LIVIVO - Search results -

Search results

Result 1 - 10 of total 75

Search options

Article ; Online: A synthetic thiol molecule releasing N-acetyl-l-cysteine and cysteamine drives early up-regulation of immunoproteasome subunits in the lymph nodes of mice infected with LP-BM5 leukemia retrovirus.

Crinelli, Rita / Monittola, Francesca / Masini, Sofia / Diotallevi, Aurora / Bartoccini, Francesca / Smietana, Michaël / Galluzzi, Luca / Magnani, Mauro / Fraternale, Alessandra

Biochimica et biophysica acta. Molecular basis of disease

2023 Volume 1870, Issue 1, Page(s) 166918

Abstract: Thiol molecules have been recently re-considered as drug candidates in viral infections because of their ability to induce redox changes which interfere with virus life cycle and modulate the host immune response. Little is known about the molecular ... ...

Abstract	Thiol molecules have been recently re-considered as drug candidates in viral infections because of their ability to induce redox changes which interfere with virus life cycle and modulate the host immune response. Little is known about the molecular mechanisms of their immunomodulatory properties. Here we show that I-152, a thiol molecule metabolized to release N-acetyl-l-cysteine and cysteamine and acting as a pro-glutathione agent, causes early up-regulation of immunoproteasome subunits in the lymph nodes of murine leukemia virus infected mice. This evidence suggests that the immunoproteasome may be modulated by thiol-based compounds with important implications in understanding redox-controlled immunoregulation.
MeSH term(s)	Mice ; Animals ; Acetylcysteine/pharmacology ; Acetylcysteine/metabolism ; Murine Acquired Immunodeficiency Syndrome/pathology ; Cysteamine/pharmacology ; Sulfhydryl Compounds ; Up-Regulation ; Retroviridae/metabolism ; Lymph Nodes/pathology ; Leukemia
Chemical Substances	Acetylcysteine (WYQ7N0BPYC) ; Cysteamine (5UX2SD1KE2) ; Sulfhydryl Compounds
Language	English
Publishing date	2023-10-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2023.166918
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.247: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: DDIT4 gene expression is switched on by a new HDAC4 function in ataxia telangiectasia.

Ricci, Anastasia / Galluzzi, Luca / Magnani, Mauro / Menotta, Michele

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2019 Volume 34, Issue 1, Page(s) 1802–1818

Abstract: Ataxia telangiectasia (AT) is a rare, severe, and ineluctably progressive multisystemic neurodegenerative disease. Histone deacetylase 4 (HDAC4) nuclear accumulation has been related to neurodegeneration in AT. Since treatment with glucocorticoid ... ...

Abstract	Ataxia telangiectasia (AT) is a rare, severe, and ineluctably progressive multisystemic neurodegenerative disease. Histone deacetylase 4 (HDAC4) nuclear accumulation has been related to neurodegeneration in AT. Since treatment with glucocorticoid analogues has been shown to improve the neurological symptoms that characterize this syndrome, the effects of dexamethasone on HDAC4 were investigated. In this paper, we describe a novel nonepigenetic function of HDAC4 induced by dexamethasone, through which it can directly modulate HIF-1a activity and promote the upregulation of the DDIT4 gene and protein expression. This new HDAC4 transcription regulation mechanism leads to a positive effect on autophagic flux, an AT-compromised biological pathway. This signaling was specifically induced by dexamethasone only in AT cell lines and can contribute in explaining the positive effects of dexamethasone observed in AT-treated patients.
MeSH term(s)	Ataxia Telangiectasia/drug therapy ; Ataxia Telangiectasia/genetics ; Cell Line ; Dexamethasone/pharmacology ; Gene Expression/drug effects ; Gene Expression/genetics ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Glucocorticoids/pharmacology ; Histone Deacetylases/genetics ; Humans ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/genetics ; Repressor Proteins/genetics ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Transcription Factors/genetics ; Transcriptional Activation/drug effects ; Transcriptional Activation/genetics ; Up-Regulation/drug effects ; Up-Regulation/genetics
Chemical Substances	DDIT4 protein, human ; Glucocorticoids ; Repressor Proteins ; Transcription Factors ; Dexamethasone (7S5I7G3JQL) ; HDAC4 protein, human (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2019-12-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201902039R
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 296: Show issues

Order via subito

Details ▾

Article: Activity of the Di-Substituted Urea-Derived Compound I-17 in

Dos Santos, José Vitorino / Medina, Jorge Mansur / Dias Teixeira, Karina Luiza / Agostinho, Daniel Marcos Julio / Chorev, Michael / Diotallevi, Aurora / Galluzzi, Luca / Aktas, Bertal Huseyin / Gazos Lopes, Ulisses

Pathogens (Basel, Switzerland)

2024 Volume 13, Issue 2

Abstract: Protein synthesis has been a very rich target for developing drugs to control prokaryotic and eukaryotic pathogens. Despite the development of new drug formulations, treating human cutaneous and ... ...

Abstract	Protein synthesis has been a very rich target for developing drugs to control prokaryotic and eukaryotic pathogens. Despite the development of new drug formulations, treating human cutaneous and visceral
Language	English
Publishing date	2024-01-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2695572-6
ISSN	2076-0817
ISSN	2076-0817
DOI	10.3390/pathogens13020104
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Transcriptional signatures in human macrophage-like cells infected by Leishmania infantum, Leishmania major and Leishmania tropica.

Diotallevi, Aurora / Bruno, Federica / Castelli, Germano / Persico, Giuseppe / Buffi, Gloria / Ceccarelli, Marcello / Ligi, Daniela / Mannello, Ferdinando / Vitale, Fabrizio / Magnani, Mauro / Galluzzi, Luca

PLoS neglected tropical diseases

2024 Volume 18, Issue 4, Page(s) e0012085

Abstract: Background: In the Mediterranean basin, three Leishmania species have been identified: L. infantum, L. major and L. tropica, causing zoonotic visceral leishmaniasis (VL), zoonotic cutaneous leishmaniasis (CL) and anthroponotic CL, respectively. Despite ... ...

Abstract	Background: In the Mediterranean basin, three Leishmania species have been identified: L. infantum, L. major and L. tropica, causing zoonotic visceral leishmaniasis (VL), zoonotic cutaneous leishmaniasis (CL) and anthroponotic CL, respectively. Despite animal models and genomic/transcriptomic studies provided important insights, the pathogenic determinants modulating the development of VL and CL are still poorly understood. This work aimed to identify host transcriptional signatures shared by cells infected with L. infantum, L. major, and L. tropica, as well as specific transcriptional signatures elicited by parasites causing VL (i.e., L. infantum) and parasites involved in CL (i.e., L. major, L. tropica). Methodology/principal findings: U937 cells differentiated into macrophage-like cells were infected with L. infantum, L. major and L. tropica for 24h and 48h, and total RNA was extracted. RNA sequencing, performed on an Illumina NovaSeq 6000 platform, was used to evaluate the transcriptional signatures of infected cells with respect to non-infected cells at both time points. The EdgeR package was used to identify differentially expressed genes (fold change > 2 and FDR-adjusted p-values < 0.05). Then, functional enrichment analysis was employed to identify the enriched ontology terms in which these genes are involved. At 24h post-infection, a common signature of 463 dysregulated genes shared among all infection conditions was recognized, while at 48h post-infection the common signature was reduced to 120 genes. Aside from a common transcriptional response, we evidenced different upregulated functional pathways characterizing L. infantum-infected cells, such as VEGFA-VEGFR2 and NFE2L2-related pathways, indicating vascular remodeling and reduction of oxidative stress as potentially important factors for visceralization. Conclusions: The identification of pathways elicited by parasites causing VL or CL could lead to new therapeutic strategies for leishmaniasis, combining the canonical anti-leishmania compounds with host-directed therapy.
MeSH term(s)	Animals ; Humans ; Leishmania tropica/genetics ; Leishmania infantum/genetics ; Leishmania major ; Leishmaniasis, Cutaneous/parasitology ; Leishmaniasis, Visceral/parasitology ; Macrophages
Language	English
Publishing date	2024-04-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2429704-5
ISSN	1935-2735 ; 1935-2735
ISSN (online)	1935-2735
ISSN	1935-2735
DOI	10.1371/journal.pntd.0012085
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The host micro-RNA cfa-miR-346 is induced in canine leishmaniasis

Buffi, Gloria / Diotallevi, Aurora / Ceccarelli, Marcello / Bruno, Federica / Castelli, Germano / Vitale, Fabrizio / Magnani, Mauro / Galluzzi, Luca

BMC Vet Res. 2022 Dec., v. 18, no. 1 p.247-247

2022

Abstract: BACKGROUND: Leishmaniases are a group of anthropo-zoonotic parasitic diseases caused by a protozoan of the Leishmania genus, affecting both humans and other vertebrates, including dogs. L. infantum is responsible for the visceral and occasionally ... ...

Abstract	BACKGROUND: Leishmaniases are a group of anthropo-zoonotic parasitic diseases caused by a protozoan of the Leishmania genus, affecting both humans and other vertebrates, including dogs. L. infantum is responsible for the visceral and occasionally cutaneous form of the disease in humans and canine leishmaniasis. Previously, we have shown that L. infantum induces a mild but significant increase in endoplasmic reticulum (ER) stress expression markers to promote parasites survival in human and murine infected macrophages. Moreover, we demonstrated that the miRNA hsa-miR-346, induced by the UPR-activated transcription factor sXBP1, was significantly upregulated in human macrophages infected with different L. infantum strains. However, the ER stress response in infected dogs, which represent an important reservoir for Leishmania parasite, was described once recently, whereas the miR-346 expression was not reported before. Therefore, this study aimed to investigate these pathways in the canine macrophage-like cell line DH82 infected by Leishmania spp. and to evaluate the presence of cfa-miR-346 in plasma of non-infected and infected dogs. The DH82 cells were infected with L. infantum and L. braziliensis parasites and the expression of cfa-mir-346 and several ER stress markers was evaluated by quantitative PCR (qPCR) at different time points. Furthermore, the cfa-miR-346 was monitored in plasma collected from non-infected dogs (n = 11) and dogs naturally infected by L. infantum (n = 18). RESULTS: The results in DH82 cells showed that cfa-mir-346 was induced at both 24 h and 48 h post-infection with all Leishmania strains but not with tunicamycin, accounting for a mechanism of induction independent from sXBP1, unlike what was previously observed in human cell lines. Moreover, the cfa-miR-346 expression analysis on plasma revealed a significant increase in infected dogs compared to non-infected dogs. CONCLUSIONS: Here for the first time, we report the upregulation of cfa-miR-346 induced by Leishmania infection in canine macrophage-like cells and plasma samples of naturally infected dogs. According to our results, the cfa-miR-346 appears to be linked to infection, and understanding its role and identifying its target genes could contribute to elucidate the mechanisms underlying the host–pathogen interaction in leishmaniasis.
Keywords	Leishmania ; cell lines ; dogs ; endoplasmic reticulum ; host-pathogen relationships ; humans ; leishmaniasis ; macrophages ; mice ; microRNA ; parasites ; quantitative polymerase chain reaction ; stress response ; transcription factors ; tunicamycin
Language	English
Dates of publication	2022-12
Size	p. 247.
Publishing place	BioMed Central
Document type	Article ; Online
ZDB-ID	2191675-5
ISSN	1746-6148
ISSN	1746-6148
DOI	10.1186/s12917-022-03359-5
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article ; Online: The host micro-RNA cfa-miR-346 is induced in canine leishmaniasis.

Buffi, Gloria / Diotallevi, Aurora / Ceccarelli, Marcello / Bruno, Federica / Castelli, Germano / Vitale, Fabrizio / Magnani, Mauro / Galluzzi, Luca

BMC veterinary research

2022 Volume 18, Issue 1, Page(s) 247

Abstract: Background: Leishmaniases are a group of anthropo-zoonotic parasitic diseases caused by a protozoan of the Leishmania genus, affecting both humans and other vertebrates, including dogs. L. infantum is responsible for the visceral and occasionally ... ...

Abstract	Background: Leishmaniases are a group of anthropo-zoonotic parasitic diseases caused by a protozoan of the Leishmania genus, affecting both humans and other vertebrates, including dogs. L. infantum is responsible for the visceral and occasionally cutaneous form of the disease in humans and canine leishmaniasis. Previously, we have shown that L. infantum induces a mild but significant increase in endoplasmic reticulum (ER) stress expression markers to promote parasites survival in human and murine infected macrophages. Moreover, we demonstrated that the miRNA hsa-miR-346, induced by the UPR-activated transcription factor sXBP1, was significantly upregulated in human macrophages infected with different L. infantum strains. However, the ER stress response in infected dogs, which represent an important reservoir for Leishmania parasite, was described once recently, whereas the miR-346 expression was not reported before. Therefore, this study aimed to investigate these pathways in the canine macrophage-like cell line DH82 infected by Leishmania spp. and to evaluate the presence of cfa-miR-346 in plasma of non-infected and infected dogs. The DH82 cells were infected with L. infantum and L. braziliensis parasites and the expression of cfa-mir-346 and several ER stress markers was evaluated by quantitative PCR (qPCR) at different time points. Furthermore, the cfa-miR-346 was monitored in plasma collected from non-infected dogs (n = 11) and dogs naturally infected by L. infantum (n = 18). Results: The results in DH82 cells showed that cfa-mir-346 was induced at both 24 h and 48 h post-infection with all Leishmania strains but not with tunicamycin, accounting for a mechanism of induction independent from sXBP1, unlike what was previously observed in human cell lines. Moreover, the cfa-miR-346 expression analysis on plasma revealed a significant increase in infected dogs compared to non-infected dogs. Conclusions: Here for the first time, we report the upregulation of cfa-miR-346 induced by Leishmania infection in canine macrophage-like cells and plasma samples of naturally infected dogs. According to our results, the cfa-miR-346 appears to be linked to infection, and understanding its role and identifying its target genes could contribute to elucidate the mechanisms underlying the host-pathogen interaction in leishmaniasis.
MeSH term(s)	Animals ; Dog Diseases/genetics ; Dog Diseases/parasitology ; Dogs ; Leishmania infantum ; Leishmaniasis, Visceral/genetics ; Leishmaniasis, Visceral/veterinary ; MicroRNAs/genetics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2022-06-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2191675-5
ISSN	1746-6148 ; 1746-6148
ISSN (online)	1746-6148
ISSN	1746-6148
DOI	10.1186/s12917-022-03359-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: In Vitro Reduced Susceptibility to Pentavalent Antimonials of a Leishmania infantum Isolate from a Human Cutaneous Leishmaniasis Case in Central Italy

Diotallevi, Aurora / Buffi, Gloria / Corbelli, Giovanni / Ceccarelli, Marcello / Ortalli, Margherita / Varani, Stefania / Magnani, Mauro / Galluzzi, Luca

Microorganisms. 2021 May 26, v. 9, no. 6

2021

Abstract: Cutaneous leishmaniasis (CL) caused by Leishmania (Leishmania) infantum is endemic in the Mediterranean basin. Here we report an autochthonous case of CL in a patient living in central Italy with an unsatisfactory response to treatment with intralesional ...

Abstract	Cutaneous leishmaniasis (CL) caused by Leishmania (Leishmania) infantum is endemic in the Mediterranean basin. Here we report an autochthonous case of CL in a patient living in central Italy with an unsatisfactory response to treatment with intralesional Meglumine Antimoniate and in vitro demonstration of reduced susceptibility to SbIII. Parasitological diagnosis was first achieved by histopathology on tissue biopsy and the patient was treated with a local infiltration of Meglumine Antimoniate. Since the clinical response at 12 weeks from the treatment’s onset was deemed unsatisfactory, two further skin biopsies were taken for histopathological examination, DNA extraction and parasite isolation. L. (L.) infantum was identified by molecular typing. The low susceptibility to Meglumine Antimoniate was confirmed in vitro: the promastigotes from the patient strain showed significantly lower susceptibility to SbIII (the active trivalent form of antimonial) compared to the reference strain MHOM/TN/80/IPT1. The patient underwent a new treatment course with intravenous liposomal Amphotericin B, reaching complete healing of the lesion. Additional studies are needed to confirm the epidemiological and clinical relevance of reduced susceptibility to SbIII of human L. (L.) infantum isolate in Italy.
Keywords	DNA ; Leishmania infantum ; amphotericin B ; biopsy ; cutaneous leishmaniasis ; histopathology ; humans ; intravenous injection ; parasites ; patients ; promastigotes ; Italy ; Mediterranean region
Language	English
Dates of publication	2021-0526
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms9061147
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article: Activation of NRF2 and ATF4 Signaling by the Pro-Glutathione Molecule I-152, a Co-Drug of N-Acetyl-Cysteine and Cysteamine

Crinelli, Rita / Zara, Carolina / Galluzzi, Luca / Buffi, Gloria / Ceccarini, Chiara / Smietana, Michael / Mari, Michele / Magnani, Mauro / Fraternale, Alessandra

Antioxidants. 2021 Jan. 26, v. 10, no. 2

2021

Abstract: I-152 combines two pro-glutathione (GSH) molecules, namely N-acetyl-cysteine (NAC) and cysteamine (MEA), to improve their potency. The co-drug efficiently increases/replenishes GSH levels in vitro and in vivo; little is known about its mechanism of ... ...

Abstract	I-152 combines two pro-glutathione (GSH) molecules, namely N-acetyl-cysteine (NAC) and cysteamine (MEA), to improve their potency. The co-drug efficiently increases/replenishes GSH levels in vitro and in vivo; little is known about its mechanism of action. Here we demonstrate that I-152 not only supplies GSH precursors, but also activates the antioxidant kelch-like ECH-associated protein 1/nuclear factor E2-related factor 2 (KEAP1/NRF2) pathway. The mechanism involves disulfide bond formation between KEAP1 cysteine residues, NRF2 stabilization and enhanced expression of the γ-glutamil cysteine ligase regulatory subunit. Accordingly, a significant increase in GSH levels, not reproduced by treatment with NAC or MEA alone, was found. Compared to its parent compounds, I-152 delivered NAC more efficiently within cells and displayed increased reactivity to KEAP1 compared to MEA. While at all the concentrations tested, I-152 activated the NRF2 pathway; high doses caused co-activation of activating transcription factor 4 (ATF4) and ATF4-dependent gene expression through a mechanism involving Atf4 transcriptional activation rather than preferential mRNA translation. In this case, GSH levels tended to decrease over time, and a reduction in cell proliferation/survival was observed, highlighting that there is a concentration threshold which determines the transition from advantageous to adverse effects. This body of evidence provides a molecular framework for the pro-GSH activity and dose-dependent effects of I-152 and shows how synergism and cross reactivity between different thiol species could be exploited to develop more potent drugs.
Keywords	antioxidants ; cell proliferation ; cross reaction ; cysteamine ; cysteine ; disulfide bonds ; dose response ; gene expression ; ligases ; mechanism of action ; synergism ; transcription factors ; transcriptional activation
Language	English
Dates of publication	2021-0126
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10020175
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article: Endoplasmic reticulum stress and unfolded protein response in infection by intracellular parasites.

Galluzzi, Luca / Diotallevi, Aurora / Magnani, Mauro

Future science OA

2017 Volume 3, Issue 3, Page(s) FSO198

Abstract: Perturbations of the physiological status of the endoplasmic reticulum (ER) trigger a specific response known as the ER stress response or unfolded protein response (UPR). In mammalian cells, the UPR is mediated by three ER transmembrane proteins (IRE1, ... ...

Abstract	Perturbations of the physiological status of the endoplasmic reticulum (ER) trigger a specific response known as the ER stress response or unfolded protein response (UPR). In mammalian cells, the UPR is mediated by three ER transmembrane proteins (IRE1, PERK and ATF6) which activate three signaling cascades to restore ER homeostasis. In recent years, a cross-talk between UPR, inflammatory and microbial sensing pathways has been elucidated. Pathogen infection can lead to UPR activation; moreover, several pathogens subvert the UPR to promote their survival and replication. While the UPR in viral and bacterial infection has been characterized, little is known about the role of UPR in intracellular parasite infection. Here, we review recent findings on UPR induction/modulation by intracellular parasites in host cells.
Language	English
Publishing date	2017-05-12
Publishing country	England
Document type	Journal Article ; Review
ISSN	2056-5623
ISSN	2056-5623
DOI	10.4155/fsoa-2017-0020
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Rapid monitoring of SARS-CoV-2 variants of concern through high-resolution melt analysis.

Diotallevi, Aurora / Buffi, Gloria / Barocci, Simone / Ceccarelli, Marcello / Bencardino, Daniela / Andreoni, Francesca / Orlandi, Chiara / Ferri, Marilisa / Vandini, Daniela / Menzo, Stefano / Carlotti, Eugenio / Casabianca, Anna / Magnani, Mauro / Galluzzi, Luca

Scientific reports

2023 Volume 13, Issue 1, Page(s) 21598

Abstract: The current global pandemic of COVID-19 is characterized by waves of infection due to the emergence of new SARS-CoV-2 variants carrying mutations on the Spike (S) protein gene. Since autumn 2020 many Variants of Concern (VOC) have been reported: Alpha/B ... ...

Abstract	The current global pandemic of COVID-19 is characterized by waves of infection due to the emergence of new SARS-CoV-2 variants carrying mutations on the Spike (S) protein gene. Since autumn 2020 many Variants of Concern (VOC) have been reported: Alpha/B.1.1.7, Beta/B.1.351, Gamma/P.1, Delta/B.1.617.2, Omicron/B.1.1.529, and sublineages. Surveillance of genomic variants is currently based on whole-genome sequencing (WGS) of viral genomes on a random fraction of samples positive to molecular tests. WGS involves high costs, extended analysis time, specialized staff, and expensive instruments compared to a PCR-based test. To rapidly identify the VOCs in positive samples, six assays based on real-time PCR and high-resolution melting (HRM) were designed on the S gene and applied to 120 oro/nasopharyngeal swab samples collected from October 2020 to June 2022 (106 positive and 14 negative samples). Overall, the assays showed 100% specificity and sensitivity compared with commercial PCR tests for COVID-19. Moreover, 104 samples out of 106 (98.1%) were correctly identified as follows: 8 Wuhan (wild type), 12 Alpha, 23 Delta, 46 Omicron BA.1/BA.1.1, 15 Omicron BA.2/BA.4/BA.5. With our lab equipment, about 10 samples can be processed every 3 h at the cost of less than € 10 ($ 10.60) per sample, including RNA extraction. The implementation of this approach could help local epidemiological surveillance and clinical decision-making.
MeSH term(s)	Humans ; SARS-CoV-2/genetics ; COVID-19/epidemiology ; Real-Time Polymerase Chain Reaction ; Biological Assay
Language	English
Publishing date	2023-12-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-48929-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito