scholarly journals Mechanisms of resistance to viruses

2002 ◽  
Vol 38 (SI 1 - 6th Conf EFPP 2002) ◽  
pp. S132-S135
Author(s):  
J.P.T. Valkonen
Keyword(s):  
Cell Death ◽  
Virus Infection ◽  
Virus Resistance ◽  
Rna Silencing ◽  
Subsequent Development ◽  
Viral Proteins ◽  
Virus Movement ◽  
Virus Infections ◽  
Viral Synergism ◽  
Multicellular Organisms

Resistance associated with a hypersensitive response (HR) and subsequent development of necrotic lesions (cell death) at the sites of virus infection can restrict virus movement in plants. Genes for HR are dominant and act on a gene-for-gene basis. Many viral proteins triggering HR have been identified. Also, several genes for HR-based virus resistance, or virus-induced cell death without resistance, have been isolated and characterized in plants, which provides novel insights to the mechanisms of virus resistance. Another international, major research frontier has formed more recently around RNA silencing, a universal RNA surveillance system and inducible virus defence mechanism in multicellular organisms. Many viral proteins interfere with different phases of RNA silencing. The data provide novel insights to break-down of resistance in mixed virus infections (viral synergism), resistance to virus movement, and recovery of plants from virus infection.

Tracking the green invaders: advances in imaging virus infection in plants

2010 ◽  
Vol 430 (1) ◽  
pp. 21-37 ◽  
Author(s):  
Jens Tilsner ◽  
Karl J. Oparka
Keyword(s):  
Virus Infection ◽  
Structural Biology ◽  
Plant Virus ◽  
Viral Proteins ◽  
Infection Process ◽  
Virus Infections ◽  
Advantages And Disadvantages ◽  
Technical Advances ◽  
Cellular Markers

Bioimaging contributes significantly to our understanding of plant virus infections. In the present review, we describe technical advances that enable imaging of the infection process at previously unobtainable levels. We highlight how such new advances in subcellular imaging are contributing to a detailed dissection of all stages of the viral infection process. Specifically, we focus on: (i) the increasingly detailed localizations of viral proteins enabled by a diversifying palette of cellular markers; (ii) approaches using fluorescence microscopy for the functional analysis of proteins in vivo; (iii) the imaging of viral RNAs; (iv) methods that bridge the gap between optical and electron microscopy; and (v) methods that are blurring the distinction between imaging and structural biology. We describe the advantages and disadvantages of such techniques and place them in the broader perspective of their utility in analysing plant virus infection.

Modes of cell death in Rauscher leukaemia virus infection

Pathology ◽  
1974 ◽  
Vol 6 (4) ◽  
pp. 315-322 ◽  
Author(s):  
K.J. Donald ◽  
L.J.L.D. van Griensen ◽  
Eveline van't Hull
Keyword(s):  
Cell Death ◽  
Virus Infection ◽  
Leukaemia Virus

The P-MAPA immunomodulator partially prevents apoptosis induced by Zika virus infection in THP-1 cells

2020 ◽  
Vol 21 ◽  
Author(s):  
Morganna C. Lima ◽  
Elisa A. N. Azevedo ◽  
Clarice N. L. de Morais ◽  
Larissa I. O. de Sousa ◽  
Bruno M. Carvalho ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Virus Infection ◽  
Virus Replication ◽  
Zika Virus ◽  
Mammalian Cells ◽  
Caspase 3 ◽  
Neurological Complications ◽  
Zika Virus Infection

Background: Zika virus is an emerging arbovirus of global importance. ZIKV infection is associated with a range of neurological complications such as the Congenital Zika Syndrome and Guillain Barré Syndrome. Despite the magnitude of recent outbreaks, there is no specific therapy to prevent or to alleviate disease pathology. Objective: To investigate the role of P-MAPA immunomodulator in Zika-infected THP-1 cells. Methods: THP-1 cells were subjected at Zika virus infection (Multiplicity of Infection = 0.5) followed by treatment with P-MAPA for until 96 hours post-infection. After that, the cell death was analyzed by annexin+/ PI+ and caspase 3/ 7+ staining by flow cytometry. In addition, the virus replication and cell proliferation were accessed by RT-qPCR and Ki67 staining, respectively. Results: We demonstrate that P-MAPA in vitro treatment significantly reduces Zika virus-induced cell death and caspase-3/7 activation on THP-1 infected cells, albeit it has no role in virus replication and cell proliferation. Conclusions: Our study reveals that P-MAPA seems to be a satisfactory alternative to inhibits the effects of Zika virus infection in mammalian cells.

scholarly journals Age influences susceptibility of brain capillary endothelial cells to La Crosse virus infection and cell death

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Rahul Basu ◽  
Vinod Nair ◽  
Clayton W. Winkler ◽  
Tyson A. Woods ◽  
Iain D. C. Fraser ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Virus Infection ◽  
La Crosse Virus ◽  
Brain Capillary ◽  
Adult Mice ◽  
Age Related ◽  
Capillary Endothelial Cells ◽  
The Brain

Abstract Background A key factor in the development of viral encephalitis is a virus crossing the blood-brain barrier (BBB). We have previously shown that age-related susceptibility of mice to the La Crosse virus (LACV), the leading cause of pediatric arbovirus encephalitis in the USA, was associated with the ability of the virus to cross the BBB. LACV infection in weanling mice (aged around 3 weeks) results in vascular leakage in the olfactory bulb/tract (OB/OT) region of the brain, which is not observed in adult mice aged > 6–8 weeks. Thus, we studied age-specific differences in the response of brain capillary endothelial cells (BCECs) to LACV infection. Methods To examine mechanisms of LACV-induced BBB breakdown and infection of the CNS, we analyzed BCECs directly isolated from weanling and adult mice as well as established a model where these cells were infected in vitro and cultured for a short period to determine susceptibility to virus infection and cell death. Additionally, we utilized correlative light electron microscopy (CLEM) to examine whether changes in cell morphology and function were also observed in BCECs in vivo. Results BCECs from weanling, but not adult mice, had detectable infection after several days in culture when taken ex vivo from infected mice suggesting that these cells could be infected in vitro. Further analysis of BCECs from uninfected mice, infected in vitro, showed that weanling BCECs were more susceptible to virus infection than adult BCECs, with higher levels of infected cells, released virus as well as cytopathic effects (CPE) and cell death. Although direct LACV infection is not detected in the weanling BCECs, CLEM analysis of brain tissue from weanling mice indicated that LACV infection induced significant cerebrovascular damage which allowed virus-sized particles to enter the brain parenchyma. Conclusions These findings indicate that BCECs isolated from adult and weanling mice have differential viral load, infectivity, and susceptibility to LACV. These age-related differences in susceptibility may strongly influence LACV-induced BBB leakage and neurovascular damage allowing virus invasion of the CNS and the development of neurological disease.

scholarly journals Identification of a small molecule as inducer of ferroptosis and apoptosis through ubiquitination of GPX4 in triple negative breast cancer cells

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yahui Ding ◽  
Xiaoping Chen ◽  
Can Liu ◽  
Weizhi Ge ◽  
Qin Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Small Molecule ◽  
Mode Of Action ◽  
Rna Silencing ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Parent Compound ◽  
Aggressive Breast Cancer

Abstract Background TNBC is the most aggressive breast cancer with higher recurrence and mortality rate than other types of breast cancer. There is an urgent need for identification of therapeutic agents with unique mode of action for overcoming current challenges in TNBC treatment. Methods Different inhibitors were used to study the cell death manner of DMOCPTL. RNA silencing was used to evaluate the functions of GPX4 in ferroptosis and apoptosis of TNBC cells and functions of EGR1 in apoptosis. Immunohistochemical assay of tissue microarray were used for investigating correlation of GPX4 and EGR1 with TNBC. Computer-aided docking and small molecule probe were used for study the binding of DMOCPTL with GPX4. Results DMOCPTL, a derivative of natural product parthenolide, exhibited about 15-fold improvement comparing to that of the parent compound PTL for TNBC cells. The cell death manner assay showed that the anti-TNBC effect of DMOCPTL mainly by inducing ferroptosis and apoptosis through ubiquitination of GPX4. The probe of DMOCPTL assay indicated that DMOCPTL induced GPX4 ubiquitination by directly binding to GPX4 protein. To the best of our knowledge, this is the first report of inducing ferroptosis through ubiquitination of GPX4. Moreover, the mechanism of GPX4 regulation of apoptosis is still obscure. Here, we firstly reveal that GPX4 regulated mitochondria-mediated apoptosis through regulation of EGR1 in TNBC cells. Compound 13, the prodrug of DMOCPTL, effectively inhibited the growth of breast tumor and prolonged the lifespan of mice in vivo, and no obvious toxicity was observed. Conclusions These findings firstly revealed novel manner to induce ferroptosis through ubiquitination of GPX4 and provided mechanism for GPX4 inducing mitochondria-mediated apoptosis through up-regulation of EGR1 in TNBC cells. Moreover, compound 13 deserves further studies as a lead compound with novel mode of action for ultimate discovery of effective anti-TNBC drug.

scholarly journals Virus Infection of Aspergillus fumigatus Compromises the Fungus in Intermicrobial Competition

Viruses ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 686
Author(s):  
Hasan Nazik ◽  
Ioly Kotta-Loizou ◽  
Gabriele Sass ◽  
Robert H. A. Coutts ◽  
David A. Stevens
Keyword(s):  
Virus Infection ◽  
Aspergillus Fumigatus ◽  
Stress Responses ◽  
Fungal Pathogens ◽  
Clinical Settings ◽  
Virus Infections ◽  
Fungal Strains ◽  
Common Reference ◽  
Strain Virus ◽  
Free Strain

Aspergillus and Pseudomonas compete in nature, and are the commonest bacterial and fungal pathogens in some clinical settings, such as the cystic fibrosis lung. Virus infections of fungi occur naturally. Effects on fungal physiology need delineation. A common reference Aspergillus fumigatus strain, long studied in two (of many) laboratories, was found infected with the AfuPmV-1 virus. One isolate was cured of virus, producing a virus-free strain. Virus from the infected strain was purified and used to re-infect three subcultures of the virus-free fungus, producing six fungal strains, otherwise isogenic. They were studied in intermicrobial competition with Pseudomonasaeruginosa. Pseudomonas culture filtrates inhibited forming or preformed Aspergillus biofilm from infected strains to a greater extent, also seen when Pseudomonas volatiles were assayed on Aspergillus. Purified iron-chelating Pseudomonas molecules, known inhibitors of Aspergillus biofilm, reproduced these differences. Iron, a stimulus of Aspergillus, enhanced the virus-free fungus, compared to infected. All infected fungal strains behaved similarly in assays. We show an important consequence of virus infection, a weakening in intermicrobial competition. Viral infection may affect the outcome of bacterial–fungal competition in nature and patients. We suggest that this occurs via alteration in fungal stress responses, the mechanism best delineated here is a result of virus-induced altered Aspergillus iron metabolism.

scholarly journals Risk factors and disposition in development of the nervous system infections

2009 ◽  
Vol 62 (9-10) ◽  
pp. 461-467
Author(s):  
Ljiljana Nesic ◽  
Predrag Canovic ◽  
Zeljko Mijailovic ◽  
Jelena Djokovic
Keyword(s):  
Risk Factors ◽  
Nervous System ◽  
Virus Infection ◽  
Lupus Erythematosus ◽  
Bacterial Infections ◽  
Heart Diseases ◽  
Final Diagnosis ◽  
Medical Documentation ◽  
Virus Infections ◽  
Number Of Patients

Introduction. Although well protected, brain is not resistant to infection agents. Acute infections of our nervous system appear more often in children and in persons who have medical history data about previous disorders, especially disorders of the nervous system. It is difficult to list possible risk factors which can be responsible for the appearance of infections of CNS and the resulting conditions. It is often difficult or impossible to determine what previous neural damage was (trauma, anoxic damages etc.) from those appearing during infections of CNS. All-inclusive anamnestic research reduces the possibility of approximate judgments. Material and methods. The research was based on the retrospective analysis of medical documentation of 275 patients. All patients were divided into three groups according to the final diagnosis. The first group consisted of 125 patients who were treated for acute virus encephalitis, the second group consisted of 125 patients who were treated for acute bacterial meningoencephalitis and the third group consisted of 25 patients who were treated for cerebritis. Discussion. In our studies sample, the youngest patient was 3 years old and the oldest was 87 years old. The highest number of patients with virus infection of the CNS was in the group under 25 years of age (45.6%). The highest number of patients with bacterial infections of the CNS and cerebritis was in the group of patients over 45 years of age (64%, 37%). Conclusion. Risk factors were more present in bacterial infections of the nervous system and cerebrit thanin virus infection of CNS. In virus infections of the CNS, 28% of patients had some risk factor, most often-chronic ethylism, diabetes mellitus and acquired heart diseases. In bacterial infections of the CNS, 64% of patients had some predisposed factor. The most frequent factor of risk in these patients were chronic otitis (21.6%) and craniotrauma (14.4%). In cerebritis, risk factors were present in 76% of patients and they were: sepsis (20%), chronic otitis (12%) and systemic lupus erythematosus (8%).

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