scholarly journals Vitamin D modulation of innate immune responses to respiratory viral infections

2016 ◽  
Vol 27 (1) ◽  
pp. e1909 ◽  
Author(s):  
Mihnea T. Zdrenghea ◽  
Heidi Makrinioti ◽  
Cristina Bagacean ◽  
Andy Bush ◽  
Sebastian L. Johnston ◽  
...  
Keyword(s):  
Vitamin D ◽  
Immune Responses ◽  
Viral Infections ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Respiratory Viral Infections

scholarly journals Innate Immune Responses to Highly Pathogenic Coronaviruses and Other Significant Respiratory Viral Infections

2020 ◽  
Vol 11 ◽  
Author(s):  
Hanaa Ahmed-Hassan ◽  
Brianna Sisson ◽  
Rajni Kant Shukla ◽  
Yasasvi Wijewantha ◽  
Nicholas T. Funderburg ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infections ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Highly Pathogenic ◽  
Respiratory Viral Infections

scholarly journals Effect of Vitamin D Supplementation on Mycobacterium tuberculosis-Induced Innate Immune Responses in a Canadian Dené First Nations Cohort

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e40692 ◽  
Author(s):  
Linda Larcombe ◽  
Pamela Orr ◽  
Emily Turner-Brannen ◽  
Caroline R. Slivinski ◽  
Peter W. Nickerson ◽  
...  
Keyword(s):  
Vitamin D ◽  
Mycobacterium Tuberculosis ◽  
Immune Responses ◽  
First Nations ◽  
Vitamin D Supplementation ◽  
Innate Immune ◽  
Innate Immune Responses

scholarly journals Autophagy receptors as viral targets

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Päivi Ylä-Anttila
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Recent Progress ◽  
Viral Infections ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Host Interaction ◽  
Autophagic Degradation ◽  
Autophagy Inhibition

AbstractActivation of autophagy is part of the innate immune response during viral infections. Autophagy involves the sequestration of endogenous or foreign components from the cytosol within double-membraned vesicles and the delivery of their content to the lysosomes for degradation. As part of innate immune responses, this autophagic elimination of foreign components is selective and requires specialized cargo receptors that function as links between a tagged foreign component and the autophagic machinery. Pathogens have evolved ways to evade their autophagic degradation to promote their replication, and recent research has shown autophagic receptors to be an important and perhaps previously overlooked target of viral autophagy inhibition. This is a brief summary of the recent progress in knowledge of virus-host interaction in the context of autophagy receptors.

scholarly journals Changes in the mitochondrial network during ectromelia virus infection of permissive L929 cells.

2014 ◽  
Vol 61 (1) ◽  
Author(s):  
Karolina P Gregorczyk ◽  
Lidia Szulc-Dąbrowska ◽  
Zbigniew Wyżewski ◽  
Justyna Struzik ◽  
Marek Niemiałtowski
Keyword(s):  
Virus Infection ◽  
Immune Responses ◽  
Viral Infections ◽  
Innate Immune ◽  
Cellular Distribution ◽  
Mitochondrial Network ◽  
Innate Immune Responses ◽  
Ectromelia Virus ◽  
L929 Cells ◽  
A Cell

Mitochondria are extremely important organelles in the life of a cell. Recent studies indicate that mitochondria also play a fundamental role in the cellular innate immune mechanisms against viral infections. Moreover, mitochondria are able to alter their shape continuously through fusion and fission. These tightly regulated processes are activated or inhibited under physiological or pathological (e.g. viral infection) conditions to help restore homeostasis. However, many types of viruses, such as orthopoxviruses, have developed various strategies to evade the mitochondrial-mediated antiviral innate immune responses. Moreover, orthopoxviruses exploit the mitochondria for their survival. Such viral activity has been reported during vaccinia virus (VACV) infection. Our study shows that the Moscow strain of ectromelia virus (ECTV-MOS), an orthopoxvirus, alters the mitochondrial network in permissive L929 cells. Upon infection, the branching structure of the mitochondrial network collapses and becomes disorganized followed by destruction of mitochondrial tubules during the late stage of infection. Small, discrete mitochondria co-localize with progeny virions, close to the cell membrane. Furthermore, clustering of mitochondria is observed around viral factories, particularly between the nucleus and viroplasm. Our findings suggest that ECTV-MOS modulates mitochondrial cellular distribution during later stages of the replication cycle, probably enabling viral replication and/or assembly as well as transport of progeny virions inside the cell. However, this requires further investigation.

scholarly journals SAMHD1 suppresses innate immune responses to viral infections and inflammatory stimuli by inhibiting the NF-κB and interferon pathways

2018 ◽  
Vol 115 (16) ◽  
pp. E3798-E3807 ◽  
Author(s):  
Shuliang Chen ◽  
Serena Bonifati ◽  
Zhihua Qin ◽  
Corine St. Gelais ◽  
Karthik M. Kodigepalli ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infections ◽  
Inflammatory Responses ◽  
Sendai Virus ◽  
Innate Immune ◽  
Type I ◽  
Innate Immune Responses ◽  
Monocytic Cells ◽  
Intracellular Dntp ◽  
Inflammatory Stimuli

Sterile alpha motif and HD-domain–containing protein 1 (SAMHD1) blocks replication of retroviruses and certain DNA viruses by reducing the intracellular dNTP pool. SAMHD1 has been suggested to down-regulate IFN and inflammatory responses to viral infections, although the functions and mechanisms of SAMHD1 in modulating innate immunity remain unclear. Here, we show that SAMHD1 suppresses the innate immune responses to viral infections and inflammatory stimuli by inhibiting nuclear factor-κB (NF-κB) activation and type I interferon (IFN-I) induction. Compared with control cells, infection of SAMHD1-silenced human monocytic cells or primary macrophages with Sendai virus (SeV) or HIV-1, or treatment with inflammatory stimuli, induces significantly higher levels of NF-κB activation and IFN-I induction. Exogenous SAMHD1 expression in cells or SAMHD1 reconstitution in knockout cells suppresses NF-κB activation and IFN-I induction by SeV infection or inflammatory stimuli. Mechanistically, SAMHD1 inhibits NF-κB activation by interacting with NF-κB1/2 and reducing phosphorylation of the NF-κB inhibitory protein IκBα. SAMHD1 also interacts with the inhibitor-κB kinase ε (IKKε) and IFN regulatory factor 7 (IRF7), leading to the suppression of the IFN-I induction pathway by reducing IKKε-mediated IRF7 phosphorylation. Interactions of endogenous SAMHD1 with NF-κB and IFN-I pathway proteins were validated in human monocytic cells and primary macrophages. Comparing splenocytes from SAMHD1 knockout and heterozygous mice, we further confirmed SAMHD1-mediated suppression of NF-κB activation, suggesting an evolutionarily conserved property of SAMHD1. Our findings reveal functions of SAMHD1 in down-regulating innate immune responses to viral infections and inflammatory stimuli, highlighting the importance of SAMHD1 in modulating antiviral immunity.

scholarly journals Cord Blood Vitamin D Status Impacts Innate Immune Responses

2011 ◽  
Vol 96 (6) ◽  
pp. 1835-1843 ◽  
Author(s):  
Valencia P. Walker ◽  
Xiaoran Zhang ◽  
Ida Rastegar ◽  
Philip T. Liu ◽  
Bruce W. Hollis ◽  
...  
Keyword(s):  
Vitamin D ◽  
Immune Responses ◽  
Cord Blood ◽  
Innate Immune ◽  
Vitamin D Status ◽  
Innate Immune Responses

scholarly journals Involvement of the TRPML Mucolipin Channels in Viral Infections and Anti-viral Innate Immune Responses

2020 ◽  
Vol 11 ◽  
Author(s):  
Giorgio Santoni ◽  
Maria Beatrice Morelli ◽  
Consuelo Amantini ◽  
Massimo Nabissi ◽  
Matteo Santoni ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infections ◽  
Innate Immune ◽  
Innate Immune Responses
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