scholarly journals Flavivirus infections induce a Golgi stress response in vertebrate and mosquito cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mercedes Viettri ◽  
José L. Zambrano ◽  
Romel Rosales ◽  
Gerson I. Caraballo ◽  
Ana Lorena Gutiérrez-Escolano ◽  
...  
Keyword(s):  
Stress Response ◽  
Golgi Complex ◽  
Stress Responses ◽  
Viral Infections ◽  
Vesicular Transport ◽  
Positive Control ◽  
Mosquito Cells ◽  
Infected Cells ◽  
The Impact ◽  
Replicative Cycle

AbstractThe stress of the Golgi apparatus is an autoregulatory mechanism that is induced to compensate for greater demand in the Golgi functions. No examples of Golgi stress responses due to physiological stimuli are known. Furthermore, the impact on this organelle of viral infections that occupy the vesicular transport during replication is unknown. In this work, we evaluated if a Golgi stress response is triggered during dengue and Zika viruses replication, two flaviviruses whose replicative cycle is heavily involved with the Golgi complex, in vertebrate and mosquito cells. Using GM-130 as a Golgi marker, and treatment with monensin as a positive control for the induction of the Golgi stress response, a significant expansion of the Golgi cisternae was observed in BHK-21, Vero E6 and mosquito cells infected with either virus. Activation of the TFE3 pathway was observed in the infected cells as indicated by the translocation from the cytoplasm to the nucleus of TFE3 and increased expression of pathway targeted genes. Of note, no sign of activation of the stress response was observed in CRFK cells infected with Feline Calicivirus (FCV), a virus released by cell lysis, not requiring vesicular transport. Finally, dilatation of the Golgi complex and translocation of TFE3 was observed in vertebrate cells expressing dengue and Zika viruses NS1, but not NS3. These results indicated that infections by dengue and Zika viruses induce a Golgi stress response in vertebrate and mosquito cells due to the increased demand on the Golgi complex imposed by virion and NS1 processing and secretion.

scholarly journals Flavivirus Infection Induce a Golgi Stress Response in Vertebrate and Mosquito Cells

2021 ◽  
Author(s):  
Mercedes Viettri ◽  
José L. Zambrano ◽  
Romel Rosales-Ramirez ◽  
Ana Lorena Gutierrez-Escolano ◽  
Juan E Ludert
Keyword(s):  
Stress Response ◽  
Golgi Complex ◽  
Stress Responses ◽  
Viral Infections ◽  
Vesicular Transport ◽  
Positive Control ◽  
Mosquito Cells ◽  
Infected Cells ◽  
Flavivirus Infection ◽  
The Impact

Abstract The stress of the Golgi apparatus is an autoregulatory mechanism that is induced to compensate for greater demand in the Golgi functions. Few examples of Golgi stress responses due to physiological stimuli are known. Furthermore, the impact on this organelle of viral infections that occupy the vesicular transport during replication is unknown. In this work, we evaluated if a Golgi stress response is triggered during dengue and Zika viruses replication, two flaviviruses whose replicative cycle is heavily involved with the Golgi complex, in vertebrate and mosquito cells. Using GM-130 as a Golgi marker, and treatment with monensin as a positive control for the induction of the Golgi stress response, a significant expansion of the Golgi cisternae was observed in BHK-21, Vero E6 and mosquito cells infected with either virus. Activation of the TFE3 pathway was observed in the infected cells as indicated by the translocation from the cytoplasm to the nucleus of TFE3. Of note, no sign of activation of the stress response was observed in CRFK cells infected with Feline Calicivirus (FCV), a virus released by cell lysis, not requiring vesicular transport. Finally, dilatation of the Golgi complex and translocation of TFE3 was observed in vertebrate cells expressing dengue and Zika viruses NS1, but not NS3. These results indicated that infections by dengue and Zika viruses induce a Golgi stress response in vertebrate and mosquito cells due to the increased demand on Golgi complex imposed by virion and NS1 processing and secretion.

scholarly journals Primed to be strong, primed to be fast: modeling benefits of microbial stress responses

2019 ◽  
Vol 95 (8) ◽  
Author(s):  
Felix Wesener ◽  
Britta Tietjen
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Defense Mechanisms ◽  
Defense Mechanism ◽  
Equation Model ◽  
Response Strategies ◽  
Early Stress ◽  
The Impact ◽  
Microbial Stress ◽  
Population Performance

ABSTRACT Organisms are prone to different stressors and have evolved various defense mechanisms. One such defense mechanism is priming, where a mild preceding stress prepares the organism toward an improved stress response. This improved response can strongly vary, and primed organisms have been found to respond with one of three response strategies: a shorter delay to stress, a faster buildup of their response or a more intense response. However, a universal comparative assessment, which response is superior under a given environmental setting, is missing. We investigate the benefits of the three improved responses for microorganisms with an ordinary differential equation model, simulating the impact of an external stress on a microbial population that is either naïve or primed. We systematically assess the resulting population performance for different costs associated with priming and stress conditions. Our results show that independent of stress type and priming costs, the stronger primed response is most beneficial for longer stress phases, while the faster and earlier responses increase population performance and survival probability under short stresses. Competition increases priming benefits and promotes the early stress response. This dependence on the ecological context highlights the importance of including primed response strategies into microbial stress ecology.

scholarly journals Reovirus Induces and Benefits from an Integrated Cellular Stress Response

2006 ◽  
Vol 80 (4) ◽  
pp. 2019-2033 ◽  
Author(s):  
Jennifer A. Smith ◽  
Stephen C. Schmechel ◽  
Arvind Raghavan ◽  
Michelle Abelson ◽  
Cavan Reilly ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stress Response ◽  
Stress Responses ◽  
Cellular Stress Response ◽  
Initiation Factor ◽  
Viral Protein Synthesis ◽  
Protein Levels ◽  
Eif2α Phosphorylation ◽  
Infected Cells ◽  
Reovirus Replication

ABSTRACT Following infection with most reovirus strains, viral protein synthesis is robust, even when cellular translation is inhibited. To gain further insight into pathways that regulate translation in reovirus-infected cells, we performed a comparative microarray analysis of cellular gene expression following infection with two strains of reovirus that inhibit host translation (clone 8 and clone 87) and one strain that does not (Dearing). Infection with clone 8 and clone 87 significantly increased the expression of cellular genes characteristic of stress responses, including the integrated stress response. Infection with these same strains decreased transcript and protein levels of P58IPK, the cellular inhibitor of the eukaryotic initiation factor 2α (eIF2α) kinases PKR and PERK. Since infection with host shutoff-inducing strains of reovirus impacted cellular pathways that control eIF2α phosphorylation and unphosphorylated eIF2α is required for translation initiation, we examined reovirus replication in a variety of cell lines with mutations that impact eIF2α phosphorylation. Our results revealed that reovirus replication is more efficient in the presence of eIF2α kinases and phosphorylatable eIF2α. When eIF2α is phosphorylated, it promotes the synthesis of ATF4, a transcription factor that controls cellular recovery from stress. We found that the presence of this transcription factor increased reovirus yields 10- to 100-fold. eIF2α phosphorylation also led to the formation of stress granules in reovirus-infected cells. Based on these results, we hypothesize that eIF2α phosphorylation facilitates reovirus replication in two ways—first, by inducing ATF4 synthesis, and second, by creating an environment that places abundant reovirus transcripts at a competitive advantage for limited translational components.

scholarly journals Effect of Combined Stressors on C. elegans Lifespan

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 667-667
Author(s):  
Bradford Hull ◽  
George Sutphin
Keyword(s):  
Heavy Metal ◽  
Stress Response ◽  
Stress Responses ◽  
Cellular Response ◽  
Multiple Stressors ◽  
Cellular Stress ◽  
Cellular Stress Response ◽  
C Elegans ◽  
Arsenic Copper ◽  
The Impact

Abstract Cellular stress is a fundamental component of age-associated disease. Cells experience many forms of stress (oxidative, heavy metal, etc.), and as we age the burden of stress and resulting damage increases while our cells’ ability to deal with the consequences becomes diminished due to dysregulation of cellular stress response pathways. By understanding how cells respond to stress we aim to slow age-associated deterioration and develop treatment targets for age-associated disease. The majority of past work has focused on understanding responses to individual stressors. In contrast, how pathology and stress responses differ in the presence of multiple stressors is relatively unknown; we investigate that here. We cultured worms on agar plates with different combinations of arsenic, copper, and DTT (which create oxidative/proteotoxic, heavy metal, and endoplasmic reticulum (ER) stress, respectively) at doses that result in 20% lifespan reduction individually and measured the effect on lifespan. We found that arsenic/copper and arsenic/DTT combinations created additive lifespan reductions while the copper/DTT combination created an antagonistic lifespan reduction when compared to controls (p<0.05). This antagonistic toxicity suggests an interaction either between the mechanisms of toxicity or the cellular response to copper and DTT. We are now evaluating the impact of copper and DTT individually and in combination on unfolded protein and heavy metal response pathways to understand the underlying mechanism of the interaction. Additionally, we are continuing to screen stressors to identify combinations that cause non-additive (synergistic or antagonistic) toxicity to build a comprehensive model of the genetic stress response network in C. elegans.

scholarly journals In-host Modelling of COVID-19 in Humans

2020 ◽  
Author(s):  
Esteban A. Hernandez-Vargas ◽  
Jorge X. Velasco-Hernandez
Keyword(s):  
Immune Responses ◽  
Target Cell ◽  
Viral Infections ◽  
Cell Model ◽  
Influenza Infection ◽  
Severe Disease ◽  
Reproductive Number ◽  
Infected Cells ◽  
Eclipse Phase ◽  
The Impact

ABSTRACTCOVID-19 pandemic has underlined the impact of emergent pathogens as a major threat for human health. The development of quantitative approaches to advance comprehension of the current outbreak is urgently needed to tackle this severe disease. In this work, several mathematical models are proposed to represent SARS-CoV-2 dynamics in infected patients. Considering different starting times of infection, parameters sets that represent infectivity of SARS-CoV-2 are computed and compared with other viral infections that can also cause pandemics.Based on the target cell model, SARS-CoV-2 infecting time between susceptible cells (mean of 30 days approximately) is much slower than those reported for Ebola (about 3 times slower) and influenza (60 times slower). The within-host reproductive number for SARS-CoV-2 is consistent to the values of influenza infection (1.7-5.35). The best model to fit the data was including immune responses, which suggest a slow cell response peaking between 5 to 10 days post onset of symptoms. The model with eclipse phase, time in a latent phase before becoming productively infected cells, was not supported. Interestingly, both, the target cell model and the model with immune responses, predict that virus may replicate very slowly in the first days after infection, and it could be below detection levels during the first 4 days post infection. A quantitative comprehension of SARS-CoV-2 dynamics and the estimation of standard parameters of viral infections is the key contribution of this pioneering work.

scholarly journals The Circadian Clock, the Immune System, and Viral Infections: The Intricate Relationship Between Biological Time and Host-Virus Interaction

Pathogens ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 83 ◽  
Author(s):  
Gianluigi Mazzoccoli ◽  
Manlio Vinciguerra ◽  
Annalucia Carbone ◽  
Angela Relógio
Keyword(s):  
Viral Infections ◽  
Mutual Influence ◽  
Biological Clock ◽  
Life Forms ◽  
The Body ◽  
Viral Agent ◽  
Biological Time ◽  
Infected Cells ◽  
Time Variations ◽  
The Impact

Living beings spend their lives and carry out their daily activities interacting with environmental situations that present space-time variations and that involve contact with other life forms, which may behave as commensals or as invaders and/or parasites. The characteristics of the environment, as well as the processes that support the maintenance of life and that characterize the execution of activities of daily life generally present periodic variations, which are mostly synchronized with the light–dark cycle determined by Earth’s rotation on its axis. These rhythms with 24-h periodicity, defined as circadian, influence events linked to the interaction between hosts and hosted microorganisms and can dramatically determine the outcome of this interplay. As for the various pathological conditions resulting from host–microorganism interactions, a particularly interesting scenario concerns infections by viruses. When a viral agent enters the body, it alters the biological processes of the infected cells in order to favour its replication and to spread to various tissues. Though our knowledge concerning the mutual influence between the biological clock and viruses is still limited, recent studies start to unravel interesting aspects of the clock–virus molecular interplay. Three different aspects of this interplay are addressed in this mini-review and include the circadian regulation of both innate and adaptive immune systems, the impact of the biological clock on viral infection itself, and finally the putative perturbations that the virus may confer to the clock leading to its deregulation.

scholarly journals Paracrine granules are cytoplasmic RNP granules distinct from stress granules assembling in response to viral infection.

2021 ◽  
Author(s):  
Valentina Iadevaia ◽  
James M Burke ◽  
Lucy Eke ◽  
Carla Moller-Levet ◽  
Roy Robert Parker ◽  
...  
Keyword(s):  
Stress Responses ◽  
Rna Binding ◽  
Viral Infections ◽  
Rna Binding Proteins ◽  
Stress Granules ◽  
Scaffolding Protein ◽  
Viral Propagation ◽  
Infected Cells ◽  
Bystander Cells ◽  
Rnp Granules

To rapidly respond and adapt to stresses, such as viral infections, cells have evolved several mechanisms, which include the activation of stress response pathways and the innate immune response. These stress responses result in the rapid inhibition of translation and condensation of stalled mRNAs, together with RNA-binding proteins and signalling components, into cytoplasmic biocondensates called stress granules. Increasing evidence suggests that stress granules contribute to antiviral defense and thus viruses need to evade these response pathways to propagate. In addition, the stress granule pathway is proposed to be dynamic and adaptable to specific stresses. We previously showed that Feline Calicivirus (FCV) impairs SGs assembly by cleaving the scaffolding protein G3BP1. We also observed that uninfected bystander cells assembled G3BP1-granules, suggesting a paracrine response trigged by the infection. We now present evidence that virus-free supernatant generated from infected cells can induce the formation of paracrine granules. They are different from canonical stress granules and exhibit specific kinetics of assembly-disassembly, protein and RNA composition and are linked to antiviral activity. We propose that this paracrine induction reflects a novel cellular defence mechanism to limit viral propagation and promote stress responses in bystander cells.

scholarly journals Relevance of oxidative stress in inhibition of eIF2 alpha phosphorylation and stress granules formation during Usutu virus infection

2021 ◽  
Vol 15 (1) ◽  
pp. e0009072
Author(s):  
Ana-Belén Blázquez ◽  
Miguel A. Martín-Acebes ◽  
Teresa Poderoso ◽  
Juan-Carlos Saiz
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Stress Responses ◽  
Stress Granules ◽  
Initiation Factor ◽  
Potential Health ◽  
Usutu Virus ◽  
Cellular Environment ◽  
Infected Cells

Usutu virus (USUV) is an African mosquito-borne flavivirus closely related to West Nile, Japanese encephalitis, Zika, and dengue viruses. USUV emerged in 1996 in Europe, where quickly spread across the continent causing a considerable number of bird deaths and varied neurological disorders in humans, including encephalitis, meningoencephalitis, or facial paralysis, thus warning about USUV as a potential health threat. USUV replication takes place on the endoplasmic reticulum (ER) of infected cells, inducing ER stress and resulting in the activation of stress-related cellular pathways collectively known as the integrated stress response (ISR). The alpha subunit of the eukaryotic initiation factor eIF2 (eIF2α), the core factor in this pathway, is phosphorylated by stress activated kinases: protein kinase R (PKR), PKR-like endoplasmic reticulum kinase (PERK), heme-regulated inhibitor kinase (HRI), and general control non-repressed 2 kinase (GCN2). Its phosphorylation results, among others, in the downstream inhibition of translation with accumulation of discrete foci in the cytoplasm termed stress granules (SGs). Our results indicated that USUV infection evades cellular stress response impairing eIF2α phosphorylation and SGs assembly induced by treatment with the HRI activator ArsNa. This protective effect was related with oxidative stress responses in USUV-infected cells. Overall, these results provide new insights into the complex connections between the stress response and flavivirus infection in order to maintain an adequate cellular environment for viral replication.

Emotions and health: The impact of emotions, emotions regulation, music, and acculturation on health

2008 ◽  
Vol 16 (3) ◽  
pp. 112-115 ◽  
Author(s):  
Stephan Bongard ◽  
Volker Hodapp ◽  
Sonja Rohrmann
Keyword(s):  
Stress Responses ◽  
Physiological Stress ◽  
Anger Expression ◽  
Domain Specific ◽  
Cardiovascular Stress ◽  
Expression Behavior ◽  
Cardio Vascular ◽  
And Coping ◽  
Relationship Of ◽  
The Impact

Abstract. Our unit investigates the relationship of emotional processes (experience, expression, and coping), their physiological correlates and possible health outcomes. We study domain specific anger expression behavior and associated cardio-vascular loads and found e.g. that particularly an open anger expression at work is associated with greater blood pressure. Furthermore, we demonstrated that women may be predisposed for the development of certain mental disorders because of their higher disgust sensitivity. We also pointed out that the suppression of negative emotions leads to increased physiological stress responses which results in a higher risk for cardiovascular diseases. We could show that relaxation as well as music activity like singing in a choir causes increases in the local immune parameter immunoglobuline A. Finally, we are investigating connections between migrants’ strategy of acculturation and health and found e.g. elevated cardiovascular stress responses in migrants when they where highly adapted to the German culture.

Childbirth and Posttraumatic Stress Responses

2006 ◽  
Vol 22 (4) ◽  
pp. 259-267 ◽  
Author(s):  
Eelco Olde ◽  
Rolf J. Kleber ◽  
Onno van der Hart ◽  
Victor J.M. Pop
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Responses ◽  
Rating Scales ◽  
Rating Scale ◽  
Stress Disorder ◽  
Traumatic Experience ◽  
Event Scale ◽  
Self Rating ◽  
The Impact

Childbirth has been identified as a possible traumatic experience, leading to traumatic stress responses and even to the development of posttraumatic stress disorder (PTSD). The current study investigated the psychometric properties of the Dutch version of the Impact of Event Scale-Revised (IES-R) in a group of women who recently gave birth (N = 435). In addition, a comparison was made between the original IES and the IES-R. The scale showed high internal consistency (α = 0.88). Using confirmatory factor analysis no support was found for a three-factor structure of an intrusion, an avoidance, and a hyperarousal factor. Goodness of fit was only reasonable, even after fitting one intrusion item on the hyperarousal scale. The IES-R correlated significantly with scores on depression and anxiety self-rating scales, as well as with scores on a self-rating scale of posttraumatic stress disorder. Although the IES-R can be used for studying posttraumatic stress reactions in women who recently gave birth, the original IES proved to be a better instrument compared to the IES-R. It is concluded that adding the hyperarousal scale to the IES-R did not make the scale stronger.

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