Innate immune responses of salmonid fish to viral infections

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.

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

Acta Biochimica Polonica ◽

10.18388/abp.2014_1940 ◽

2014 ◽

Vol 61 (1) ◽

Cited By ~ 4

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.

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

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1801213115 ◽

2018 ◽

Vol 115 (16) ◽

pp. E3798-E3807 ◽

Cited By ~ 34

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.

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Innate Immune Responses to Viral Infections

Viral Immunology ◽

10.1089/vim.2014.1501 ◽

2014 ◽

Vol 27 (4) ◽

pp. 139-139

Author(s):

David L. Woodland

Keyword(s):

Immune Responses ◽

Viral Infections ◽

Innate Immune ◽

Innate Immune Responses

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

Frontiers in Immunology ◽

10.3389/fimmu.2020.00739 ◽

2020 ◽

Vol 11 ◽

Cited By ~ 2

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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Dissection of measles virus V protein in relation to its ability to block alpha/beta interferon signal transduction

Journal of General Virology ◽

10.1099/vir.0.80308-0 ◽

2004 ◽

Vol 85 (10) ◽

pp. 2991-2999 ◽

Cited By ~ 106

Author(s):

Shinji Ohno ◽

Nobuyuki Ono ◽

Makoto Takeda ◽

Kaoru Takeuchi ◽

Yusuke Yanagi

Keyword(s):

Immune Responses ◽

Measles Virus ◽

Viral Infections ◽

Terminal Region ◽

Innate Immune ◽

Innate Immune Responses ◽

Wild Type ◽

Antagonist Activity ◽

V Protein ◽

P Protein

Interferon (IFN)-α and -β are the main cytokines for innate immune responses against viral infections. To replicate efficiently in the hosts, viruses have evolved various countermeasures to the IFN response. The V protein of measles virus (MV) has been shown to block IFN-α/β signalling. Here, the wild-type IC-B strain of MV was shown to grow comparably in the presence and absence of IFN-α, whereas replication of the Edmonston tag strain recovered from cloned DNA was strongly suppressed in its presence. The V protein of the IC-B strain, but not the Edmonston tag strain, blocked IFN-α signalling. The V protein of the Edmonston strain from the ATCC also inhibited IFN-α signalling. There were three amino acid differences between the V proteins of the Edmonston ATCC and tag strains, and substitutions of both residues at positions 110 and 272 were required for the Edmonston ATCC V protein to lose IFN-antagonist activity. The P protein of the IC-B strain, which shares the N-terminal 231 aa residues with the V protein, also inhibited IFN-α signalling. Indeed, fragments comprising only those 231 residues of the IC-B and Edmonston ATCC V proteins, but not the Edmonston tag V protein, were able to block IFN-α signalling. However, the N-terminal region of the Edmonston tag V protein, when attached to the C-terminal region of the Edmonston ATCC V protein, inhibited IFN-α signalling. Taken together, our results indicate that both the N- and C-terminal regions contribute to the IFN-antagonist activity of the MV V protein.

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Immunity and Viral Infections: Modulating Antiviral Response via CRISPR–Cas Systems

Viruses ◽

10.3390/v13071373 ◽

2021 ◽

Vol 13 (7) ◽

pp. 1373

Author(s):

Sergey Brezgin ◽

Anastasiya Kostyusheva ◽

Ekaterina Bayurova ◽

Elena Volchkova ◽

Vladimir Gegechkori ◽

...

Keyword(s):

Infectious Diseases ◽

Immune Responses ◽

Viral Infections ◽

Antiviral Agents ◽

Innate Immune ◽

Host Factors ◽

Innate Immune Responses ◽

Host Interactions ◽

Translational Studies ◽

Short Time

Viral infections cause a variety of acute and chronic human diseases, sometimes resulting in small local outbreaks, or in some cases spreading across the globe and leading to global pandemics. Understanding and exploiting virus–host interactions is instrumental for identifying host factors involved in viral replication, developing effective antiviral agents, and mitigating the severity of virus-borne infectious diseases. The diversity of CRISPR systems and CRISPR-based tools enables the specific modulation of innate immune responses and has contributed impressively to the fields of virology and immunology in a very short time. In this review, we describe the most recent advances in the use of CRISPR systems for basic and translational studies of virus–host interactions.

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