targets for antiviral drug development. Here, we have manually curated the literature to assemble a unique dataset of 1311 coronavirus-host protein-protein interactions. Functional enrichment and network-based analyses showed coronavirus connections to RNA processing and translation, DNA damage and pathogen sensing, interferon production, and metabolic pathways. In particular, this global analysis pinpointed overlooked interactions with translation modulators (GIGYF2-EIF4E2), components of the nuclear pore, proteins involved in mitochondria homeostasis (PHB, PHB2, STOML2), and methylation pathways (MAT2A/B). Finally, interactome data provided a rational for the antiviral activity of some drugs inhibiting coronaviruses replication. Altogether, this work describing the current landscape of coronavirus-host interactions provides valuable hints for understanding the pathophysiology of coronavirus infections and developing effective antiviral therapies.
MeSH term(s)	Animals ; Betacoronavirus/physiology ; COVID-19 ; Coronavirus/chemistry ; Coronavirus/metabolism ; Coronavirus Infections/metabolism ; Coronavirus Infections/virology ; Databases, Protein ; Host-Pathogen Interactions/physiology ; Humans ; Mitochondrial Proteins/metabolism ; Pandemics ; Pneumonia, Viral/metabolism ; Pneumonia, Viral/virology ; Protein Interaction Maps ; SARS-CoV-2 ; Transcription Factors/metabolism ; Viral Proteins/metabolism ; Virus Replication/genetics
Chemical Substances	Mitochondrial Proteins ; Transcription Factors ; Viral Proteins
Keywords	covid19
Language	English
Publishing date	2020-08-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1479-5876
ISSN (online)	1479-5876
DOI	10.1186/s12967-020-02480-z
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