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1.
New Microbiol ; 47(2): 123-136, 2024 Jul.
Article in English | MEDLINE | ID: mdl-39023521

ABSTRACT

The escalating global population poses formidable challenges to addressing pressing environmental concerns, hindering progress towards sustainable development goals. Unregulated human activities, particularly the excessive reliance on fossil fuels and unsustainable agricultural practices, contribute to pollution, climate change, and resource depletion. Inadequate waste management systems exacerbate environmental degradation and pose risks to public health. Leveraging biological resources and urban/industrial waste emerges as a promising solution. Various waste materials, such as food waste and agro-industrial by-products, have been efficiently repurposed into valuable bio-based products. This review explores the diverse applications of agricultural and food waste repurposing, including microbial production of biopolymers and biosurfactants, as well as the extraction of biologically active compounds for potential antimicrobial drugs.


Subject(s)
Anti-Infective Agents , Anti-Infective Agents/pharmacology , Humans , Biomass , Waste Management/methods , Biocompatible Materials , Waste Products/analysis
2.
Antiviral Res ; 216: 105664, 2023 08.
Article in English | MEDLINE | ID: mdl-37414288

ABSTRACT

Recent evidence suggests that lipids play a crucial role in viral infections beyond their traditional functions of supplying envelope and energy, and creating protected niches for viral replication. In the case of Zika virus (ZIKV), it alters host lipids by enhancing lipogenesis and suppressing ß-oxidation to generate viral factories at the endoplasmic reticulum (ER) interface. This discovery prompted us to hypothesize that interference with lipogenesis could serve as a dual antiviral and anti-inflammatory strategy to combat the replication of positive sense single-stranded RNA (ssRNA+) viruses. To test this hypothesis, we examined the impact of inhibiting N-Acylethanolamine acid amidase (NAAA) on ZIKV-infected human Neural Stem Cells. NAAA is responsible for the hydrolysis of palmitoylethanolamide (PEA) in lysosomes and endolysosomes. Inhibition of NAAA results in PEA accumulation, which activates peroxisome proliferator-activated receptor-α (PPAR-α), directing ß-oxidation and preventing inflammation. Our findings indicate that inhibiting NAAA through gene-editing or drugs moderately reduces ZIKV replication by approximately one log10 in Human Neural Stem Cells, while also releasing immature virions that have lost their infectivity. This inhibition impairs furin-mediated prM cleavage, ultimately blocking ZIKV maturation. In summary, our study highlights NAAA as a host target for ZIKV infection.


Subject(s)
Zika Virus Infection , Zika Virus , Humans , Amidohydrolases/antagonists & inhibitors , Amidohydrolases/metabolism , Anti-Inflammatory Agents/pharmacology , Inflammation/drug therapy , Zika Virus Infection/drug therapy
3.
Antiviral Res ; 206: 105398, 2022 10.
Article in English | MEDLINE | ID: mdl-35985406

ABSTRACT

A marked reorganization of internal membranes occurs in the cytoplasm of cells infected by single stranded positive-sense RNA viruses. Most cell compartments change their asset to provide lipids for membrane rearrangement into replication organelles, where to concentrate viral proteins and enzymes while hiding from pathogen pattern recognition molecules. Because the endoplasmic reticulum is a central hub for lipid metabolism, when viruses hijack the organelle to form their replication organelles, a cascade of events change the intracellular environment. This results in a marked increase in lipid consumption, both by lipolysis and lipophagy of lipid droplets. In addition, lipids are used to produce energy for viral replication. At the same time, inflammation is started by signalling lipids, where lysosomal processing plays a relevant role. This review is aimed at providing an overview on what takes place after human class IV viruses have released their genome into the host cell and the consequences on lipid metabolism, including lysosomes.


Subject(s)
Positive-Strand RNA Viruses , RNA Viruses , Endoplasmic Reticulum/metabolism , Humans , Lipids , Lysosomes/metabolism , RNA, Viral/metabolism , Virus Replication
4.
Viruses ; 14(5)2022 05 17.
Article in English | MEDLINE | ID: mdl-35632821

ABSTRACT

Lipids play a crucial role in the entry and egress of viruses, regardless of whether they are naked or enveloped. Recent evidence shows that lipid involvement in viral infection goes much further. During replication, many viruses rearrange internal lipid membranes to create niches where they replicate and assemble. Because of the close connection between lipids and inflammation, the derangement of lipid metabolism also results in the production of inflammatory stimuli. Due to its pivotal function in the viral life cycle, lipid metabolism has become an area of intense research to understand how viruses seize lipids and to design antiviral drugs targeting lipid pathways. Palmitoylethanolamide (PEA) is a lipid-derived peroxisome proliferator-activated receptor-α (PPAR-α) agonist that also counteracts SARS-CoV-2 entry and its replication. Our work highlights for the first time the antiviral potency of PEA against SARS-CoV-2, exerting its activity by two different mechanisms. First, its binding to the SARS-CoV-2 S protein causes a drop in viral infection of ~70%. We show that this activity is specific for SARS-CoV-2, as it does not prevent infection by VSV or HSV-2, other enveloped viruses that use different glycoproteins and entry receptors to mediate their entry. Second, we show that in infected Huh-7 cells, treatment with PEA dismantles lipid droplets, preventing the usage of these vesicular bodies by SARS-CoV-2 as a source of energy and protection against innate cellular defenses. This is not surprising since PEA activates PPAR-α, a transcription factor that, once activated, generates a cascade of events that leads to the disruption of fatty acid droplets, thereby bringing about lipid droplet degradation through ß-oxidation. In conclusion, the present work demonstrates a novel mechanism of action for PEA as a direct and indirect antiviral agent against SARS-CoV-2. This evidence reinforces the notion that treatment with this compound might significantly impact the course of COVID-19. Indeed, considering that the protective effects of PEA in COVID-19 are the current objectives of two clinical trials (NCT04619706 and NCT04568876) and given the relative lack of toxicity of PEA in humans, further preclinical and clinical tests will be needed to fully consider PEA as a promising adjuvant therapy in the current COVID-19 pandemic or against emerging RNA viruses that share the same route of replication as coronaviruses.


Subject(s)
COVID-19 Drug Treatment , SARS-CoV-2 , Amides , Antiviral Agents/pharmacology , Antiviral Agents/therapeutic use , Ethanolamines , Humans , Palmitic Acids/pharmacology , Pandemics , Pisum sativum , Peroxisome Proliferator-Activated Receptors , Spike Glycoprotein, Coronavirus
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