Novel Biomolecules Modulating Innate Immune Responses against Virus Infection
The innate immune response against viruses is fundamental for the host to survive infections. Foreign viral pathogens are sensed by a set of germline-encoded pattern-recognition receptors triggering a rapid response, including a variety of defense mechanisms, such as DNA damage response, cellular stress response pathways, inflammasome pathways or regulated cell death responses. Central to the innate host defense is the type I interferon pathway inducing antiviral proteins to control infection and alert other cells. These innate responses are observed at the intra-cellular, tissue and systemic level. The responses not only include the activity of proteins, positive and negative regulators of the innate signaling cascades, but are also regulated by lipids, polysaccharides, nucleic acids and other metabolites.
This Special Issue aims to highlight novel involvement of all kinds of biomolecules in the innate response to mammalian virus infections, including, but not limited to, second messengers, miRNAs, nucleotides and novel cellular factors. These biomolecules may modulate intracellular innate signaling, affect cell–cell communication or change the biology of the host cell. The biomolecules could interfere with cellular signaling responding to viruses, could directly target or repress viruses at any stage or indirectly regulate dependency or restricting proteins or protein complexes.
We encourage the submission of reviews but also welcome original research papers.
- constitutive and induced expression of antiviral factors
- mediators of cell resistance
- biomolecules mediating system- or tissue-wide innate response
- biomolecules regulating the innate response
|Journal Name||Impact Factor||CiteScore||Launched Year||First Decision (median)||APC|
|5.5||8.3||2011||19.2 Days||CHF 2700|
|3.7||5.1||2012||16.4 Days||CHF 2700|
|4.3||9.6||2015||17.9 Days||CHF 1600|
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Published Papers (7 papers)
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Abstract: The highly conserved trans-acting response element (TAR) present in the RNA genome of human immunodeficiency virus 1 (HIV-1) is a stably folded hairpin structure involved in viral replication. However, TAR is also sensed by viral sensors, leading to antiviral immunity. While high variation in the TAR RNA structure renders the virus replication incompetent, effects on viral sensing remain unclear. Here, we investigated the role of TAR RNA structure and stability on viral sensing. TAR mutants with deletions in the TAR hairpin that enhanced thermodynamic stability increased antiviral responses. Strikingly, TAR mutants with lower stability due to destabilization of the TAR hairpin also increased antiviral responses without affecting pro-inflammatory responses. Moreover, mutations that affected the TAR RNA sequence also enhanced specific antiviral responses. Our data suggest that mutations in TAR of replication-incompetent viruses can still induce immune responses via viral sensors, hereby underscoring the robustness of HIV-1 RNA sensing mechanisms.
Melissa Stunnenberg1, John L. van Hamme1, Atze T. Das2, Ben Berkhout2 and Teunis B.H. Geijtenbeek1
1Amsterdam UMC, University of Amsterdam, Department of Experimental Immunology, Amsterdam Institute for Infection & Immunity, Meibergdreef 9, Amsterdam, Netherlands.
2Amsterdam UMC, University of Amsterdam, Laboratory of Experimental Virology, Department of Medical Microbiology, Meibergdreef 9, Amsterdam, Netherlands.