scholarly journals Viral Manipulation of the Host Epigenome as a Driver of Virus-Induced Oncogenesis

2021 ◽  
Vol 9 (6) ◽  
pp. 1179
Author(s):  
Shimaa Hassan AbdelAziz Soliman ◽  
Arturo Orlacchio ◽  
Fabio Verginelli
Keyword(s):  
Viral Infection ◽  
Host Cell ◽  
Tumor Development ◽  
Oncogenic Viruses ◽  
Comprehensive Understanding ◽  
Global Impact ◽  
Epigenetic Machinery ◽  
Histone Modifiers ◽  
High Fraction ◽  
Potential Use

Tumorigenesis due to viral infection accounts for a high fraction of the total global cancer burden (15–20%) of all human cancers. A comprehensive understanding of the mechanisms by which viral infection leads to tumor development is extremely important. One of the main mechanisms by which viruses induce host cell proliferation programs is through controlling the host’s epigenetic machinery. In this review, we dissect the epigenetic pathways through which oncogenic viruses can integrate their genome into host cell chromosomes and lead to tumor progression. In addition, we highlight the potential use of drugs based on histone modifiers in reducing the global impact of cancer development due to viral infection.

scholarly journals Modelling Degradation and Replication Kinetics of the Zika Virus In Vitro Infection

Viruses ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 547
Author(s):  
Veronika Bernhauerová ◽  
Veronica V. Rezelj ◽  
Marco Vignuzzi
Keyword(s):  
Mathematical Model ◽  
Viral Infection ◽  
Host Cell ◽  
Decay Time ◽  
Zika Virus ◽  
Infectious Virus ◽  
Numerical Characterization ◽  
The Mathematical Model

Mathematical models of in vitro viral kinetics help us understand and quantify the main determinants underlying the virus–host cell interactions. We aimed to provide a numerical characterization of the Zika virus (ZIKV) in vitro infection kinetics, an arthropod-borne emerging virus that has gained public recognition due to its association with microcephaly in newborns. The mathematical model of in vitro viral infection typically assumes that degradation of extracellular infectious virus proceeds in an exponential manner, that is, each viral particle has the same probability of losing infectivity at any given time. We incubated ZIKV stock in the cell culture media and sampled with high frequency for quantification over the course of 96 h. The data showed a delay in the virus degradation in the first 24 h followed by a decline, which could not be captured by the model with exponentially distributed decay time of infectious virus. Thus, we proposed a model, in which inactivation of infectious ZIKV is gamma distributed and fit the model to the temporal measurements of infectious virus remaining in the media. The model was able to reproduce the data well and yielded the decay time of infectious ZIKV to be 40 h. We studied the in vitro ZIKV infection kinetics by conducting cell infection at two distinct multiplicity of infection and measuring viral loads over time. We fit the mathematical model of in vitro viral infection with gamma distributed degradation time of infectious virus to the viral growth data and identified the timespans and rates involved within the ZIKV-host cell interplay. Our mathematical analysis combined with the data provides a well-described example of non-exponential viral decay dynamics and presents numerical characterization of in vitro infection with ZIKV.

scholarly journals Tumour viruses and innate immunity

2017 ◽  
Vol 372 (1732) ◽  
pp. 20160267 ◽  
Author(s):  
Sharon E. Hopcraft ◽  
Blossom Damania
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Viral Infection ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Host Cells ◽  
Oncogenic Viruses ◽  
Barr Virus ◽  
Human T Cell ◽  
Epstein Barr

Host cells sense viral infection through pattern recognition receptors (PRRs), which detect pathogen-associated molecular patterns (PAMPs) and stimulate an innate immune response. PRRs are localized to several different cellular compartments and are stimulated by viral proteins and nucleic acids. PRR activation initiates signal transduction events that ultimately result in an inflammatory response. Human tumour viruses, which include Kaposi's sarcoma-associated herpesvirus, Epstein–Barr virus, human papillomavirus, hepatitis C virus, hepatitis B virus, human T-cell lymphotropic virus type 1 and Merkel cell polyomavirus, are detected by several different PRRs. These viruses engage in a variety of mechanisms to evade the innate immune response, including downregulating PRRs, inhibiting PRR signalling, and disrupting the activation of transcription factors critical for mediating the inflammatory response, among others. This review will describe tumour virus PAMPs and the PRRs responsible for detecting viral infection, PRR signalling pathways, and the mechanisms by which tumour viruses evade the host innate immune system. This article is part of the themed issue ‘Human oncogenic viruses’.

scholarly journals Efficacy of Garlic and Onion against virus

2019 ◽  
Vol 10 (4) ◽  
pp. 3578-3586 ◽  
Author(s):  
Neha Sharma
Keyword(s):  
Viral Infection ◽  
Host Cell ◽  
Antiviral Effect ◽  
Viral Assembly ◽  
Organosulfur Compounds ◽  
Phospholipid Membrane ◽  
Safe Alternative ◽  
Virus Attachment ◽  
Current Scenario ◽  
Pass Through

In the current scenario, pharmaceutical industry is dependent on chemical based drugs to treat viral infection. However, these drugs are known to induce many side effects in human body. There is pressing need to promote safe alternative to chemical based antiviral drugs. Onion and garlic are natural sources which are known to possess antiviral properties. It is well known that onion and garlic are rich source of organosulfur compounds. Organosulfur compounds like quercetin and allicin are associated with inhibition of viral infection. These chemicals can hinder virus attachment to host cell, alter transcription and translation of viral genome in host cell and also affect viral assembly. Quercetin can affect entry and attachment of Enterovirus and Influenza virus on host cell. This compound also has ability to inhibit RNA polymerase which is necessary for viral replication. Quercetin also inhibit process by which virus alter signalling pathway in host cell. Organosulfur compounds like allicin, diallyl trisulfide and ajoene are main chemicals which impart antiviral property to garlic. It is known that allicin can pass through phospholipid membrane of cell and can further contribute in inhibiting viral multiplication. Considering numerous studies which corroborate antiviral effect of onion and garlic, this paper recommends consumption of these plants as a safe alternative to prevent virus infection.

scholarly journals Global Transcriptional Responses of Pseudomonas aeruginosa to Phage PRR1 Infection

2007 ◽  
Vol 82 (5) ◽  
pp. 2324-2329 ◽  
Author(s):  
Janne J. Ravantti ◽  
Tanja M. Ruokoranta ◽  
A. Marika Alapuranen ◽  
Dennis H. Bamford
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Viral Infection ◽  
Host Cell ◽  
Cell Function ◽  
Growth Conditions ◽  
Growth Cycle ◽  
Global Changes ◽  
Mrna Levels ◽  
Transcriptional Responses ◽  
Number Of Genes

ABSTRACT The infectious cycles of viruses are known to cause dramatic changes to host cell function. The development of microarray technology has provided means to monitor host cell responses to viral infection at the level of global changes in mRNA levels. We have applied this methodology to investigate gene expression changes caused by a small, icosahedral, single-stranded-RNA phage, PRR1 (a member of the Leviviridae family), on its host, Pseudomonas aeruginosa, at different times during its growth cycle. Viral infection in this system resulted in changes in expression levels of <4% of P. aeruginosa genes. Interestingly, the number of genes affected by viral infection was significantly lower than the number of genes affected by changes in growth conditions during the experiment. Compared with a similar study that focused on the complex, double-stranded-DNA bacterial virus PRD1, it was evident that there were no universal responses to viral infection. However, in both cases, translation was affected in infected cells.

Ayurvedic system a new possible safe and effective way to get rid of this critical nCOVID-19 pandemic situation- A review

2021 ◽  
Vol 07 ◽  
Author(s):  
Sumel Ashique ◽  
Navjot K Sandhu
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Viral Infection ◽  
Traditional Medicine ◽  
Host Cell ◽  
Western Medicine ◽  
Treatment Strategies ◽  
Unani Medicine ◽  
System A ◽  
The World

: The nCOVID-19 virus has become the most threatening infections disease all over the world. From the beginning till today a large number of researches is going on to develop appropriate therapeutics that can prevent and cure this viral infection successfully. But unfortunately, modern western medicine could not find any effective drug having no toxic effects on host cell. TCM (traditional Chinese Medicine) has shown promising effect against nCOVID-19. This TCM contains natural occurring herbal decoctions which showed promising blocking of viral progression in host cell. These ayurvedic formulations containing homeopathic medicine, unani medicine and yoga to challenge the virus. The traditional medicine system is unable to cure properly but it can be a possible preventing strategy to stop this virus pandemicity. This review focuses how the ayurvedic medicines, homeopathic treatment strategies and yoga can impact to prevent the viral infection.

scholarly journals Hijacking of Lipid Droplets by Hepatitis C, Dengue and Zika Viruses—From Viral Protein Moonlighting to Extracellular Release

2020 ◽  
Vol 21 (21) ◽  
pp. 7901 ◽  
Author(s):  
Alexandra P.M. Cloherty ◽  
Andrea D. Olmstead ◽  
Carla M.S. Ribeiro ◽  
François Jean
Keyword(s):  
Hepatitis C ◽  
Viral Infection ◽  
Host Cell ◽  
Lipid Droplets ◽  
Viral Proteins ◽  
Biological Properties ◽  
Protein Functions ◽  
Associated Proteins ◽  
Viral Lifecycle ◽  
Moonlighting Functions

Hijacking and manipulation of host cell biosynthetic pathways by human enveloped viruses are essential for the viral lifecycle. Flaviviridae members, including hepatitis C, dengue and Zika viruses, extensively manipulate host lipid metabolism, underlining the importance of lipid droplets (LDs) in viral infection. LDs are dynamic cytoplasmic organelles that can act as sequestration platforms for a unique subset of host and viral proteins. Transient recruitment and mobilization of proteins to LDs during viral infection impacts host-cell biological properties, LD functionality and canonical protein functions. Notably, recent studies identified LDs in the nucleus and also identified that LDs are transported extracellularly via an autophagy-mediated mechanism, indicating a novel role for autophagy in Flaviviridae infections. These developments underline an unsuspected diversity and localization of LDs and potential moonlighting functions of LD-associated proteins during infection. This review summarizes recent breakthroughs concerning the LD hijacking activities of hepatitis C, dengue and Zika viruses and potential roles of cytoplasmic, nuclear and extracellular LD-associated viral proteins during infection.

scholarly journals African Swine Fever Virus Blocks the Host Cell Antiviral Inflammatory Response through a Direct Inhibition of PKC-θ-Mediated p300 Transactivation

2008 ◽  
Vol 83 (2) ◽  
pp. 969-980 ◽  
Author(s):  
Aitor G. Granja ◽  
Elena G. Sánchez ◽  
Prado Sabina ◽  
Manuel Fresno ◽  
Yolanda Revilla
Keyword(s):  
Gene Expression ◽  
Inflammatory Response ◽  
Viral Infection ◽  
Host Cell ◽  
Expression Pattern ◽  
African Swine Fever Virus ◽  
Gene Expression Pattern ◽  
African Swine Fever ◽  
Fever Virus ◽  
Amino Terminal

ABSTRACT During a viral infection, reprogramming of the host cell gene expression pattern is required to establish an adequate antiviral response. The transcriptional coactivators p300 and CREB binding protein (CBP) play a central role in this regulation by promoting the assembly of transcription enhancer complexes to specific promoters of immune and proinflammatory genes. Here we show that the protein A238L encoded by African swine fever virus counteracts the host cell inflammatory response through the control of p300 transactivation during the viral infection. We demonstrate that A238L inhibits the expression of the inflammatory regulators cyclooxygenase-2 (COX-2) and tumor necrosis factor alpha (TNF-α) by preventing the recruitment of p300 to the enhanceosomes formed on their promoters. Furthermore, we report that A238L inhibits p300 activity during the viral infection and that its amino-terminal transactivation domain is essential in the A238L-mediated inhibition of the inflammatory response. Importantly, we found that the residue serine 384 of p300 is required for the viral protein to accomplish its inhibitory function and that ectopically expressed PKC-θ completely reverts this inhibition, thus indicating that this signaling pathway is disrupted by A238L during the viral infection. Furthermore, we show here that A238L does not affect PKC-θ enzymatic activity, but the molecular mechanism of this viral inhibition relies on the lack of interaction between PKC-θ and p300. These findings shed new light on how viruses alter the host cell antiviral gene expression pattern through the blockade of the p300 activity, which represents a new and sophisticated viral mechanism to evade the inflammatory and immune defense responses.

scholarly journals Zebrafish RPZ5 Degrades Phosphorylated IRF7 To Repress Interferon Production

2019 ◽  
Vol 93 (21) ◽  
Author(s):  
Long-Feng Lu ◽  
Xiao-Yu Zhou ◽  
Can Zhang ◽  
Zhuo-Cong Li ◽  
Dan-Dan Chen ◽  
...  
Keyword(s):  
Viral Infection ◽  
Host Cell ◽  
Negative Regulator ◽  
Regulatory Factor ◽  
Lower Vertebrate ◽  
Fish Viruses ◽  
Viral Proliferation ◽  
Balance Mechanism ◽  
Insight Into ◽  
Inducible Gene

ABSTRACT Interferon (IFN) production activated by phosphorylated interferon regulatory factor 7 (IRF7) is a pivotal process during host antiviral infection. For viruses, suppressing the host IFN response is beneficial for viral proliferation; in such cases, evoking host-derived IFN negative regulators would be very useful for viruses. Here, we report that the zebrafish rapunzel 5 (RPZ5) protein which activated by virus degraded phosphorylated IRF7 is activated by TANK-binding kinase 1 (TBK1), leading to a reduction in IFN production. Upon viral infection, zebrafish rpz5 was significantly upregulated, as was ifn, in response to the stimulation. Overexpression of RPZ5 blunted the IFN expression induced by both viral and retinoic acid-inducible gene I (RIG-I) like-receptor (RLR) factors. Subsequently, RPZ5 interacted with RLRs but did not affect the stabilization of the proteins in the normal state. Interestingly, RPZ5 degraded the phosphorylated IRF7 under TBK1 activation through K48-linked ubiquitination. Finally, the overexpression of RPZ5 remarkably reduced the host cell antiviral capacity. These findings suggest that zebrafish RPZ5 is a negative regulator of phosphorylated IRF7 and attenuates IFN expression during viral infection, providing insight into the IFN balance mechanism in fish. IMPORTANCE The phosphorylation of IRF7 is helpful for host IFN production to defend against viral infection; thus, it is a potential target for viruses to mitigate the antiviral response. We report that the fish RPZ5 is an IFN negative regulator induced by fish viruses and degrades the phosphorylated IRF7 activated by TBK1, leading to IFN suppression and promotion of viral proliferation. These findings reveal a novel mechanism for interactions between the host cell and viruses in the lower vertebrate.

scholarly journals Navigating the Host Cell Response during Entry into Sites of Latent Cytomegalovirus Infection

Pathogens ◽  
2018 ◽  
Vol 7 (1) ◽  
pp. 30 ◽  
Author(s):  
Matthew Murray ◽  
Nicholas Peters ◽  
Matthew Reeves
Keyword(s):  
Viral Infection ◽  
Host Cell ◽  
Innate Immune ◽  
Host Responses ◽  
Hostile Environment ◽  
Innate Immune Responses ◽  
Cellular Functions ◽  
Surface Receptors ◽  
Host Cell Response ◽  
The Impact

The host cell represents a hostile environment that viruses must counter in order to establish infection. Human cytomegalovirus (HCMV) is no different and encodes a multitude of functions aimed at disabling, re-directing or hijacking cellular functions to promulgate infection. However, during the very early stages of infection the virus relies on the outcome of interactions between virion components, cell surface receptors and host signalling pathways to promote an environment that supports infection. In the context of latent infection—where the virus establishes an infection in an absence of many gene products specific for lytic infection—these initial interactions are crucial events. In this review, we will discuss key host responses triggered by viral infection and how, in turn, the virus ameliorates the impact on the establishment of non-lytic infections of cells. We will focus on strategies to evade intrinsic antiviral and innate immune responses and consider their impact on viral infection. Finally, we will consider the hypothesis that the very early events upon viral infection are important for dictating the outcome of infection and consider the possibility that events that occur during entry into non-permissive cells are unique and thus contribute to the establishment of latency.

Sign in / Sign up

Export Citation Format

Share Document