To see the other types of publications on this topic, follow the link: Virus Physiological Processes.
Journal articles on the topic 'Virus Physiological Processes'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Virus Physiological Processes.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Pyrih, O. V. "INCREASED VIRAL-RESISTANCE OF YELLOW LUPINE UNDER THE ACTION OF MICROBIAL PREPARATIONS AND PHYSIOLOGICALLY ACTIVE SUBSTANCES." Agriciltural microbiology 24 (October 9, 2016): 59–63. http://dx.doi.org/10.35868/1997-3004.24.59-63.
Full textAbstract:
The influence of microbial preparations and physiologically active substances on the reproduction bean yellow mosaic virus in yellow lupine plants has been investigated. It was established that the action of microbial preparations on the limitation of the viral infection development is explained by the influence of exogenous physiologically active substances, which are contained in preparations and produced by the microorganisms introduced in agrocenosis, on the forming of endogenous phytohormone pool. Therefore, it optimizes a number of physiological processes of the plants and activates their defence reactions.
2
Zhao, Shizhen, and Honggang Wang. "EVA1A Plays an Important Role by Regulating Autophagy in Physiological and Pathological Processes." International Journal of Molecular Sciences 22, no. 12 (June 8, 2021): 6181. http://dx.doi.org/10.3390/ijms22126181.
Full textAbstract:
Eva-1 homolog A (EVA1A) is regarded as TMEM166 (transmembrane protein 166) or FAM176A (family with sequence similarity 176) and a lysosome and endoplasmic reticulum-associated protein involved in regulating autophagy and apoptosis. EVA1A regulates embryonic neurogenesis, cardiac remodeling, islet alpha-cell functions, acute liver failure, and hepatitis B virus replication. However, the related mechanisms are not fully clear. Autophagy is a process in which cells transfer pathogens, abnormal proteins and organelles to lysosomes for degradation. It plays an important role in various physiological and pathological processes, including cancer, aging, neurodegeneration, infection, heart disease, development, cell differentiation and nutritional starvation. Recently, there are many studies on the important role of EVA1A in many physiological and pathological processes by regulating autophagy. However, the related molecular mechanisms need further study. Therefore, we summarize the above-mentioned researches about the role of EVA1A in physiological and pathological processes through regulating autophagy in order to provide theoretical basis for future researches.
3
Štrukelj, Melita, Jaka RAZINGER, Barbara GRUBAR, Uroš ŽIBRAT, Irena MAVRIČ PLEŠKO, Dominik Vodnik, and Gregor UREK. "Fiziološki odziv žlahtne vinske trte Vitis vinifera L. na okužbo z zvijanjem listov vinske trte povezanih virusov (GLRaV-1 in GLRaV-1 + GLRaV-3)." Acta agriculturae Slovenica 107, no. 2 (October 26, 2016): 519. http://dx.doi.org/10.14720/aas.2016.107.2.22.
Full textAbstract:
Grapevine leafroll disease is one of the most severe viral diseases of grapevine caused by Grapevine leafroll-associated viruses (GLRaVs). Physiological processes were monitored on grapevines with single (GLRaV-1) and mixed (GLRaV-1 and GLRaV -3) viral infection under greenhouse conditions from June to September, in vegetation period 2014. In the mid of the season (July) negative effects of the virus infections on physiological processes were more severe in mixed than in single infection. The net-photosynthesis (Pn) of the leaves infected with GLRaV-1 and GLRaV-3 reached only a half of the Pn in GLRaV-1 infected grapevines. Similar reduction was found for stomatal conductance, transpiration and parameters related to photochemical efficiency (electron transport rate).
4
Williams, C. K. "Development and use of virus-vectored immunocontraception." Reproduction, Fertility and Development 9, no. 1 (1997): 169. http://dx.doi.org/10.1071/r96063.
Full textAbstract:
Virus-vectored immunocontraception (VVIC) is perceived to present biological risks, real or baseless, which create social and political constraints to deploying VVIC for managing vertebrate pests. Developing and deploying VVIC must be justified and address biological, social and political risks. Future needs for pest management will influence deployment of VVIC. Projections of human society and pest impact on agriculture and conservation suggest increasing need for cost-beneficial strategies. Best strategies are likely to integrate various methods, possibly including forms of VVIC. Processes identifying future pest impacts and roles for VVIC are shown using the rabbit in Australia. Present research developing VVIC aims to test physiological feasibility, to develop it for specific pests, and address aspects of ecological feasibility. Minimizing biological risks through choosing species-specific antigens and, if possible, viral vectors, is central and overseen by regulatory authorities. International collaborators study related valued species to develop protective strategies. Excellent science can withstand legal or public challenge to safe and cost-beneficial VVIC if aided by information needed by the public exposed to media distortion of scientific debate, complex argument and concepts of probability and risk. Sound science needs support from strategies for public processes to enable cost-beneficial management of vertebrate pests.
5
Li, Xiaofei, Qi Wang, Yanni Gao, Xiaole Qi, Yongqiang Wang, Honglei Gao, Yulong Gao, and Xiaomei Wang. "Quantitative iTRAQ LC-MS/MS Proteomics Reveals the Proteome Profiles of DF-1 Cells after Infection with Subgroup J Avian Leukosis Virus." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/395307.
Full textAbstract:
Avian leukosis virus subgroup J (ALV-J) is an avian oncogenic retrovirus that can induce various clinical tumors and has caused severe economic losses in China. To improve our understanding of the host cellular responses to virus infection and the pathogenesis of ALV-J infection, we applied isobaric tags for relative and absolute quantification (iTRAQ) labeling coupled with multidimensional liquid chromatography-tandem mass spectrometry to detect the protein changes in DF-1 cells infected and mock-infected with ALV-J. A total of 75 cellular proteins were significantly changed, including 33 upregulated proteins and 42 downregulated proteins. The reliability of iTRAQ-LC MS/MS was confirmed via real-time PCR. Most of these proteins were related to the physiological functions of metabolic processes, biosynthetic processes, responses to stimuli, protein binding, signal transduction, cell cytoskeleton, and so forth. We also found some proteins that play important roles in apoptosis and oncogenicity. The differentially expressed proteins identified may provide valuable information to elucidate the pathogenesis of virus infection and virus-host interactions.
6
Monette, Anne, and Andrew J. Mouland. "Zinc and Copper Ions Differentially Regulate Prion-Like Phase Separation Dynamics of Pan-Virus Nucleocapsid Biomolecular Condensates." Viruses 12, no. 10 (October 18, 2020): 1179. http://dx.doi.org/10.3390/v12101179.
Full textAbstract:
Liquid-liquid phase separation (LLPS) is a rapidly growing research focus due to numerous demonstrations that many cellular proteins phase-separate to form biomolecular condensates (BMCs) that nucleate membraneless organelles (MLOs). A growing repertoire of mechanisms supporting BMC formation, composition, dynamics, and functions are becoming elucidated. BMCs are now appreciated as required for several steps of gene regulation, while their deregulation promotes pathological aggregates, such as stress granules (SGs) and insoluble irreversible plaques that are hallmarks of neurodegenerative diseases. Treatment of BMC-related diseases will greatly benefit from identification of therapeutics preventing pathological aggregates while sparing BMCs required for cellular functions. Numerous viruses that block SG assembly also utilize or engineer BMCs for their replication. While BMC formation first depends on prion-like disordered protein domains (PrLDs), metal ion-controlled RNA-binding domains (RBDs) also orchestrate their formation. Virus replication and viral genomic RNA (vRNA) packaging dynamics involving nucleocapsid (NC) proteins and their orthologs rely on Zinc (Zn) availability, while virus morphology and infectivity are negatively influenced by excess Copper (Cu). While virus infections modify physiological metal homeostasis towards an increased copper to zinc ratio (Cu/Zn), how and why they do this remains elusive. Following our recent finding that pan-retroviruses employ Zn for NC-mediated LLPS for virus assembly, we present a pan-virus bioinformatics and literature meta-analysis study identifying metal-based mechanisms linking virus-induced BMCs to neurodegenerative disease processes. We discover that conserved degree and placement of PrLDs juxtaposing metal-regulated RBDs are associated with disease-causing prion-like proteins and are common features of viral proteins responsible for virus capsid assembly and structure. Virus infections both modulate gene expression of metalloproteins and interfere with metal homeostasis, representing an additional virus strategy impeding physiological and cellular antiviral responses. Our analyses reveal that metal-coordinated virus NC protein PrLDs initiate LLPS that nucleate pan-virus assembly and contribute to their persistence as cell-free infectious aerosol droplets. Virus aerosol droplets and insoluble neurological disease aggregates should be eliminated by physiological or environmental metals that outcompete PrLD-bound metals. While environmental metals can control virus spreading via aerosol droplets, therapeutic interference with metals or metalloproteins represent additional attractive avenues against pan-virus infection and virus-exacerbated neurological diseases.
7
Hing, Stephanie, Edward J. Narayan, R. C. Andrew Thompson, and Stephanie S. Godfrey. "The relationship between physiological stress and wildlife disease: consequences for health and conservation." Wildlife Research 43, no. 1 (2016): 51. http://dx.doi.org/10.1071/wr15183.
Full textAbstract:
Wildlife populations are under increasing pressure from a variety of threatening processes, ranging from climate change to habitat loss, that can incite a physiological stress response. The stress response influences immune function, with potential consequences for patterns of infection and transmission of disease among and within wildlife, domesticated animals and humans. This is concerning because stress may exacerbate the impact of disease on species vulnerable to extinction, with consequences for biodiversity conservation globally. Furthermore, stress may shape the role of wildlife in the spread of emerging infectious diseases (EID) such as Hendra virus (HeV) and Ebola virus. However, we still have a limited understanding of the influence of physiological stress on infectious disease in wildlife. We highlight key reasons why an improved understanding of the relationship between stress and wildlife disease could benefit conservation, and animal and public health, and discuss approaches for future investigation. In particular, we recommend that increased attention be given to the influence of anthropogenic stressors including climate change, habitat loss and management interventions on disease dynamics in wildlife populations.
8
Filgueira, Luis, Alexey Larionov, and Nils Lannes. "The Influence of Virus Infection on Microglia and Accelerated Brain Aging." Cells 10, no. 7 (July 20, 2021): 1836. http://dx.doi.org/10.3390/cells10071836.
Full textAbstract:
Microglia are the resident immune cells of the central nervous system contributing substantially to health and disease. There is increasing evidence that inflammatory microglia may induce or accelerate brain aging, by interfering with physiological repair and remodeling processes. Many viral infections affect the brain and interfere with microglia functions, including human immune deficiency virus, flaviviruses, SARS-CoV-2, influenza, and human herpes viruses. Especially chronic viral infections causing low-grade neuroinflammation may contribute to brain aging. This review elucidates the potential role of various neurotropic viruses in microglia-driven neurocognitive deficiencies and possibly accelerated brain aging.
9
López-Cortés, Georgina I., Miryam Palacios-Pérez, Margarita M. Hernández-Aguilar, Hannya F. Veledíaz, and Marco V. José. "Human Coronavirus Cell Receptors Provide Challenging Therapeutic Targets." Vaccines 11, no. 1 (January 13, 2023): 174. http://dx.doi.org/10.3390/vaccines11010174.
Full textAbstract:
Coronaviruses interact with protein or carbohydrate receptors through their spike proteins to infect cells. Even if the known protein receptors for these viruses have no evolutionary relationships, they do share ontological commonalities that the virus might leverage to exacerbate the pathophysiology. ANPEP/CD13, DPP IV/CD26, and ACE2 are the three protein receptors that are known to be exploited by several human coronaviruses. These receptors are moonlighting enzymes involved in several physiological processes such as digestion, metabolism, and blood pressure regulation; moreover, the three proteins are expressed in kidney, intestine, endothelium, and other tissues/cell types. Here, we spot the commonalities between the three enzymes, the physiological functions of the enzymes are outlined, and how blocking either enzyme results in systemic deregulations and multi-organ failures via viral infection or therapeutic interventions is addressed. It can be difficult to pinpoint any coronavirus as the target when creating a medication to fight them, due to the multiple processes that receptors are linked to and their extensive expression.
10
Horníková, Lenka, Kateřina Bruštíková, Sandra Huérfano, and Jitka Forstová. "Nuclear Cytoskeleton in Virus Infection." International Journal of Molecular Sciences 23, no. 1 (January 5, 2022): 578. http://dx.doi.org/10.3390/ijms23010578.
Full textAbstract:
The nuclear lamina is the main component of the nuclear cytoskeleton that maintains the integrity of the nucleus. However, it represents a natural barrier for viruses replicating in the cell nucleus. The lamina blocks viruses from being trafficked to the nucleus for replication, but it also impedes the nuclear egress of the progeny of viral particles. Thus, viruses have evolved mechanisms to overcome this obstacle. Large viruses induce the assembly of multiprotein complexes that are anchored to the inner nuclear membrane. Important components of these complexes are the viral and cellular kinases phosphorylating the lamina and promoting its disaggregation, therefore allowing virus egress. Small viruses also use cellular kinases to induce lamina phosphorylation and the subsequent disruption in order to facilitate the import of viral particles during the early stages of infection or during their nuclear egress. Another component of the nuclear cytoskeleton, nuclear actin, is exploited by viruses for the intranuclear movement of their particles from the replication sites to the nuclear periphery. This study focuses on exploitation of the nuclear cytoskeleton by viruses, although this is just the beginning for many viruses, and promises to reveal the mechanisms and dynamic of physiological and pathological processes in the nucleus.
11
Zhou, Yong, Juan Pu, and Yuping Wu. "The Role of Lipid Metabolism in Influenza A Virus Infection." Pathogens 10, no. 3 (March 5, 2021): 303. http://dx.doi.org/10.3390/pathogens10030303.
Full textAbstract:
Influenza A virus (IAV) is an important zoonotic pathogen that can cause disease in animals such as poultry and pigs, and it can cause infection and even death in humans, posing a serious threat to public health. IAV is an enveloped virus that relies on host cell metabolic systems, especially lipid metabolism systems, to complete its life cycle in host cells. On the other side, host cells regulate their metabolic processes to prevent IAV replication and maintain their normal physiological functions. This review summarizes the roles of fatty acid, cholesterol, phospholipid and glycolipid metabolism in IAV infection, proposes future research challenges, and looks forward to the prospective application of lipid metabolism modification to limit IAV infection, which will provide new directions for the development of anti-influenza drugs.
12
Schabla, N. Max, Koushik Mondal, and Patrick C. Swanson. "DCAF1 (VprBP): emerging physiological roles for a unique dual-service E3 ubiquitin ligase substrate receptor." Journal of Molecular Cell Biology 11, no. 9 (December 24, 2018): 725–35. http://dx.doi.org/10.1093/jmcb/mjy085.
Full textAbstract:
Abstract Cullin-RING ligases (CRLs) comprise a large group of modular eukaryotic E3 ubiquitin ligases. Within this family, the CRL4 ligase (consisting of the Cullin4 [CUL4] scaffold protein, the Rbx1 RING finger domain protein, the DNA damage-binding protein 1 [DDB1], and one of many DDB1-associated substrate receptor proteins) has been intensively studied in recent years due to its involvement in regulating various cellular processes, its role in cancer development and progression, and its subversion by viral accessory proteins. Initially discovered as a target for hijacking by the human immunodeficiency virus accessory protein r, the normal targets and function of the CRL4 substrate receptor protein DDB1–Cul4-associated factor 1 (DCAF1; also known as VprBP) had remained elusive, but newer studies have begun to shed light on these questions. Here, we review recent progress in understanding the diverse physiological roles of this DCAF1 in supporting various general and cell type-specific cellular processes in its context with the CRL4 E3 ligase, as well as another HECT-type E3 ligase with which DCAF1 also associates, called EDD/UBR5. We also discuss emerging questions and areas of future study to uncover the dynamic roles of DCAF1 in normal physiology.
13
Nagy, Gábor, Ágota Bányai, and Béla Illés. "The Impact of the Pandemic on Global Logistics Processes." Advanced Logistic Systems - Theory and Practice 14, no. 1 (2020): 39–48. http://dx.doi.org/10.32971/als.2020.008.
Full textAbstract:
The COVID-19 pandemic reminded society that, in addition to natural disasters, epidemics are also part of our past, present and future. Even if we cannot prevent the emergence of dangerous viruses, we must be prepared to mitigate their impact on society. It is clear that the COVID-19 epidemic, in addition to its severe physiological effects, has caused significant economic damage worldwide. Global supply chains in different industries face significant challenges. Not only is the economy affected by the virus; society as a whole is affected, leading to dramatic changes in the behaviour of businesses and consumers. The global supply chains that have shown a high level of stability and resilience in recent decades now face a number of disruptive factors. The pandemic adversely affected the entire chain in terms of both manufacturing and logistics processes, as well as a significant shift in demand. The pandemic highlighted the need to focus on three key areas to increase the resilience of supply chains: risk and flexibility, global transparency, and rapid response and decision-making. It can be concluded that the changes caused by the epidemic will make global supply chains shorter and more transparent through renewed strategies such as digitization, the tools of which are the building blocks of the DSN.
14
Iqbal, Javaid, and Uli Mueller. "Virus infection causes specific learning deficits in honeybee foragers." Proceedings of the Royal Society B: Biological Sciences 274, no. 1617 (April 17, 2007): 1517–21. http://dx.doi.org/10.1098/rspb.2007.0022.
Full textAbstract:
In both mammals and invertebrates, virus infections can impair a broad spectrum of physiological functions including learning and memory formation. In contrast to the knowledge on the conserved mechanisms underlying learning, the effects of virus infection on different aspects of learning are barely known. We use the honeybee ( Apis mellifera ), a well-established model system for studying learning, to investigate the impact of deformed wing virus (DWV) on learning. Injection of DWV into the haemolymph of forager leads to a RT-PCR detectable DWV signal after 3 days. The detailed behavioural analysis of DWV-infected honeybees shows an increased responsiveness to water and low sucrose concentrations, an impaired associative learning and memory formation, but intact non-associative learning like sensitization and habituation. This contradicts all present studies in non-infected bees, where increased sucrose responsiveness is linked to improved associative learning and to changes in non-associative learning. Thus, DWV seems to interfere with molecular mechanism of learning by yet unknown processes that may include viral effects on the immune system and on gene expression.
15
Patton, Holly K., Zhen-Hong Zhou, James K. Bubien, Etty N. Benveniste, and Dale J. Benos. "gp120-induced alterations of human astrocyte function: Na+/H+exchange, K+conductance, and glutamate flux." American Journal of Physiology-Cell Physiology 279, no. 3 (September 1, 2000): C700—C708. http://dx.doi.org/10.1152/ajpcell.2000.279.3.c700.
Full textAbstract:
Many human immunodeficiency virus (HIV)-infected patients suffer from impaired neurological function and dementia. This facet of the disease has been termed acquired immunodeficiency syndrome (AIDS)-associated dementia complex (ADC). Several cell types, including astrocytes and neurons, are not productively infected by virus but are involved in ADC pathophysiology. Previous studies of rat astrocytes showed that an HIV coat protein (gp120) accelerated astrocyte Na+/H+exchange and that the resultant intracellular alkalinization activated a pH-sensitive K+conductance. The present experiments were conducted to determine whether gp120 affected human astrocytes in the same fashion. It was found that primary human astrocytes express a pH-sensitive K+conductance that was activated on intracellular alkalinization. Also, gp120 treatment of whole cell clamped human astrocytes activated this conductance specifically. Furthermore, gp120 inhibited glutamate uptake by primary human astrocytes. These altered physiological processes could contribute to pathophysiological changes in HIV-infected brains. Because the gp120-induced cell physiological changes were partially inhibited by dimethylamiloride (an inhibitor of Na+/H+exchange), our findings suggest that modification of human astrocyte Na+/H+exchange activity may provide a means of addressing some of the neurological complications of HIV infection.
16
Bota, Josefina, Enrico Cretazzo, Rafael Montero, Joan Rosselló, and Josep Cifre. "Grapevine fleck virus (GFkV) elimination in a selected clone of Vitis vinifera L. cv. Manto Negro and its effects on photosynthesis." OENO One 48, no. 1 (January 31, 2014): 11. http://dx.doi.org/10.20870/oeno-one.2014.48.1.1653.
Full textAbstract:
<p style="text-align: justify;"><strong>Aims</strong>: The use of healthy propagating material is required to control grapevine viruses. The aim of this work was to eliminate <em>Grapevine fleck virus</em> (GFkV) from a Manto Negro clone, a local grapevine variety, in order to include this material in certification programs. Additionally, the effects of virus elimination on photosynthesis and related parameters were evaluated.</p><p style="text-align: justify;"><strong>Methods and results</strong>: Two method combinations for virus elimination were evaluated: (1) field thermotherapy and shoot tip culture and (2) chamber thermotherapy and shoot tip culture. GFkV elimination was tested by double antibody sandwich-enzyme-linked immunosorbent assay (DAS-ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). The results suggest that a natural field thermotherapy prior to shoot tip culture is effective, making unnecessary the chamber thermotherapy treatment. Additionally, the effects of virus elimination on gas exchanges, chlorophyll fluorescence, electron transport rate (ETR), protein and pigment content were evaluated. The results indicate that GFkV infection affects physiological processes, especially stomatal conductance (g<sub>s</sub>), whereas photosynthesis, protein, pigment content, ETR, and fluorescence parameters were not significantly changed. </p><p style="text-align: justify;"><strong>Conclusion</strong>: This study described a simple and rapid method that requires only one medium for virus elimination (GFkV). Beyond its sanitation potential, the use of larger explants (1-3 mm) ensures the integrity of the clone. The presence of the virus affects physiological processes, especially g<sub>s</sub>, demonstrating the beneficial effect of eliminating GFkV. <strong></strong></p><p style="text-align: justify;"><strong>Significance and impact of the study</strong>: The described method has the potential to produce GFkV-free rooted plantlets faster than other methods while being potentially safer in maintaining the genetic and phenotypic stability of the regenerated clone. The beneficial effects of GFkV elimination provide evidence for the importance to detect this virus prior to the inclusion of clones in certification programs.</p>
17
Malgras, Mathilde, Magali Garcia, Clément Jousselin, Charles Bodet, and Nicolas Lévêque. "The Antiviral Activities of Poly-ADP-Ribose Polymerases." Viruses 13, no. 4 (March 30, 2021): 582. http://dx.doi.org/10.3390/v13040582.
Full textAbstract:
The poly-adenosine diphosphate (ADP)-ribose polymerases (PARPs) are responsible for ADP-ribosylation, a reversible post-translational modification involved in many cellular processes including DNA damage repair, chromatin remodeling, regulation of translation and cell death. In addition to these physiological functions, recent studies have highlighted the role of PARPs in host defenses against viruses, either by direct antiviral activity, targeting certain steps of virus replication cycle, or indirect antiviral activity, via modulation of the innate immune response. This review focuses on the antiviral activity of PARPs, as well as strategies developed by viruses to escape their action.
18
Kwasnik, Malgorzata, Wojciech Socha, Bartosz Czech, Magdalena Wasiak, Jerzy Rola, and Wojciech Rozek. "Protein-Coding Region Derived Small RNA in Exosomes from Influenza A Virus–Infected Cells." International Journal of Molecular Sciences 24, no. 1 (January 3, 2023): 867. http://dx.doi.org/10.3390/ijms24010867.
Full textAbstract:
Exosomes may function as multifactorial mediators of cell-to-cell communication, playing crucial roles in both physiological and pathological processes. Exosomes released from virus-infected cells may contain RNA and proteins facilitating infection spread. The purpose of our study was to analyze how the small RNA content of exosomes is affected by infection with the influenza A virus (IAV). Exosomes were isolated by ultracentrifugation after hemadsorption of virions and their small RNA content was identified using high-throughput sequencing. As compared to mock-infected controls, 856 RNA transcripts were significantly differentially expressed in exosomes from IAV-infected cells, including fragments of 458 protein-coding (pcRNA), 336 small, 28 long intergenic non-coding RNA transcripts, and 33 pseudogene transcripts. Upregulated pcRNA species corresponded mainly to proteins associated with translation and antiviral response, and the most upregulated among them were RSAD2, CCDC141 and IFIT2. Downregulated pcRNA species corresponded to proteins associated with the cell cycle and DNA packaging. Analysis of differentially expressed pseudogenes showed that in most cases, an increase in the transcription level of pseudogenes was correlated with an increase in their parental genes. Although the role of exosome RNA in IAV infection remains undefined, the biological processes identified based on the corresponding proteins may indicate the roles of some of its parts in IAV replication.
19
Mavri, Maša, Katja Spiess, Mette Marie Rosenkilde, Catrin Sian Rutland, Milka Vrecl, and Valentina Kubale. "Methods for Studying Endocytotic Pathways of Herpesvirus Encoded G Protein-Coupled Receptors." Molecules 25, no. 23 (December 3, 2020): 5710. http://dx.doi.org/10.3390/molecules25235710.
Full textAbstract:
Endocytosis is a fundamental process involved in trafficking of various extracellular and transmembrane molecules from the cell surface to its interior. This enables cells to communicate and respond to external environments, maintain cellular homeostasis, and transduce signals. G protein-coupled receptors (GPCRs) constitute a family of receptors with seven transmembrane alpha-helical domains (7TM receptors) expressed at the cell surface, where they regulate physiological and pathological cellular processes. Several herpesviruses encode receptors (vGPCRs) which benefits the virus by avoiding host immune surveillance, supporting viral dissemination, and thereby establishing widespread and lifelong infection, processes where receptor signaling and/or endocytosis seem central. vGPCRs are rising as potential drug targets as exemplified by the cytomegalovirus-encoded receptor US28, where its constitutive internalization has been exploited for selective drug delivery in virus infected cells. Therefore, studying GPCR trafficking is of great importance. This review provides an overview of the current knowledge of endocytic and cell localization properties of vGPCRs and methodological approaches used for studying receptor internalization. Using such novel approaches, we show constitutive internalization of the BILF1 receptor from human and porcine γ-1 herpesviruses and present motifs from the eukaryotic linear motif (ELM) resources with importance for vGPCR endocytosis.
20
Asai, Risa, Ai Kato, and Yasushi Kawaguchi. "Epstein–Barr virus protein kinase BGLF4 interacts with viral transactivator BZLF1 and regulates its transactivation activity." Journal of General Virology 90, no. 7 (July 1, 2009): 1575–81. http://dx.doi.org/10.1099/vir.0.010462-0.
Full textAbstract:
BGLF4 is a serine/threonine protein kinase encoded by Epstein–Barr virus. One of the physiological substrates of BGLF4 is viral transactivator BZLF1. In the present study, it was demonstrated that alanine substitution of the serine residue at position 209 (S209A) in BZLF1 eliminated phosphorylation of the protein by BGLF4 in vitro. The S209A mutation in BZLF1, as well as a K102I mutation in BGLF4, which inactivated catalytic activity of the viral kinase, also inhibited formation of a stable BGLF4–BZLF1 complex and downregulation of BZLF1 autotransactivation activity mediated by BGLF4. These results indicate that formation of a stable complex of BGLF4–BZLF1 enables downregulation of BZLF1 autoregulation activity and it appears that BGLF4 phosphorylation of BZLF1 may be involved in these processes.
21
Fani, Mona, Milad Zandi, Majid Rezayi, Nastaran Khodadad, Hadis Langari, and Iraj Amiri. "The Role of microRNAs in the Viral Infections." Current Pharmaceutical Design 24, no. 39 (March 14, 2019): 4659–67. http://dx.doi.org/10.2174/1381612825666190110161034.
Full textAbstract:
MicroRNAs (miRNAs) are non-coding RNAs with 19 to 24 nucleotides which are evolutionally conserved. MicroRNAs play a regulatory role in many cellular functions such as immune mechanisms, apoptosis, and tumorigenesis. The main function of miRNAs is the post-transcriptional regulation of gene expression via mRNA degradation or inhibition of translation. In fact, many of them act as an oncogene or tumor suppressor. These molecular structures participate in many physiological and pathological processes of the cell. The virus can also produce them for developing its pathogenic processes. It was initially thought that viruses without nuclear replication cycle such as Poxviridae and RNA viruses can not code miRNA, but recently, it has been proven that RNA viruses can also produce miRNA. The aim of this articles is to describe viral miRNAs biogenesis and their effects on cellular and viral genes.
22
Elesela, Srikanth, and Nicholas W. Lukacs. "Role of Mitochondria in Viral Infections." Life 11, no. 3 (March 11, 2021): 232. http://dx.doi.org/10.3390/life11030232.
Full textAbstract:
Viral diseases account for an increasing proportion of deaths worldwide. Viruses maneuver host cell machinery in an attempt to subvert the intracellular environment favorable for their replication. The mitochondrial network is highly susceptible to physiological and environmental insults, including viral infections. Viruses affect mitochondrial functions and impact mitochondrial metabolism, and innate immune signaling. Resurgence of host-virus interactions in recent literature emphasizes the key role of mitochondria and host metabolism on viral life processes. Mitochondrial dysfunction leads to damage of mitochondria that generate toxic compounds, importantly mitochondrial DNA, inducing systemic toxicity, leading to damage of multiple organs in the body. Mitochondrial dynamics and mitophagy are essential for the maintenance of mitochondrial quality control and homeostasis. Therefore, metabolic antagonists may be essential to gain a better understanding of viral diseases and develop effective antiviral therapeutics. This review briefly discusses how viruses exploit mitochondrial dynamics for virus proliferation and induce associated diseases.
23
Umeda, Rie, Tomohiro Nishizawa, and Osamu Nureki. "Crystallization of the human tetraspanin protein CD9." Acta Crystallographica Section F Structural Biology Communications 75, no. 4 (April 1, 2019): 254–59. http://dx.doi.org/10.1107/s2053230x1801840x.
Full textAbstract:
The tetraspanin family of proteins with four membrane-spanning proteins function in a wide range of physiological processes in higher organisms, including cell migration and proliferation, cell fusion, fertilization and virus infection. Although the recently reported structure of CD81 unveiled the basic architecture of this family for the first time, further structural and functional studies are required in order to understand the mechanistic details of the complicated functions of the tetraspanin-family proteins. In this study, attempts were made to crystallize human CD9, a representative member of the tetraspanin family, and it was demonstrated that the truncation of a variable region in the second long extracellular loop significantly improved crystal growth.
24
Golem, Sheetal, and James N. Culver. "Tobacco mosaic virus Induced Alterations in the Gene Expression Profile of Arabidopsis thaliana." Molecular Plant-Microbe Interactions® 16, no. 8 (August 2003): 681–88. http://dx.doi.org/10.1094/mpmi.2003.16.8.681.
Full textAbstract:
In this study, mRNA profiles generated from cDNA microarrays were used to identify gene expression changes in Arabidopsis thaliana ecotype Shahdara infected with Tobacco mosaic virus (TMV). Shahdara is a susceptible TMV host, permitting rapid accumulations of virus in both inoculated and systemic tissues, accompanied by defined disease symptoms that include stunting, necrosis, and leaf curling. Gene expression profiles were monitored in whole tissues of inoculated leaves at four days postinoculation (dpi) and in systemically infected leaves at 14 dpi. Microarrays contained cDNAs representing between 8,000 and 10,000 Arabidopsis genes. Expression analysis identified 68 genes that displayed significant and consistent changes in expression levels, either up or down, in either TMV inoculated or systemically infected tissues, or both. Identified TMV-responsive genes encode a diverse array of functional proteins that include transcription factors, antioxidants, metabolic enzymes, and transporters. Thus, the TMV infection process has a significant impact on a wide array of cellular processes that likely reflect the biochemical and physiological changes involved in the development of this disease syndrome.
25
Laing, Eric, Spencer Sterling, Dawn Weir, Chelsi Beauregard, Ina Smith, Sasha Larsen, Lin-Fa Wang, Andrew Snow, Brian Schaefer, and Christopher Broder. "Enhanced Autophagy Contributes to Reduced Viral Infection in Black Flying Fox Cells." Viruses 11, no. 3 (March 14, 2019): 260. http://dx.doi.org/10.3390/v11030260.
Full textAbstract:
Bats are increasingly implicated as hosts of highly pathogenic viruses. The underlying virus–host interactions and cellular mechanisms that promote co-existence remain ill-defined, but physiological traits such as flight and longevity are proposed to drive these adaptations. Autophagy is a cellular homeostatic process that regulates ageing, metabolism, and intrinsic immune defense. We quantified basal and stimulated autophagic responses in black flying fox cells, and demonstrated that although black flying fox cells are susceptible to Australian bat lyssavirus (ABLV) infection, viral replication is dampened in these bat cells. Black flying fox cells tolerated prolonged ABLV infection with less cell death relative to comparable human cells, suggesting post-entry mechanisms interference with virus replication. An elevated basal autophagic level was observed and autophagy was induced in response to high virus doses. Pharmacological stimulation of the autophagy pathway reduced virus replication, indicating autophagy acts as an anti-viral mechanism. Enhancement of basal and virus-induced autophagy in bat cells connects related reports that long-lived species possess homeostatic processes that dampen oxidative stress and macromolecule damage. Exemplifying the potential that evolved cellular homeostatic adaptations like autophagy may secondarily act as anti-viral mechanisms, enabling bats to serve as natural hosts to an assortment of pathogenic viruses. Furthermore, our data suggest autophagy-inducing drugs may provide a novel therapeutic strategy for combating lyssavirus infection.
26
Azouz, Francine, Komal Arora, Keeton Krause, Vivek Nerurkar, and Mukesh Kumar. "Integrated MicroRNA and mRNA Profiling in Zika Virus-Infected Neurons." Viruses 11, no. 2 (February 16, 2019): 162. http://dx.doi.org/10.3390/v11020162.
Full textAbstract:
Zika virus (ZIKV) infections have caused a wide spectrum of neurological diseases, such as Guillain-Barré syndrome, myelitis, meningoencephalitis, and congenital microcephaly. No effective therapies currently exist for treating patients infected with ZIKV. MicroRNAs (miRNAs) are a group of small RNAs involved in the regulation of a wide variety of cellular and physiological processes. In this study, we analyzed digital miRNA and mRNA profiles in ZIKV-infected primary mouse neurons using the nCounter technology. A total of 599 miRNAs and 770 mRNAs were examined. We demonstrate that ZIKV infection causes global downregulation of miRNAs with only few upregulated miRNAs. ZIKV-modulated miRNAs including miR-155, miR-203, miR-29a, and miR-124-3p are known to play critical role in flavivirus infection, anti-viral immunity and brain injury. ZIKV infection also results in downregulation of miRNA processing enzymes. In contrast, ZIKV infection induces dramatic upregulation of anti-viral, inflammatory and apoptotic genes. Furthermore, our data demonstrate an inverse correlation between ZIKV-modulated miRNAs and target host mRNAs induced by ZIKV. Biofunctional analysis revealed that ZIKV-modulated miRNAs and mRNAs regulate the pathways related to neurological development and neuroinflammatory responses. Functional studies targeting specific miRNA are warranted to develop therapeutics for the management of ZIKV neurological disease.
27
Dharancy, Sébastien, Maud Lemoine, Philippe Mathurin, Lawrence Serfaty, and Laurent Dubuquoy. "Peroxisome Proliferator-Activated Receptors in HCV-Related Infection." PPAR Research 2009 (2009): 1–5. http://dx.doi.org/10.1155/2009/357204.
Full textAbstract:
The topic of peroxisome proliferator-activated receptors has been developed in the field of hepatology allowing envisaging therapeutic strategies for the most frequent chronic liver diseases such as chronic infection with hepatitis C virus (HCV). PPARs contribute to wide physiological processes within the liver such as lipid/glucid metabolisms, inflammatory response, cell differentiation, and cell cycle. In vitro experiments and animal studies showed that PPAR discloses anti-inflammatory property, and PPAR discloses anti-inflammatory, antifibrogenic, and antiproliferative properties in the liver. Experimental and human studies showed impaired PPARs expression and function during HCV infection. The available nonhepatotoxic agonists of PPARs may constitute a progress in the therapeutic management of patients chronically infected with HCV.
28
Ipinmoroti, Ayodeji O., and Qiana L. Matthews. "Extracellular Vesicles: Roles in Human Viral Infections, Immune-Diagnostic, and Therapeutic Applications." Pathogens 9, no. 12 (December 17, 2020): 1056. http://dx.doi.org/10.3390/pathogens9121056.
Full textAbstract:
Membrane-bound vesicles that are released from cells are increasingly being studied as a medium of intercellular communication, as these act to shuttle functional proteins, such as lipids, DNA, rRNA, and miRNA, between cells during essential physiological processes. Extracellular vesicles (EVs), most commonly exosomes, are consistently produced by virus-infected cells, and they play crucial roles in mediating communication between infected and uninfected cells. Notably, pathophysiological roles for EVs have been established in various viral infections, including human immune deficiency virus (HIV), coronavirus (CoV), and human adenovirus (HAdv). Retroviruses, such as HIV, modulate the production and composition of EVs, and critically, these viruses can exploit EV formation, secretion, and release pathways to promote infection, transmission, and intercellular spread. Consequently, EV production has been investigated as a potential tool for the development of improved viral infection diagnostics and therapeutics. This review will summarize our present knowledge of EV–virus relationships, focusing on their known roles in pathophysiological pathways, immunomodulatory mechanisms, and utility for biomarker discovery. This review will also discuss the potential for EVs to be exploited as diagnostic and treatment tools for viral infection.
29
Tsai, Ching-Yi, Weijun Zhang, S. Allie, and Edward Usherwood. "MiR-155 modulates effector and memory CD8 T cell differentiation in response to murine γ herpes virus. (110.13)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 110.13. http://dx.doi.org/10.4049/jimmunol.188.supp.110.13.
Full textAbstract:
Abstract MicroRNAs (miRNAs) have emerged as a major regulatory network with profound effects on many physiological processes. They are particularly important for determining cell fate decisions. Several processes mediate CD8 T cell differentiation. While many studies have revealed the importance of transcriptional and epigenetic regulation, it is likely that miRNAs also contribute to this programming. miRNAs are critical in determining B and CD4 T cell lineage, yet little is known about their effect on CD8 T cell differentiation. Studies with in vitro skewed central memory CD8 T cells show a down regulation of miR-155 relative to skewed effector memory cells. Using murine gammaherpesvirus 68 as a model, we examined the influence of miR-155 on CD8 differentiation in vivo. Our results showed lowered CD8 responses in the absence of miR-155 accompanied by a phenotypic skewing towards a memory precursor phenotype at the acute phase, which resulted in more central memory cells. The resulting memory cells in the absence of miR-155 were as functionally competent as their wild type counterparts, as revealed by their ability to recall to the same antigen. Our data indicate the importance of mIR-155 in effector differentiation, which may be a critical piece of the puzzle in CD8 differentiation giving useful information for vaccine research.
30
Zaeck, Luca, Madlin Potratz, Antonia Klein, Conrad M. Freuling, Thomas Müller, and Stefan Finke. "High-Resolution 3D Imaging of Virus Infections in Solvent-Cleared Organs: Novel Insights into Virus Replication and Tropism In Vivo." Proceedings 50, no. 1 (June 17, 2020): 75. http://dx.doi.org/10.3390/proceedings2020050075.
Full textAbstract:
The visualization of infection processes in relevant tissues and organs using microscopy methods reveals a unique link between the distribution, tropism, and abundance of pathogens and the physiological structure of the respective organ. To dissect virus replication and the host reaction in vivo at both a global and a single-cell level, conventional 2D imaging approaches can only provide limited insight. However, pathological studies of infected organ material are still mostly restricted to the immunostaining of thin sections from paraffin-embedded or frozen samples. While the 3D analysis of large tissue volumes is possible via laborious serial sectioning, a variety of problems and artifacts remain. Modern immunostaining-compatible tissue clearing techniques allow for the seamless 3D visualization of infection sites in optically cleared thick tissues sections or even entire organs. Benefiting from pure optical slicing, this approach enables the acquisition of multicolor high-volume 3D image stacks for coherent qualitative and quantitative analyses of the infection and its surrounding cellular environment. Here, we demonstrate the utility and power of this methodology by visualizing virus infections in different target tissues. For instance, we reconstructed the cellular context of rabies virus infection sites in mouse brain tissue, allowing a thorough investigation and quantitative analysis of rabies virus cell tropism. The systematic comparison of different rabies viruses with varying pathogenicity revealed a remarkable difference for highly virulent street rabies viruses and attenuated lab strains. While the virus protein expression was readily detectable at a comparable level in both neurons and non-neuronal glial cells from brains of mice infected with street rabies viruses, it was virtually absent in glial cells of lab strain-infected mice. These data provide novel and detailed insights into the pathogenesis of virus infections and substantially contribute to an improved understanding of virus–host interactions in vivo.
31
Rosenberg, Avi Z., Weiying Yu, D. Ashley Hill, Christine A. Reyes, and David A. Schwartz. "Placental Pathology of Zika Virus: Viral Infection of the Placenta Induces Villous Stromal Macrophage (Hofbauer Cell) Proliferation and Hyperplasia." Archives of Pathology & Laboratory Medicine 141, no. 1 (September 28, 2016): 43–48. http://dx.doi.org/10.5858/arpa.2016-0401-oa.
Full textAbstract:
Context.—The placenta is an important component in understanding the fetal response to intrauterine Zika virus infection, but the pathologic changes in this organ remain largely unknown. Hofbauer cells are fetal-derived macrophages normally present in the chorionic villous stroma. They have been implicated in a variety of physiological and pathologic processes, in particular involving infectious agents. Objectives.—To characterize the fetal and maternal responses and viral localization in the placenta following Zika virus transmission to an 11 weeks' gestation fetus. The clinical course was notable for prolonged viremia in the mother and extensive neuronal necrosis in the fetus. The fetus was delivered at 21 weeks' gestation after pregnancy termination. Design.—The placenta was evaluated by using immunohistochemistry for inflammatory cells (macrophages/monocytes [Hofbauer cells], B and T lymphocytes) and proliferating cells, and an RNA probe to Zika virus. The fetal brain and the placenta were previously found to be positive for Zika virus RNA by reverse transcription–polymerase chain reaction. Results.—The placenta demonstrated prominently enlarged, hydropic chorionic villi with hyperplasia and focal proliferation of Hofbauer cells. The degree of Hofbauer cell hyperplasia gave an exaggerated immature appearance to the villi. No acute or chronic villitis, villous necrosis, remote necroinflammatory abnormalities, chorioamnionitis, funisitis, or hemorrhages were present. An RNA probe to Zika virus was positive in villous stromal cells, presumably Hofbauer cells. Conclusions.—Zika virus placental infection induces proliferation and prominent hyperplasia of Hofbauer cells in the chorionic villi but does not elicit villous necrosis or a maternal or fetal lymphoplasmacellular or acute inflammatory cell reaction.
32
Li, Manjin, Dan Xing, Duo Su, Di Wang, Heting Gao, Cejie Lan, Zhenyu Gu, Tongyan Zhao, and Chunxiao Li. "Transcriptome Analysis of Responses to Dengue Virus 2 Infection in Aedes albopictus (Skuse) C6/36 Cells." Viruses 13, no. 2 (February 22, 2021): 343. http://dx.doi.org/10.3390/v13020343.
Full textAbstract:
Dengue virus (DENV), a member of the Flavivirus genus of the Flaviviridae family, can cause dengue fever (DF) and more serious diseases and thus imposes a heavy burden worldwide. As the main vector of DENV, mosquitoes are a serious hazard. After infection, they induce a complex host–pathogen interaction mechanism. Our goal is to further study the interaction mechanism of viruses in homologous, sensitive, and repeatable C6/36 cell vectors. Transcriptome sequencing (RNA-Seq) technology was applied to the host transcript profiles of C6/36 cells infected with DENV2. Then, bioinformatics analysis was used to identify significant differentially expressed genes and the associated biological processes. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to verify the sequencing data. A total of 1239 DEGs were found by transcriptional analysis of Aedes albopictus C6/36 cells that were infected and uninfected with dengue virus, among which 1133 were upregulated and 106 were downregulated. Further bioinformatics analysis showed that the upregulated DEGs were significantly enriched in signaling pathways such as the MAPK, Hippo, FoxO, Wnt, mTOR, and Notch; metabolic pathways and cellular physiological processes such as autophagy, endocytosis, and apoptosis. Downregulated DEGs were mainly enriched in DNA replication, pyrimidine metabolism, and repair pathways, including BER, NER, and MMR. The qRT-PCR results showed that the concordance between the RNA-Seq and RT-qPCR data was very high (92.3%). The results of this study provide more information about DENV2 infection of C6/36 cells at the transcriptome level, laying a foundation for further research on mosquito vector–virus interactions. These data provide candidate antiviral genes that can be used for further functional verification in the future.
33
Fu, Xiaotian, Xinyi Jiang, Xinye Chen, Liqian Zhu, and Gaiping Zhang. "The Differential Expression of Mitochondrial Function-Associated Proteins and Antioxidant Enzymes during Bovine Herpesvirus 1 Infection: A Potential Mechanism for Virus Infection-Induced Oxidative Mitochondrial Dysfunction." Mediators of Inflammation 2019 (March 18, 2019): 1–10. http://dx.doi.org/10.1155/2019/7072917.
Full textAbstract:
Reactive oxidative species (ROS) are important inflammatory mediators. Electrons escaping from the mitochondrial electron transport chain (ETC) during oxidative phosphorylation (OXPHOS) in the mitochondrial respiratory chain (RC) complexes contribute to ROS production. The cellular antioxidant enzymes are important for maintaining ROS release at the physiological levels. It has been reported that BoHV-1 infection induces overproduction of ROS and oxidative mitochondrial dysfunction in cell cultures. In this study, we found that chemical interruption of RC complexes by TTFA (an inhibitor of RC complex II), NaN3 (an inhibitor of RC complex IV), and oligomycin A (an inhibitor of ATP synthase) consistently decreased virus productive infection, suggesting that the integral processes of RC complexes are important for the virus replication. The virus infection significantly increased the expression of subunit SDHB (succinate dehydrogenase) and MTCO1 (cytochrome c oxidase subunit I), critical components of RC complexes II and IV, respectively. The expression of antioxidant enzymes including superoxide dismutase 1 (SOD1), SOD2, catalase (CAT), and glutathione peroxidase 4 (GPX4) was differentially affected following the virus infection. The protein TFAM (transcription factor A, mitochondrial) stimulated by either nuclear respiratory factor 1 (NRF1) or NRF2 is a key regulator of mitochondrial biogenesis. Interestingly, the virus infection at the late stage (at 16 h after infection) stimulated TFAM expression but decreased the levels of both NRF1 and NRF2, indicating that virus infection activated TFAM signaling independent of either NRF1 or NRF2. Overall, this study provided evidence that BoHV-1 infection altered the expression of molecules associated with RC complexes, antioxidant enzymes, and mitochondrial biogenesis-related signaling NRF1/NRF2/TFAM, which correlated with the previous report that virus infection induces ROS overproduction and mitochondrial dysfunction.
34
Magyar-Tábori, Katalin, Nóra Mendler-Drienyovszki, Alexandra Hanász, László Zsombik, and Judit Dobránszki. "Phytotoxicity and Other Adverse Effects on the In Vitro Shoot Cultures Caused by Virus Elimination Treatments: Reasons and Solutions." Plants 10, no. 4 (March 31, 2021): 670. http://dx.doi.org/10.3390/plants10040670.
Full textAbstract:
In general, in vitro virus elimination is based on the culture of isolated meristem, and in addition thermotherapy, chemotherapy, electrotherapy, and cryotherapy can also be applied. During these processes, plantlets suffer several stresses, which can result in low rate of survival, inhibited growth, incomplete development, or abnormal morphology. Even though the in vitro cultures survive the treatment, further development can be inhibited; thus, regeneration capacity of treated in vitro shoots or explants play also an important role in successful virus elimination. Sensitivity of genotypes to treatments is very different, and the rate of destruction largely depends on the physiological condition of plants as well. Exposure time of treatments affects the rate of damage in almost every therapy. Other factors such as temperature, illumination (thermotherapy), type and concentration of applied chemicals (chemo- and cryotherapy), and electric current intensity (electrotherapy) also may have a great impact on the rate of damage. However, there are several ways to decrease the harmful effect of treatments. This review summarizes the harmful effects of virus elimination treatments applied on tissue cultures reported in the literature. The aim of this review is to expound the solutions that can be used to mitigate phytotoxic and other adverse effects in practice.
35
D'Apuzzo, Massimo, Georgia Mandolesi, Gerald Reis, and Erin M. Schuman. "Abundant GFP Expression and LTP in Hippocampal Acute Slices by In Vivo Injection of Sindbis Virus." Journal of Neurophysiology 86, no. 2 (August 1, 2001): 1037–42. http://dx.doi.org/10.1152/jn.2001.86.2.1037.
Full textAbstract:
Virus-mediated gene transfer into neurons is a powerful tool for the analysis of neuronal structure and function. Recombinant sindbis virus has been previously used to study protein function in hippocampal neuron cultures as well as in hippocampal organotypic slice cultures. Nevertheless, some concern still exists about the physiological relevance of these cultured preparations. Acute hippocampal slices are a widely used preparation for the study of synaptic transmission, but currently recombinant gene delivery is usually achieved only through time-consuming transgenic techniques. In this study, we show that a subregion of the CA1 area in acute hippocampal slices can be specifically altered to express a gene of interest. A sindbis virus vector carrying an enhanced green fluorescent protein (EGFP) reporter was injected in vivo into the hippocampus of adult rats. After 18 h, rats were killed, and acute hippocampal slices, infected in the CA1 field, were analyzed morphologically and electrophysiologically. Infected slices showed healthy and stable electrophysiological responses as well as long-term potentiation. In addition, infected pyramidal cells were readily recognized in living slices by two-photon imaging. Specifically, the introduction of an EGFP-Actin fusion protein greatly enhanced the detection of fine processes and dendritic spines. We propose this technique as an efficient tool for studying gene function in adult hippocampal neurons.
36
Haas de Mello, Aline Haas, Tianshuang Liu, Roberto P. Garofalo, and Antonella Casola. "Hydrogen Sulfide Donor GYY4137 Rescues NRF2 Activation in Respiratory Syncytial Virus Infection." Antioxidants 11, no. 7 (July 21, 2022): 1410. http://dx.doi.org/10.3390/antiox11071410.
Full textAbstract:
Respiratory syncytial virus (RSV) can cause severe respiratory illness in infants, immunocompromised, and older adults. Despite its burden, no vaccine or specific treatment is available. RSV infection is associated with increased reactive oxygen species (ROS) production, degradation of the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2), and decreased antioxidant enzymes (AOEs), leading to oxidative damage and lung injury. Hydrogen sulfide (H2S) is an endogenous gaseous molecule that plays a physiological role in numerous cellular processes and a protective role in multiple pathological conditions, displaying vasoactive, cytoprotective, anti-inflammatory, and antioxidant activities. H2S can promote NRF2 activation through the sulfhydration of Kelch-like ECH-associated protein 1, the cytoplasmic repressor of NRF2. Here we investigated whether increasing cellular H2S levels could rescue NRF2 and NRF2-dependent gene expression in RSV-infected primary airway epithelial cells. We found that treatment with the H2S donor GYY4137 significantly increased NRF2 levels and AOEs gene expression by decreasing KEAP1 levels, and by modulating pathways involved in RSV-induced NRF2 degradation, such as NRF2 ubiquitination, and promyelocytic leukemia (PML) protein levels. These results suggest that the administration of exogenous H2S can positively impact the altered redox balance associated with RSV infection, which represents an important determinant of RSV-induced lung disease.
37
Monroy-Ramirez, Hugo Christian, Marina Galicia-Moreno, Ana Sandoval-Rodriguez, Alejandra Meza-Rios, Arturo Santos, and Juan Armendariz-Borunda. "PPARs as Metabolic Sensors and Therapeutic Targets in Liver Diseases." International Journal of Molecular Sciences 22, no. 15 (August 2, 2021): 8298. http://dx.doi.org/10.3390/ijms22158298.
Full textAbstract:
Carbohydrates and lipids are two components of the diet that provide the necessary energy to carry out various physiological processes to help maintain homeostasis in the body. However, when the metabolism of both biomolecules is altered, development of various liver diseases takes place; such as metabolic-associated fatty liver diseases (MAFLD), hepatitis B and C virus infections, alcoholic liver disease (ALD), and in more severe cases, hepatocelular carcinoma (HCC). On the other hand, PPARs are a family of ligand-dependent transcription factors with an important role in the regulation of metabolic processes to hepatic level as well as in other organs. After interaction with specific ligands, PPARs are translocated to the nucleus, undergoing structural changes to regulate gene transcription involved in lipid metabolism, adipogenesis, inflammation and metabolic homeostasis. This review aims to provide updated data about PPARs’ critical role in liver metabolic regulation, and their involvement triggering the genesis of several liver diseases. Information is provided about their molecular characteristics, cell signal pathways, and the main pharmacological therapies that modulate their function, currently engaged in the clinic scenario, or in pharmacological development.
38
Li, Yuwan, Keke Wu, Sen Zeng, Linke Zou, Xiaowen Li, Chen Xu, Bingke Li, et al. "The Role of Mitophagy in Viral Infection." Cells 11, no. 4 (February 17, 2022): 711. http://dx.doi.org/10.3390/cells11040711.
Full textAbstract:
Mitophagy, which is able to selectively clear excess or damaged mitochondria, plays a vital role in the quality control of mitochondria and the maintenance of normal mitochondrial functions in eukaryotic cells. Mitophagy is involved in many physiological and pathological processes, including apoptosis, innate immunity, inflammation, cell differentiation, signal transduction, and metabolism. Viral infections cause physical dysfunction and thus pose a significant threat to public health. An accumulating body of evidence reveals that some viruses hijack mitophagy to enable immune escape and self-replication. In this review, we systematically summarize the pathway of mitophagy initiation and discuss the functions and mechanisms of mitophagy in infection with classical swine fever virus and other specific viruses, with the aim of providing a theoretical basis for the prevention and control of related diseases.
39
Rajsbaum, Ricardo, and Preeti Bharaj. "Unanchored Polyubiquitin Chains and Innate Immune Sensing of Influenza Virus Infection." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 63.1. http://dx.doi.org/10.4049/jimmunol.196.supp.63.1.
Full textAbstract:
Abstract Innate immune responses are initiated when pattern recognition receptors detect incoming microbes and trigger signaling pathways leading to production of inflammatory cytokines and type-I interferons (IFNs). These signaling pathways are regulated by different cellular processes including the ubiquitin (Ub) system. Proteins covalently attached to K48-linked polyUb are targeted for degradation by the proteasome, whereas protein modification with K63-linked polyUb may have non-proteolytic-activating functions. Unanchored Ub chains that are not covalently attached to any protein are also important for kinase activation. We recently reported that the E3 ligase TRIM6 synthesizes unanchored K48-linked polyUb chains, which activate the IKKɛ kinase for induction of an antiviral response. To better understand the physiological role of unanchored polyUb during virus infection, we developed a system to isolate ubiquitin-interacting proteins from the lungs of influenza-infected mice. By using a proteomics approach we identified three RNA helicases that interact with unanchored polyUb chains in vivo. Knockdown analyses of these RNA helicases resulted in decreased IFN induction upon influenza virus infection, suggesting that they may be involved in viral RNA recognition. Therefore, unanchored polyUb chains are emerging as important players in viral sensing and innate immune signaling. Our approach provides a new strategy for the identification of Ub-binding proteins from in vivo samples.
40
Suzuki, Nobuhiro, Kazuyuki Maruyama, Miho Moriyama, and Donald L. Nuss. "Hypovirus Papain-Like Protease p29 Functions in trans To Enhance Viral Double-Stranded RNA Accumulation and Vertical Transmission." Journal of Virology 77, no. 21 (November 1, 2003): 11697–707. http://dx.doi.org/10.1128/jvi.77.21.11697-11707.2003.
Full textAbstract:
ABSTRACT The prototypic hypovirus CHV1-EP713 attenuates virulence (hypovirulence) and alters several physiological processes of the chestnut blight fungus Cryphonectria parasitica. The papain-like protease, p29, and the highly basic protein, p40, derived, respectively, from the N-terminal and C-terminal portions of the CHV1-EP713-encoded open reading frame (ORF) A polyprotein, p69, both contribute to reduced pigmentation and sporulation. The p29 coding region was shown to suppress pigmentation and asexual sporulation in the absence of virus infection in transformed C. parasitica, whereas transformants containing the p40-coding domain exhibited a wild-type, untransformed phenotype. Deletion of either p29 or p40 from the viral genome also results in reduced accumulation of viral RNA. We now show that p29, but not p40, functions in trans to enhance genomic RNA accumulation and vertical transmission of p29 deletion mutant viruses. The frequency of virus transmission through conidia was found to decrease with reduced accumulation of viral genomic double-stranded RNA (dsRNA): from almost 100% for wild-type virus to ∼50% for Δp29, and 10 to 20% for Δp69. When expressed from a chromosomally integrated cDNA copy, p29 elevated viral dsRNA accumulation and transmission for Δp29 mutant virus to the level shown by wild-type virus. Increased viral RNA accumulation levels were also observed for a Δp69 mutant lacking almost the entire ORF A sequence. Such enhancements were not detected in transgenic fungal colonies expressing p40. Mutation of p29 residues Cys70 or Cys72, strictly conserved in hypovirus p29 and potyvirus HC-Pro, resulted in the loss of both p29-mediated suppressive activity in virus-free transgenic C. parasitica and in trans enhancement of RNA accumulation and transmission, suggesting a linkage between these functional activities. These results suggest that p29 is an enhancer of viral dsRNA accumulation and vertical virus transmission through asexual spores.
41
McCLURE, HEATHER H., CHARLES R. MARTINEZ, J. JOSH SNODGRASS, J. MARK EDDY, ROBERTO A. JIMÉNEZ, LAURA E. ISIORDIA, and THOMAS W. McDADE. "DISCRIMINATION-RELATED STRESS, BLOOD PRESSURE AND EPSTEIN-BARR VIRUS ANTIBODIES AMONG LATIN AMERICAN IMMIGRANTS IN OREGON, US." Journal of Biosocial Science 42, no. 4 (February 24, 2010): 433–61. http://dx.doi.org/10.1017/s0021932010000039.
Full textAbstract:
SummaryPerceived discrimination has been linked to poor health outcomes among ethnic and racial minorities in the United States, though the relationship of discrimination-related stress to immigrant health is not well understood. This article reports findings from a preliminary study that examined blood pressure and Epstein-Barr virus antibody levels in relation to self-reported indicators of stress, acculturation and social support among 79 adult immigrant Latino farm workers in Oregon, US. Findings show that increases in discrimination-related stress predicted elevated systolic blood pressure (SBP) and Epstein-Barr virus antibody levels among male participants. Though female participants reported similar levels of discrimination stress, this perceived stress was not reflected in biological measures. Among women, greater English language engagement was linked to higher SBP, and more years in the US was associated with higher diastolic blood pressure. Study results suggest that male and female immigrants' physiological responses to stress may be influenced in distinctive ways by processes of adjustment to life in the US. If replicated, the finding that discrimination stress predicts elevated SBP may have clinical and public health implications given that elevated SBP is an established risk factor for cardiovascular disease.
42
Wrzesińska, Barbara, Agnieszka Zmienko, Lam Dai Vu, Ive De Smet, and Aleksandra Obrępalska-Stęplowska. "Multiple cellular compartments engagement in Nicotiana benthamiana-peanut stunt virus-satRNA interactions revealed by systems biology approach." Plant Cell Reports 40, no. 7 (May 24, 2021): 1247–67. http://dx.doi.org/10.1007/s00299-021-02706-4.
Full textAbstract:
Abstract Key message PSV infection changed the abundance of host plant’s transcripts and proteins associated with various cellular compartments, including ribosomes, chloroplasts, mitochondria, the nucleus and cytosol, affecting photosynthesis, translation, transcription, and splicing. Abstract Virus infection is a process resulting in numerous molecular, cellular, and physiological changes, a wide range of which can be analyzed due to development of many high-throughput techniques. Plant RNA viruses are known to replicate in the cytoplasm; however, the roles of chloroplasts and other cellular structures in the viral replication cycle and in plant antiviral defense have been recently emphasized. Therefore, the aim of this study was to analyze the small RNAs, transcripts, proteins, and phosphoproteins affected during peanut stunt virus strain P (PSV-P)–Nicotiana benthamiana interactions with or without satellite RNA (satRNA) in the context of their cellular localization or functional connections with particular cellular compartments to elucidate the compartments most affected during pathogenesis at the early stages of infection. Moreover, the processes associated with particular cell compartments were determined. The ‘omic’ results were subjected to comparative data analyses. Transcriptomic and small RNA (sRNA)–seq data were obtained to provide new insights into PSV-P–satRNA–plant interactions, whereas previously obtained proteomic and phosphoproteomic data were used to broaden the analysis to terms associated with cellular compartments affected by virus infection. Based on the collected results, infection with PSV-P contributed to changes in the abundance of transcripts and proteins associated with various cellular compartments, including ribosomes, chloroplasts, mitochondria, the nucleus and the cytosol, and the most affected processes were photosynthesis, translation, transcription, and mRNA splicing. Furthermore, sRNA-seq and phosphoproteomic analyses indicated that kinase regulation resulted in decreases in phosphorylation levels. The kinases were associated with the membrane, cytoplasm, and nucleus components.
43
Nugmanova, Dzhamilia, Inna Kozlova, and Roman Kupriyanov. "The peculiarities of Adaptation of First-Year Students to the University during COVID-19 Pandemic in Russia." Revista de Psicología Clínica con Niños y Adolescentes 9, no. 2 (May 2022): 32–38. http://dx.doi.org/10.21134/rpcna.2022.09.2.4.
Full textAbstract:
The speed and efficiency of student adaptation largely determines the success of the educational process. This is especially true for university freshmen, as the older adolescent organism, with its specific neurophysiological characteristics, is very sensitive to changes in the environment. The situation with SARS-CoV-2 virus (COVID-19) pandemic has added to the problem of adaptation. The present study aims to examine the influence of the COVID-19 pandemic on the first-year students’ adaptation to university studies in Russia. The study involves 692 freshmen with an average age of 18.7, majority of women (80.6%), from three Russian universities: Kazan National Research Technological University, Kazan Federal University and Kazan Aviation University. The results show that during the COVID-19 period statistically significant changes occurred in almost all the adaptation components: physiological adaptation (p < .0001), socio-psychological adaptation (p < .05), academic adaptation (p < .05). There was a decrease in the level of physiological adaptation, while socio-psychological adaptation and academic adaptation increased. Comparison by gender during the COVID-19 period shows differences between adaptation processes of men and women. Comparison of foreign students with Russian citizens during the COVID-19 period demonstrates that foreign students stand out in socio-cultural adaptation (4.94 - foreigners, 4.64 - citizens of Russia, p < .05), physiological adaptation (5.36 - foreigners, 4.36 - citizens of Russia, p < .00001) and academic adaptation (5.28 - foreigners, 4.99 - citizens of Russia, p < .05)
44
Hančević, Katarina, Mate Čarija, Sandra Radić Brkanac, Emanuel Gaši, Matevž Likar, Goran Zdunić, Marjana Regvar, and Tomislav Radić. "Grapevine Leafroll-Associated Virus 3 in Single and Mixed Infections Triggers Changes in the Oxidative Balance of Four Grapevine Varieties." International Journal of Molecular Sciences 24, no. 1 (December 20, 2022): 8. http://dx.doi.org/10.3390/ijms24010008.
Full textAbstract:
: With the aim to characterize changes caused by grapevine leafroll-associated virus 3 (GLRaV-3) singly or in coinfection with other viruses and to potentially determine genotype-specific or common markers of viral infection, thirty-six parameters, including nutrient status, oxidative stress parameters, and primary metabolism as well as symptoms incidence were investigated in ‘Cabernet Franc,’ ‘Merlot,’ ‘Pinot Noir,’ and ‘Tribidrag’ grapevine varieties. Host responses were characterized by changes in cellular redox state rather than disturbances in nutrient status and primary metabolic processes. Superoxide dismutase, hydrogen peroxide, and proteins were drastically affected regardless of the type of isolate, the host, and the duration of the infection, so they present cellular markers of viral infection. No clear biological pattern could be ascertained for each of the GLRaV-3 genotypes. There is a need to provide a greater understanding of virus epidemiology in viticulture due to the increasing natural disasters and climate change to provide for global food production security. Finding grape varieties that will be able to cope with those changes can aid in this task. Among the studied grapevine varieties, autochthonous ‘Tribidrag’ seems to be more tolerant to symptoms development despite numerous physiological changes caused by viruses.
45
Jan Fada, Behdokht, Eleazar Reward, and Haidong Gu. "The Role of ND10 Nuclear Bodies in Herpesvirus Infection: A Frenemy for the Virus?" Viruses 13, no. 2 (February 3, 2021): 239. http://dx.doi.org/10.3390/v13020239.
Full textAbstract:
Nuclear domains 10 (ND10), a.k.a. promyelocytic leukemia nuclear bodies (PML-NBs), are membraneless subnuclear domains that are highly dynamic in their protein composition in response to cellular cues. They are known to be involved in many key cellular processes including DNA damage response, transcription regulation, apoptosis, oncogenesis, and antiviral defenses. The diversity and dynamics of ND10 residents enable them to play seemingly opposite roles under different physiological conditions. Although the molecular mechanisms are not completely clear, the pro- and anti-cancer effects of ND10 have been well established in tumorigenesis. However, in herpesvirus research, until the recently emerged evidence of pro-viral contributions, ND10 nuclear bodies have been generally recognized as part of the intrinsic antiviral defenses that converge to the incoming viral DNA to inhibit the viral gene expression. In this review, we evaluate the newly discovered pro-infection influences of ND10 in various human herpesviruses and analyze their molecular foundation along with the traditional antiviral functions of ND10. We hope to shed light on the explicit role of ND10 in both the lytic and latent cycles of herpesvirus infection, which is imperative to the delineation of herpes pathogenesis and the development of prophylactic/therapeutic treatments for herpetic diseases.
46
Forterre, Alexis, Hiroaki Komuro, Shakhlo Aminova, and Masako Harada. "A Comprehensive Review of Cancer MicroRNA Therapeutic Delivery Strategies." Cancers 12, no. 7 (July 9, 2020): 1852. http://dx.doi.org/10.3390/cancers12071852.
Full textAbstract:
In the field of molecular oncology, microRNAs (miRNAs) and their role in regulating physiological processes and cancer pathogenesis have been a revolutionary discovery over the last decade. It is now considered that miRNA dysregulation influences critical molecular pathways involved in tumor progression, invasion, angiogenesis and metastasis in a wide range of cancer types. Hence, altering miRNA levels in cancer cells has promising potential as a therapeutic intervention, which is discussed in many other articles in this Special Issue. Some of the most significant hurdles in therapeutic miRNA usage are the stability and the delivery system. In this review, we cover a comprehensive update on the challenges and strategies for the development of therapeutic miRNA delivery systems that includes virus-based delivery, non-viral delivery (artificial lipid-based vesicles, polymer-based or chemical structures), and recently emerged extracellular vesicle (EV)-based delivery systems.
47
Sorel, Océane, and Benjamin G. Dewals. "MicroRNAs in large herpesvirus DNA genomes: recent advances." Biomolecular Concepts 7, no. 4 (August 1, 2016): 229–39. http://dx.doi.org/10.1515/bmc-2016-0017.
Full textAbstract:
AbstractMicroRNAs (miRNAs) are small non-coding RNAs (ncRNAs) that regulate gene expression. They alter mRNA translation through base-pair complementarity, leading to regulation of genes during both physiological and pathological processes. Viruses have evolved mechanisms to take advantage of the host cells to multiply and/or persist over the lifetime of the host. Herpesviridae are a large family of double-stranded DNA viruses that are associated with a number of important diseases, including lymphoproliferative diseases. Herpesviruses establish lifelong latent infections through modulation of the interface between the virus and its host. A number of reports have identified miRNAs in a very large number of human and animal herpesviruses suggesting that these short non-coding transcripts could play essential roles in herpesvirus biology. This review will specifically focus on the recent advances on the functions of herpesvirus miRNAs in infection and pathogenesis.
48
Ishikawa, Hinata, Md Matiur Rahman, Marika Yamauchi, Shigeo Takashima, Yoshiko Wakihara, Yuji O. Kamatari, Kaori Shimizu, Ayaka Okada, and Yasuo Inoshima. "mRNA Profile in Milk Extracellular Vesicles from Bovine Leukemia Virus-Infected Cattle." Viruses 12, no. 6 (June 20, 2020): 669. http://dx.doi.org/10.3390/v12060669.
Full textAbstract:
Milk extracellular vesicles (EVs) form an excellent source of mRNAs, microRNAs (miRNAs), proteins, and lipids that represent the physiological and pathological status of the host. Recent studies have reported milk EVs as novel biomarkers for many infectious diseases in both humans and animals. For example, miRNAs in milk EVs from cattle were used for early detection of bacterial infection in the mammary gland. Based on these findings, we hypothesized that mRNAs in milk EVs are suitable for gaining a better understanding of the pathogenesis of bovine leukemia virus (BLV) infection and prognosis of the clinical stage in cattle. For that purpose, milk EVs were isolated from BLV-infected and uninfected cattle, and mRNAs were investigated using microarray analysis. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed mainly focusing on the differentially expressed genes (DEGs) in milk EVs from BLV-infected cattle. GO and KEGG analyses suggested the DEGs in milk EVs from BLV-infected cattle had involved in diverse molecular functions, biological processes, and distinct disease-related pathways. The present study suggested that BLV infection causes profound effects on host cellular activity, changing the mRNA expression profile in milk EVs obtained from BLV-infected cattle. Overall, our results suggested that the mRNA profile in milk EVs to be a key factor for monitoring the clinical stage of BLV infection. This is the first report of mRNA profiling of milk EVs obtained from BLV-infected cattle.
49
Martinez, Miguel Angel, Cristina Tural, and Sandra Franco. "Circulating MicroRNAs as a Tool for Diagnosis of Liver Disease Progression in People Living with HIV-1." Viruses 14, no. 6 (May 24, 2022): 1118. http://dx.doi.org/10.3390/v14061118.
Full textAbstract:
MicroRNAs (miRNAs) are small, non-coding RNAs that post-transcriptionally regulate gene expression by binding specific cell mRNA targets, preventing their translation. miRNAs are implicated in the regulation of important physiological and pathological pathways. Liver disease, including injury, fibrosis, metabolism dysregulation, and tumor development disrupts liver-associated miRNAs. In addition to their effect in the originating tissue, miRNAs can also circulate in body fluids. miRNA release is an important form of intercellular communication that plays a role in the physiological and pathological processes underlying multiple diseases. Circulating plasma levels of miRNAs have been identified as potential disease biomarkers. One of the main challenges clinics face is the lack of available noninvasive biomarkers for diagnosing and predicting the different stages of liver disease (e.g., nonalcoholic fatty liver disease and nonalcoholic steatohepatitis), particularly among individuals infected with human immunodeficiency virus type 1 (HIV-1). Liver disease is a leading cause of death unrelated to acquired immunodeficiency syndrome (AIDS) among people living with HIV-1 (PLWH). Here, we review and discuss the utility of circulating miRNAs as biomarkers for early diagnosis, prognosis, and assessment of liver disease in PLWH. Remarkably, the identification of dysregulated miRNA expression may also identify targets for new therapeutics.
50
Bartoloni, Stefania, Stefano Leone, and Filippo Acconcia. "Unexpected Impact of a Hepatitis C Virus Inhibitor on 17β-Estradiol Signaling in Breast Cancer." International Journal of Molecular Sciences 21, no. 10 (May 12, 2020): 3418. http://dx.doi.org/10.3390/ijms21103418.
Full textAbstract:
17β-Estradiol (E2) controls diverse physiological processes, including cell proliferation, through its binding to estrogen receptor α (ERα). E2:ERα signaling depends on both the receptor subcellular localization (e.g., nucleus, plasma membrane) and intracellular ERα abundance. Indeed, the control of ERα levels is necessary for the effects of E2, and E2 itself induces ERα degradation and cell proliferation in parallel. Thus, the modulation of intracellular ERα levels is a critical parameter for E2-induced cell proliferation. Therefore, we used this parameter as a bait to identify compounds that influence ERα levels and E2-dependent proliferation in breast cancer (BC) cells from a library of Food and Drug Administration (FDA)-approved drugs. We found that telaprevir (Tel) reduces ERα levels and inhibits BC cell proliferation. Tel is an inhibitor of the hepatitis C virus (HCV) NS3/4A serine protease, but its effect on E2:ERα signaling has not been investigated. Here, for the first time, we analyzed the effects of Tel on intracellular ERα levels and E2:ERα signaling to cell proliferation in different ERα-expressing BC cell lines. Overall, our findings demonstrate that Tel reduces intracellular ERα levels, deregulates E2:ERα signaling and inhibits E2-induced proliferation in BC cells and suggest the potential drug repurposing of Tel for the treatment of BC.