The interplay between viruses and the immune system of bats

2017 ◽  
Vol 38 (1) ◽  
pp. 30
Author(s):  
Stacey Leech ◽  
Michelle L Baker
Keyword(s):  
Immune System ◽  
Viral Replication ◽  
Viral Infections ◽  
Clinical Signs ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Highly Pathogenic ◽  
Vertebrate Hosts ◽  
And Migration ◽  
Respiratory Coronavirus

Bats are an abundant and diverse group of mammals with an array of unique characteristics, including their well-known roles as natural reservoirs for a variety of viruses. These include the deadly zoonotic paramyxoviruses; Hendra (HeV) and Nipah (NiV)1,2, lyssaviruses3, coronaviruses such as severe acute respiratory coronavirus (SARS-CoV)4 and filoviruses such as Marburg5. Although these viruses are highly pathogenic in other species, including humans, bats rarely show clinical signs of disease whilst maintaining the ability to transmit virus to susceptible vertebrate hosts. In addition, bats are capable of clearing experimental infections with henipaviruses, filoviruses and lyssaviruses at doses of infection that are lethal in other mammals6–12. Curiously, the ability of bats to tolerate viral infections does not appear to extend to extracellular pathogens such as bacteria, fungi and parasites13. Over the past few years, considerable headway has been made into elucidating the mechanisms responsible for the ability of bats to control viral replication, with evidence for unique differences in the innate immune responses of bats14–20. However, many questions remain around mechanisms responsible for the ability of bats to co-exist with viruses, including their ability to tolerate constitutive immune activation, the triggers associated with viral spillover events and the sites of viral replication. Although bats appear to have all of the major components of the immune system present in other species, their unique ecological characteristics (including flight, high density populations and migration) combined with their long co-evolutionary history with viruses has likely shaped their immune response resulting in an equilibrium between the host and its pathogens.

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 Commensal and Opportunistic Bacteria Present in the Microbiota in Atlantic Cod (Gadus morhua) Larvae Differentially Alter the Hosts’ Innate Immune Responses

2021 ◽  
Vol 10 (1) ◽  
pp. 24
Author(s):  
Ragnhild Inderberg Vestrum ◽  
Torunn Forberg ◽  
Birgit Luef ◽  
Ingrid Bakke ◽  
Per Winge ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Atlantic Cod ◽  
Innate Immune ◽  
Rrna Gene ◽  
Innate Immune Responses ◽  
Transcriptional Responses ◽  
Gut Morphology ◽  
Germ Free ◽  
Opportunistic Bacteria

The roles of host-associated bacteria have gained attention lately, and we now recognise that the microbiota is essential in processes such as digestion, development of the immune system and gut function. In this study, Atlantic cod larvae were reared under germ-free, gnotobiotic and conventional conditions. Water and fish microbiota were characterised by 16S rRNA gene analyses. The cod larvae’s transcriptional responses to the different microbial conditions were analysed by a custom Agilent 44 k oligo microarray. Gut development was assessed by transmission electron microscopy (TEM). Water and fish microbiota differed significantly in the conventional treatment and were dominated by different fast-growing bacteria. Our study indicates that components of the innate immune system of cod larvae are downregulated by the presence of non-pathogenic bacteria, and thus may be turned on by default in the early larval stages. We see indications of decreased nutrient uptake in the absence of bacteria. The bacteria also influence the gut morphology, reflected in shorter microvilli with higher density in the conventional larvae than in the germ-free larvae. The fact that the microbiota alters innate immune responses and gut morphology demonstrates its important role in marine larval development.

scholarly journals Mitochondria surveillance systems trigger innate immune responses to bacterial pathogens via AMPK pathway in C. elegans

2020 ◽  
Author(s):  
Shouyong Ju ◽  
Hanqiao Chen ◽  
Shaoying Wang ◽  
Jian Lin ◽  
Raffi V Aroian ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Innate Immune ◽  
Surveillance Systems ◽  
Innate Immune Responses ◽  
Energy Status ◽  
Microbial Infection ◽  
C Elegans ◽  
Host Interaction ◽  
Intracellular Energy

AbstractPathogen recognition and triggering pattern of host innate immune system is critical to understanding pathogen-host interaction. It is generally accepted that the microbial infection can be recognized by host via pattern-triggered immunity (PTI) or effector-triggered immunity (ETI) responses. Recently, non-PRR-mediated cellular surveillance systems have been reported as an important supplement strategy to PTI and ETI responses. However, the mechanism of how surveillance systems sense pathogens and trigger innate immune responses is largely unknown. In the present study, using Bacillus thuringiensis-Caenorhabditis elegans as a model, we found a new approach for surveillance systems to sense the pathogens through no-PPRs patterns. We reported C. elegans can monitor intracellular energy status through the mitochondrial surveillance system to triggered innate immune responses against pathogenic attack via AMP-activated protein kinase (AMPK). Consider that the mitochondria surveillance systems and AMPK are conserved components from worms to mammals, our study suggests that disrupting mitochondrial homeostasis to activate the immune system through AMPK-dependent pathways may widely existing in animals.

scholarly journals The neuropeptide receptor NMUR-1 regulates the specificity of C. elegans innate immunity against pathogen infection

2021 ◽  
Author(s):  
Phillip Wibisono ◽  
Shawndra Wibisono ◽  
Jan Watteyne ◽  
Chia-Hui Chen ◽  
Durai Sellegounder ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Immune Responses ◽  
Adaptive Immune System ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Immune Genes ◽  
C Elegans ◽  
Adaptive Immune ◽  
Functional Assays

A key question in current immunology is how the innate immune system generates high levels of specificity. Like most invertebrates, Caenorhabditis elegans does not have an adaptive immune system and relies solely on innate immunity to defend itself against pathogen attacks, yet it can still differentiate different pathogens and launch distinct innate immune responses. Here, we have found that functional loss of NMUR-1, a neuronal GPCR homologous to mammalian receptors for the neuropeptide neuromedin U, has diverse effects on C. elegans survival against various bacterial pathogens. Transcriptomic analyses and functional assays revealed that NMUR-1 modulates C. elegans transcription activity by regulating the expression of transcription factors, which, in turn, controls the expression of distinct immune genes in response to different pathogens. Our study has uncovered a molecular basis for the specificity of C. elegans innate immunity that could provide mechanistic insights into understanding the specificity of vertebrate innate immunity.

Cellular and molecular insights on the regulation of innate immune responses to experimental aspergillosis in chicken and turkey poults

2020 ◽  
Author(s):  
Tobias Vahsen ◽  
Laura Zapata ◽  
Rodrigo Guabiraba ◽  
Elise Melloul ◽  
Nathalie Cordonnier ◽  
...  
Keyword(s):  
Immune Responses ◽  
Aspergillus Fumigatus ◽  
Inflammatory Responses ◽  
Clinical Signs ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Lung Lesions ◽  
Turkey Poults ◽  
Cd8 T Lymphocyte ◽  
Fungal Immunity

Abstract Across the world, many commercial poultry flocks and captive birds are threatened by infection with Aspergillus fumigatus. Susceptibility to aspergillosis varies among birds; among galliform birds specifically, morbidity and mortality rates seem to be greater in turkeys than in chickens. Little is known regarding the features of avian immune responses after inhalation of Aspergillus conidia, and to date, scarce information on inflammatory responses during aspergillosis exists. Thus, in the present study, we aimed to improve our understanding of the interactions between A. fumigatus and economically relevant galliform birds in terms of local innate immune responses. Intra-tracheal aerosolization of A. fumigatus conidia in turkey and chicken poults led to more severe clinical signs and lung lesions in turkeys, but leukocyte recovery from lung lavages was higher in chickens at 1dpi only. Interestingly, only chicken CD8+ T lymphocyte proportions increased after infection. Furthermore, the lungs of infected chickens showed an early upregulation of pro-inflammatory cytokines, including IL-1β, IFN-γ and IL-6, whereas in turkeys, most of these cytokines showed a downregulation or a delayed upregulation. These results confirmed the importance of an early pro-inflammatory response to ensure the development of an appropriate anti-fungal immunity to avoid Aspergillus dissemination in the respiratory tract. In conclusion, we show for the first time that differences in local innate immune responses between chickens and turkeys during aspergillosis may determine the outcome of the disease. Lay Summary Aspergillus fumigatus infection may cause mortality in poultry, depending on species sensitivity. This study confirms the earlier activation of chickens’ pro-inflammatory effectors to control Aspergillus dissemination, whereas turkeys’ immune response enables the exacerbation of lung lesions.

scholarly journals Lassa Virus, but Not Highly Pathogenic New World Arenaviruses, Restricts Immunostimulatory Double-Stranded RNA Accumulation during Infection

2020 ◽  
Vol 94 (9) ◽  
Author(s):  
Elizabeth J. Mateer ◽  
Junki Maruyama ◽  
Galen E. Card ◽  
Slobodan Paessler ◽  
Cheng Huang
Keyword(s):  
Immune Responses ◽  
Innate Immune ◽  
Lassa Virus ◽  
Innate Immune Responses ◽  
Highly Pathogenic ◽  
Double Stranded Rna ◽  
L Protein ◽  
Biochemical Assays ◽  
Infected Cells ◽  
First Time

ABSTRACT The arenaviruses Lassa virus (LASV), Junín virus (JUNV), and Machupo virus (MACV) can cause severe and fatal diseases in humans. Although these pathogens are closely related, the host immune responses to these virus infections differ remarkably, with direct implications for viral pathogenesis. LASV infection is immunosuppressive, with a very low-level interferon response. In contrast, JUNV and MACV infections stimulate a robust interferon (IFN) response in a retinoic acid-inducible gene I (RIG-I)-dependent manner and readily activate protein kinase R (PKR), a known host double-stranded RNA (dsRNA) sensor. In response to infection with RNA viruses, host nonself RNA sensors recognize virus-derived dsRNA as danger signals and initiate innate immune responses. Arenavirus nucleoproteins (NPs) contain a highly conserved exoribonuclease (ExoN) motif, through which LASV NP has been shown to degrade virus-derived immunostimulatory dsRNA in biochemical assays. In this study, we for the first time present evidence that LASV restricts dsRNA accumulation during infection. Although JUNV and MACV NPs also have the ExoN motif, dsRNA readily accumulated in infected cells and often colocalized with dsRNA sensors. Moreover, LASV coinfection diminished the accumulation of dsRNA and the IFN response in JUNV-infected cells. The disruption of LASV NP ExoN with a mutation led to dsRNA accumulation and impaired LASV replication in minigenome systems. Importantly, both LASV NP and RNA polymerase L protein were required to diminish the accumulation of dsRNA and the IFN response in JUNV infection. For the first time, we discovered a collaboration between LASV NP ExoN and L protein in limiting dsRNA accumulation. Our new findings provide mechanistic insights into the differential host innate immune responses to highly pathogenic arenavirus infections. IMPORTANCE Arenavirus NPs contain a highly conserved DEDDh ExoN motif, through which LASV NP degrades virus-derived, immunostimulatory dsRNA in biochemical assays to eliminate the danger signal and inhibit the innate immune response. Nevertheless, the function of NP ExoN in arenavirus infection remains to be defined. In this study, we discovered that LASV potently restricts dsRNA accumulation during infection and minigenome replication. In contrast, although the NPs of JUNV and MACV also harbor the ExoN motif, dsRNA readily formed during JUNV and MACV infections, accompanied by IFN and PKR responses. Interestingly, LASV NP alone was not sufficient to limit dsRNA accumulation. Instead, both LASV NP and L protein were required to restrict immunostimulatory dsRNA accumulation. Our findings provide novel and important insights into the mechanism for the distinct innate immune response to these highly pathogenic arenaviruses and open new directions for future studies.

scholarly journals Canonical and Noncanonical Autophagy as Potential Targets for COVID-19

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1619 ◽  
Author(s):  
Melissa Bello-Perez ◽  
Isabel Sola ◽  
Beatriz Novoa ◽  
Daniel J. Klionsky ◽  
Alberto Falco
Keyword(s):  
Molecular Mechanisms ◽  
Viral Infections ◽  
Current Knowledge ◽  
Therapeutic Targets ◽  
Innate Immune ◽  
Interacting Proteins ◽  
Innate Immune Responses ◽  
Molecular Machinery ◽  
Autophagy Pathway

The SARS-CoV-2 pandemic necessitates a review of the molecular mechanisms underlying cellular infection by coronaviruses, in order to identify potential therapeutic targets against the associated new disease (COVID-19). Previous studies on its counterparts prove a complex and concomitant interaction between coronaviruses and autophagy. The precise manipulation of this pathway allows these viruses to exploit the autophagy molecular machinery while avoiding its protective apoptotic drift and cellular innate immune responses. In turn, the maneuverability margins of such hijacking appear to be so narrow that the modulation of the autophagy, regardless of whether using inducers or inhibitors (many of which are FDA-approved for the treatment of other diseases), is usually detrimental to viral replication, including SARS-CoV-2. Recent discoveries indicate that these interactions stretch into the still poorly explored noncanonical autophagy pathway, which might play a substantial role in coronavirus replication. Still, some potential therapeutic targets within this pathway, such as RAB9 and its interacting proteins, look promising considering current knowledge. Thus, the combinatory treatment of COVID-19 with drugs affecting both canonical and noncanonical autophagy pathways may be a turning point in the fight against this and other viral infections, which may also imply beneficial prospects of long-term protection.

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 Mechanisms of Severe Acute Respiratory Syndrome Pathogenesis and Innate Immunomodulation

2008 ◽  
Vol 72 (4) ◽  
pp. 672-685 ◽  
Author(s):  
Matthew Frieman ◽  
Ralph Baric
Keyword(s):  
Innate Immune ◽  
Open Reading Frames ◽  
Innate Immune Responses ◽  
Highly Pathogenic ◽  
Host Interactions ◽  
Host Cell Signaling ◽  
Robust Model ◽  
Pathogenic Viruses ◽  
End Stage ◽  
Reading Frames

SUMMARY The modulation of the immune response is a common practice of many highly pathogenic viruses. The emergence of the highly pathogenic coronavirus severe acute respiratory virus (SARS-CoV) serves as a robust model system to elucidate the virus-host interactions that mediate severe end-stage lung disease in humans and animals. Coronaviruses encode the largest positive-sense RNA genome of ∼30 kb, encode a variety of replicase and accessory open reading frames that are structurally unique, and encode novel enzymatic functions among RNA viruses. These viruses have broad or specific host ranges, suggesting the possibility of novel strategies for targeting and regulating host innate immune responses following virus infection. Using SARS-CoV as a model, we review the current literature on the ability of coronaviruses to interact with and modify the host intracellular environment during infection. These studies are revealing a rich set of novel viral proteins that engage, modify, and/or disrupt host cell signaling and nuclear import machinery for the benefit of virus replication.

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