The Amphibian (Xenopus laevis) Type I Interferon Response to Frog Virus 3: New Insight into Ranavirus Pathogenicity

The global amphibian declines are compounded by ranavirus infections such as Frog Virus 3 (FV3), and amphibian tadpoles more frequently succumb to these pathogens than adult animals. Amphibian gastrointestinal tracts represent a major route of ranavirus entry, and viral pathogenesis often leads to hemorrhaging and necrosis within this tissue. Alas, the differences between tadpole and adult amphibian immune responses to intestinal ranavirus infections remain poorly defined. As interferon (IFN) cytokine responses represent a cornerstone of vertebrate antiviral immunity, it is pertinent that the tadpoles and adults of the anuran Xenopus laevis frog mount disparate IFN responses to FV3 infections. Presently, we compared the tadpole and adult X. laevis responses to intestinal FV3 infections. Our results indicate that FV3-challenged tadpoles mount more robust intestinal type I and III IFN responses than adult frogs. These tadpole antiviral responses appear to be mediated by myeloid cells, which are recruited into tadpole intestines in response to FV3 infections. Conversely, myeloid cells bearing similar cytology already reside within the intestines of healthy (uninfected) adult frogs, possibly accounting for some of the anti-FV3 resistance of these animals. Further insight into the differences between tadpole and adult frog responses to ranaviral infections is critical to understanding the facets of susceptibility and resistance to these pathogens.

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Molecular Insight Into the IRE1α-Mediated Type I Interferon Response Induced by Proteasome Impairment in Myeloid Cells of the Brain

Frontiers in Immunology ◽

10.3389/fimmu.2019.02900 ◽

2019 ◽

Vol 10 ◽

Cited By ~ 3

Author(s):

Maja Studencka-Turski ◽

Gonca Çetin ◽

Heike Junker ◽

Frédéric Ebstein ◽

Elke Krüger

Keyword(s):

Type I Interferon ◽

Myeloid Cells ◽

Interferon Response ◽

Type I ◽

The Brain ◽

Insight Into

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Faculty Opinions recommendation of Lymphotoxin-mediated crosstalk between B cells and splenic stroma promotes the initial type I interferon response to cytomegalovirus.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1104493.560531 ◽

2008 ◽

Author(s):

Ann Hill

Keyword(s):

B Cells ◽

Type I Interferon ◽

Interferon Response ◽

Type I

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Faculty Opinions recommendation of USP15 regulates type I interferon response and is required for pathogenesis of neuroinflammation.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.726829800.793527398 ◽

2017 ◽

Author(s):

Benedict Michael ◽

Mark Ellul

Keyword(s):

Type I Interferon ◽

Interferon Response ◽

Type I

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Viral Invasion and Type I Interferon Response Characterize the Immunophenotypes during COVID-19 Infection

SSRN Electronic Journal ◽

10.2139/ssrn.3555695 ◽

2020 ◽

Cited By ~ 8

Author(s):

Lai Wei ◽

Siqi Ming ◽

Bin Zou ◽

Yongjian Wu ◽

Zhongsi Hong ◽

...

Keyword(s):

Type I Interferon ◽

Interferon Response ◽

Type I

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Positive natural selection in primate genes of the type I interferon response

BMC Ecology and Evolution ◽

10.1186/s12862-021-01783-z ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Elena N. Judd ◽

Alison R. Gilchrist ◽

Nicholas R. Meyerson ◽

Sara L. Sawyer

Keyword(s):

Natural Selection ◽

Positive Selection ◽

Type I Interferon ◽

Interferon Response ◽

Type I ◽

Sequence Alignments ◽

Multiple Sequence ◽

Multiple Sequence Alignments ◽

Interferon Stimulated Genes ◽

Interferon Induction

Abstract Background The Type I interferon response is an important first-line defense against viruses. In turn, viruses antagonize (i.e., degrade, mis-localize, etc.) many proteins in interferon pathways. Thus, hosts and viruses are locked in an evolutionary arms race for dominance of the Type I interferon pathway. As a result, many genes in interferon pathways have experienced positive natural selection in favor of new allelic forms that can better recognize viruses or escape viral antagonists. Here, we performed a holistic analysis of selective pressures acting on genes in the Type I interferon family. We initially hypothesized that the genes responsible for inducing the production of interferon would be antagonized more heavily by viruses than genes that are turned on as a result of interferon. Our logic was that viruses would have greater effect if they worked upstream of the production of interferon molecules because, once interferon is produced, hundreds of interferon-stimulated proteins would activate and the virus would need to counteract them one-by-one. Results We curated multiple sequence alignments of primate orthologs for 131 genes active in interferon production and signaling (herein, “induction” genes), 100 interferon-stimulated genes, and 100 randomly chosen genes. We analyzed each multiple sequence alignment for the signatures of recurrent positive selection. Counter to our hypothesis, we found the interferon-stimulated genes, and not interferon induction genes, are evolving significantly more rapidly than a random set of genes. Interferon induction genes evolve in a way that is indistinguishable from a matched set of random genes (22% and 18% of genes bear signatures of positive selection, respectively). In contrast, interferon-stimulated genes evolve differently, with 33% of genes evolving under positive selection and containing a significantly higher fraction of codons that have experienced selection for recurrent replacement of the encoded amino acid. Conclusion Viruses may antagonize individual products of the interferon response more often than trying to neutralize the system altogether.

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