scholarly journals Recognition of Reovirus RNAs by the Innate Immune System

Viruses ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 667
Author(s):  
Andrew T. Abad ◽  
Pranav Danthi
Keyword(s):  
Innate Immune ◽  
Immune Recognition ◽  
Mammalian Orthoreovirus ◽  
Host Detection ◽  
Dsrna Viruses ◽  
Sensor Proteins ◽  
Host Virus Interactions ◽  
Virus Interactions ◽  
Gain Access ◽  
Genomic Material

Mammalian orthoreovirus (reovirus) is a dsRNA virus, which has long been used as a model system to study host–virus interactions. One of the earliest interactions during virus infection is the detection of the viral genomic material, and the consequent induction of an interferon (IFN) based antiviral response. Similar to the replication of related dsRNA viruses, the genomic material of reovirus is thought to remain protected by viral structural proteins throughout infection. Thus, how innate immune sensor proteins gain access to the viral genomic material, is incompletely understood. This review summarizes currently known information about the innate immune recognition of the reovirus genomic material. Using this information, we propose hypotheses about host detection of reovirus.

scholarly journals Unraveling the Underlying Interaction Mechanism Between Dabie bandavirus and Innate Immune Response

2021 ◽  
Vol 12 ◽  
Author(s):  
Chuan-min Zhou ◽  
Xue-jie Yu
Keyword(s):  
Interaction Mechanism ◽  
Innate Immune ◽  
Type I ◽  
Innate Immune Responses ◽  
Structural Protein ◽  
Antiviral Responses ◽  
Host Virus Interactions ◽  
Virus Interactions ◽  
Severe Fever

The genus Bandavirus consists of seven tick-borne bunyaviruses, among which four are known to infect humans. Dabie bandavirus, severe fever with thrombocytopenia syndrome virus (SFTSV), poses serious threats to public health worldwide. SFTSV is a tick-borne virus mainly reported in China, South Korea, and Japan with a mortality rate of up to 30%. To date, most immunology-related studies focused on the antagonistic role of SFTSV non-structural protein (NSs) in sequestering RIG-I-like-receptors (RLRs)-mediated type I interferon (IFN) induction and type I IFN mediated signaling pathway. It is still elusive whether the interaction of SFTSV and other conserved innate immune responses exists. As of now, no specific vaccines or therapeutics are approved for SFTSV prevention or treatments respectively, in part due to a lack of comprehensive understanding of the molecular interactions occurring between SFTSV and hosts. Hence, it is necessary to fully understand the host-virus interactions including antiviral responses and viral evasion mechanisms. In this review, we highlight the recent progress in understanding the pathogenesis of SFTS and speculate underlying novel mechanisms in response to SFTSV infection.

scholarly journals To TRIM or not to TRIM: the balance of host–virus interactions mediated by the ubiquitin system

2019 ◽  
Vol 100 (12) ◽  
pp. 1641-1662 ◽  
Author(s):  
Adam Hage ◽  
Ricardo Rajsbaum
Keyword(s):  
Innate Immunity ◽  
Viral Replication ◽  
Viral Infections ◽  
Ubiquitin Ligases ◽  
Innate Immune ◽  
Future Research ◽  
Post Translational Modifications ◽  
Ubiquitin System ◽  
Host Virus Interactions ◽  
Virus Interactions

The innate immune system responds rapidly to protect against viral infections, but an overactive response can cause harmful damage. To avoid this, the response is tightly regulated by post-translational modifications (PTMs). The ubiquitin system represents a powerful PTM machinery that allows for the reversible linkage of ubiquitin to activate and deactivate a target’s function. A precise enzymatic cascade of ubiquitin-activating, conjugating and ligating enzymes facilitates ubiquitination. Viruses have evolved to take advantage of the ubiquitin pathway either by targeting factors to dampen the antiviral response or by hijacking the system to enhance their replication. The tripartite motif (TRIM) family of E3 ubiquitin ligases has garnered attention as a major contributor to innate immunity. Many TRIM family members limit viruses either indirectly as components in innate immune signalling, or directly by targeting viral proteins for degradation. In spite of this, TRIMs and other ubiquitin ligases can be appropriated by viruses and repurposed as valuable tools in viral replication. This duality of function suggests a new frontier of research for TRIMs and raises new challenges for discerning the subtleties of these pro-viral mechanisms. Here, we review current findings regarding the involvement of TRIMs in host–virus interactions. We examine ongoing developments in the field, including novel roles for unanchored ubiquitin in innate immunity, the direct involvement of ubiquitin ligases in promoting viral replication, recent controversies on the role of ubiquitin and TRIM25 in activation of the pattern recognition receptor RIG-I, and we discuss the implications these studies have on future research directions.

scholarly journals The molecular footprints of COVID-19

2020 ◽  
Vol 45 (3) ◽  
pp. 241-248
Author(s):  
Engin Yilmaz ◽  
Yakut Akyön ◽  
Muhittin Serdar
Keyword(s):  
Reaction Time ◽  
Changing Environment ◽  
The Third ◽  
The Past ◽  
The People ◽  
The World ◽  
The Future ◽  
Host Virus Interactions ◽  
Virus Interactions

AbstractCOVID-19 is the third spread of animal coronavirus over the past two decades, resulting in a major epidemic in humans after SARS and MERS. COVID-19 is responsible of the biggest biological earthquake in the world. In the global fight against COVID-19 some serious mistakes have been done like, the countries’ misguided attempts to protect their economies, lack of international co-operation. These mistakes that the people had done in previous deadly outbreaks. The result has been a greater economic devastation and the collapse of national and international trust for all. In this constantly changing environment, if we have a better understanding of the host-virus interactions than we can be more prepared to the future deadly outbreaks. When encountered with a disease which the causative is unknown, the reaction time and the precautions that should be taken matters a great deal. In this review we aimed to reveal the molecular footprints of COVID-19 scientifically and to get an understanding of the pandemia. This review might be a highlight to the possible outbreaks.

scholarly journals Poxviral Strategies to Overcome Host Cell Apoptosis

Pathogens ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 6
Author(s):  
Chathura D. Suraweera ◽  
Mark G. Hinds ◽  
Marc Kvansakul
Keyword(s):  
Viral Infections ◽  
B Cell Lymphoma ◽  
Intrinsic Apoptosis ◽  
Host Cell Apoptosis ◽  
Successful Infection ◽  
Infected Cells ◽  
Host Virus Interactions ◽  
Almost All ◽  
Virus Interactions ◽  
Multicellular Organisms

Apoptosis is a form of cellular suicide initiated either via extracellular (extrinsic apoptosis) or intracellular (intrinsic apoptosis) cues. This form of programmed cell death plays a crucial role in development and tissue homeostasis in multicellular organisms and its dysregulation is an underlying cause for many diseases. Intrinsic apoptosis is regulated by members of the evolutionarily conserved B-cell lymphoma-2 (Bcl-2) family, a family that consists of pro- and anti-apoptotic members. Bcl-2 genes have also been assimilated by numerous viruses including pox viruses, in particular the sub-family of chordopoxviridae, a group of viruses known to infect almost all vertebrates. The viral Bcl-2 proteins are virulence factors and aid the evasion of host immune defenses by mimicking the activity of their cellular counterparts. Viral Bcl-2 genes have proved essential for the survival of virus infected cells and structural studies have shown that though they often share very little sequence identity with their cellular counterparts, they have near-identical 3D structures. However, their mechanisms of action are varied. In this review, we examine the structural biology, molecular interactions, and detailed mechanism of action of poxvirus encoded apoptosis inhibitors and how they impact on host–virus interactions to ultimately enable successful infection and propagation of viral infections.

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