Virology, Journal Year: 2025, Volume and Issue: 605, P. 110462 - 110462
Published: Feb. 21, 2025
Language: Английский
Cellular and Molecular Immunology, Journal Year: 2023, Volume and Issue: 21(2), P. 171 - 183
Published: Nov. 20, 2023
Abstract An ancient conflict between hosts and pathogens has driven the innate adaptive arms of immunity. Knowledge about this interplay can not only help us identify biological mechanisms but also reveal pathogen vulnerabilities that be leveraged therapeutically. The humoral response to SARS-CoV-2 infection been focus intense research, role immune system received significantly less attention. Here, we review current knowledge various means employs evade defense systems. We consider immunity in vaccines phenomenon long COVID.
Language: Английский
Citations
51
Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)
Published: Jan. 13, 2025
Autophagy dysfunction is associated with changes in autophagy-related genes. Various factors are connected to autophagy, and the mechanism regulating autophagy highly complicated. Epigenetic changes, such as aberrant expression of histone demethylase, actively not only oncogenesis but also inflammatory responses. Among post-translational modifications, lysine methylation holds significant importance. There over 30 members demethylases (KDMs), which act epigenetic regulators physiological processes diseases. Importantly, KDMs abnormally expressed regulation cellular inflammation, representing a crucial affecting inflammation-related This article reviewed function proteins inflammation. Specifically, It focused on specific regulatory mechanisms underlying activation or inhibition well their abnormal By analyzing each KDM modification, this review provides reliable theoretical basis for clinical decision marking regarding abnormalities
Language: Английский
Citations
2
Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14
Published: Aug. 24, 2023
Multicellular organisms are constantly subjected to pathogens that might be harmful. Although insects lack an adaptive immune system, they possess highly effective anti-infective mechanisms. Bacterial phagocytosis and parasite encapsulation some forms of cellular responses. Insects often defend themselves against infections through a humoral response. This phenomenon includes the secretion antimicrobial peptides into hemolymph. Specific receptors for detecting infection required recognition foreign such as proteins recognize glucans peptidoglycans, together referred PGRPs βGRPs. Activation these leads stimulation signaling pathways which further activates genes encoding peptides. Some instances JAK-STAT, Imd, Toll. The host response frequently accompanies has, however, been circumvented by diseases, may have assisted evolve their own complicated systems. role ncRNAs in insect immunology has discussed several notable studies reviews. paper examines most recent research on regulatory function during insect-pathogen crosstalk, including insect- pathogen-encoded miRNAs lncRNAs, provides overview important effector mechanisms activated diverse pathogen invaders.
Language: Английский
Citations
30
Cells, Journal Year: 2024, Volume and Issue: 13(2), P. 123 - 123
Published: Jan. 9, 2024
The COVID-19 pandemic has brought to the forefront intricate relationship between SARS-CoV-2 and its impact on neurological complications, including potential links neurodegenerative processes, characterized by a dysfunction of protein quality control systems ER stress. This review article explores role systems, such as Unfolded Protein Response (UPR), Endoplasmic Reticulum-Associated Degradation (ERAD), Ubiquitin–Proteasome System (UPS), autophagy molecular chaperones, in infection. Our hypothesis suggests that produces stress exploits leading disruption proteostasis cannot be solved host cell. culminates cell death may represent link neurodegeneration.
Language: Английский
Citations
12
The FASEB Journal, Journal Year: 2025, Volume and Issue: 39(1)
Published: Jan. 10, 2025
Abstract Hantaan virus (HTNV) infection causes severe hemorrhagic fever with renal syndrome (HFRS) in humans and the infectious process can be regulated by autophagy. The phosphatase tensin homolog (PTEN) protein has antiviral effects plays a critical role autophagy pathway. However, relationship between PTEN HTNV is not clear whether PTEN‐regulated involves replication unknown. Here, we identified that inhibits expression vitro vivo. glycoprotein Gc promotes ubiquitination degradation through 26S‐proteasome pathway via E3 ubiquitin ligase NEDD4. In addition, knockdown of prevents increases production, while overexpression induces autophagosome formation which wrap particles, thus leading to restrain production progeny viruses. Altogether, our findings reveal autophagy, highlighting potential importance treatment HFRS diseases.
Language: Английский
Citations
1
The Journal of Steroid Biochemistry and Molecular Biology, Journal Year: 2025, Volume and Issue: 249, P. 106710 - 106710
Published: Feb. 20, 2025
The interaction between vitamin D and the immune system is perhaps most well recognised extraskeletal facet of D, encompassing early studies therapy for TB leprosy through to more recent links with autoimmune disease. However, spotlight on function has been particularly intense in last five years following COVID-19 pandemic. This was due, part, many association status infection disease prognosis, as smaller number clinical trials supplementation. a potential role also stemmed from basic biology that provides plausible mechanistic rationale beneficial effects improved health setting respiratory infection. aim this review summarise different strands evidence supporting effect COVID-19, how modified during pandemic itself, new aspects are likely arise near future. Key topics feature are: antibacterial versus antiviral innate responses 1,25-dihydroxyvitamin (1,25(OH)2D); 1α-hydroxylase (CYP27B1) activity metabolism 25-hydroxyvitamin (25(OH)D) beyond antigen-presenting cells; advances cell target gene (notably changes metabolic profile). Whilst much interest era focused public health, continued evolution our understanding interacts components continues support health.
Language: Английский
Citations
1
Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: April 8, 2025
Chronic inflammation is an important component of many diseases, including autoimmune intracellular infections, dysbiosis and degenerative diseases. An element this state the mainly positive feedback between inflammatory cytokines, reactive oxygen species (ROS), nitric oxide (NO), increased calcium, hypoxia-inducible factor 1-alpha (HIF-1α) stabilisation mitochondrial oxidative stress, which, under normal conditions, enhance response against pathogens. Autophagy nuclear erythroid 2-related 2 (Nrf2)-mediated antioxidant are negatively coupled with above-mentioned elements to maintain defence at a level appropriate severity infection. The current review first attempt build multidimensional model cellular self-regulation chronic inflammation. It describes feedbacks involved in explains possible pathways by which becomes chronic. multiplicity suggests that symptomatic treatment should focus on inhibiting multiple effectively suppress all dysregulated inflammation, calcium mito-stress other metabolic disturbances.
Language: Английский
Citations
1
Frontiers in Cellular and Infection Microbiology, Journal Year: 2023, Volume and Issue: 13
Published: Aug. 25, 2023
Since December 2019, the world has been facing viral pandemic called COVID-19 (Coronavirus disease 2019) caused by a new beta-coronavirus named severe acute respiratory syndrome coronavirus-2, or SARS-CoV-2. patients may present with wide range of symptoms, from asymptomatic to requiring intensive care support. The form is often marked an altered immune response and cytokine storm. Advanced age, age-related underlying diseases, including metabolic syndromes, appear contribute increased severity mortality suggesting role for mitochondria in pathogenesis. Furthermore, since system associated its damage-related molecular patterns (mtDAMPs), host mitochondrial play important during infections. Viruses have evolved modulate function survival proliferation, which turn could lead cellular stress progression. Recent studies focused on possible roles SARS-CoV-2 infection. It suggested that hijacking be key factor In this review, we discuss infections infection based past knowledge. Paying attention will help better understand pathophysiology achieve effective methods prevention, diagnosis, treatment.
Language: Английский
Citations
17
Cells, Journal Year: 2024, Volume and Issue: 13(2), P. 183 - 183
Published: Jan. 18, 2024
Rabies virus (RABV) is a single-stranded negative-sense RNA belonging to the Rhabdoviridae family and Lyssavirus genus, which highly neurotropic can infect almost all warm-blooded animals, including humans. Autophagy apoptosis are two evolutionarily conserved genetically regulated processes that maintain cellular organismal homeostasis, respectively. recycles unnecessary or dysfunctional intracellular organelles molecules in cell, whereas eliminates damaged unwanted cells an organism. Studies have shown RABV induce both autophagy target cells. To advance our understanding of pathogenesis rabies, this paper reviews molecular mechanisms induced by effects events on replication.
Language: Английский
Citations
8
PLoS Pathogens, Journal Year: 2024, Volume and Issue: 20(1), P. e1011958 - e1011958
Published: Jan. 16, 2024
Autophagy-related protein 7 (ATG7) is an essential autophagy effector enzyme. Although it well known that plays crucial roles in the infections with various viruses including influenza A virus (IAV), function and underlying mechanism of ATG7 infection pathogenesis IAV remain poorly understood. Here, vitro studies showed had profound effects on replication IAV. Depletion markedly attenuated IAV, whereas overexpression facilitated viral replication. conditional knockout mice were further employed exhibited significantly resistant to infections, as evidenced by a lower degree tissue injury, slower body weight loss, better survival, than wild type animals challenged either (RNA virus) or pseudorabies (DNA virus). Interestingly, we found promoted autophagy-dependent -independent manners, inhibition failed completely block upregulation ATG7. To determine autophagy-independent mechanism, transcriptome analysis was utilized demonstrated restrained production interferons (IFNs). Loss obviously enhanced expression I III IFNs ATG7-depleted cells mice, impaired interferon response infection. Consistently, our experiments suppressed IRF3 activation during Furthermore, identified long noncoding RNA (lncRNA) GAPLINC critical regulator involved promotion Importantly, both inactivation IFN caused mediated through control over expression, suggesting contributes suppression antiviral immunity Together, these results uncover which suppresses host innate establish role for ATG7/GAPLINC/IRF3 axis regulating pathogenesis.
Language: Английский
Citations
7