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J Virol
2021 May 24;9512:. doi: 10.1128/JVI.00215-21.
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TLR5-Mediated Reactivation of Quiescent Ranavirus FV3 in Xenopus Peritoneal Macrophages.
Samanta M
,
Yim J
,
De Jesús Andino F
,
Paiola M
,
Robert J
.
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Ranaviruses such as frog virus 3 (FV3) are large double-stranded DNA (dsDNA) viruses causing emerging infectious diseases leading to extensive morbidity and mortality of amphibians and other ectothermic vertebrates worldwide. Among the hosts of FV3, some are highly susceptible, whereas others are resistant and asymptomatic carriers that can take part in disseminating the infectious virus. To date, the mechanisms involved in the processes of FV3 viral persistence associated with subclinical infection transitioning to lethal outbreaks remain unknown. Investigation in Xenopus laevis has revealed that in asymptomatic FV3 carrier animals, inflammation induced by heat-killed (HK) Escherichia coli stimulation can provoke the relapse of active infection. Since Toll-like receptors (TLRs) are critical for recognizing microbial molecular patterns, we investigated their possible involvement in inflammation-induced FV3 reactivation. Among the 10 different TLRs screened for changes in expression levels following FV3 infection and HK E. coli stimulation, only TLR5 and TLR22, both of which recognize bacterial products, showed differential expression, and only the TLR5 ligand flagellin was able to induce FV3 reactivation similarly to HK E. coli Furthermore, only the TLR5 ligand flagellin induced FV3 reactivation in peritoneal macrophages both in vitro and in vivo These data indicate that the TLR5 signaling pathway can trigger FV3 reactivation and suggest a role of secondary bacterial infections or microbiome alterations (stress or pollution) in initiating sudden deadly disease outbreaks in amphibian populations with detectable persistent asymptomatic ranavirus.IMPORTANCE This study in the amphibian Xenopus laevis provides new evidence of the critical role of macrophages in the persistence of ranaviruses in a quiescent state as well as in the reactivation of these pathogens into a virulent infection. Among the multiple microbial sensors expressed by macrophages, our data underscore the preponderant involvement of TLR5 stimulation in triggering the reactivation of quiescent FV3 in resident peritoneal macrophages, unveiling a mechanistic connection between the reactivation of persisting ranavirus infection and bacterial coinfection. This suggests a role for secondary bacterial infections or microbiome alterations (stress or pollution) in initiating sudden deadly disease outbreaks in amphibian populations with detectable persistent asymptomatic ranavirus.
Alvarez-Carbonell,
Toll-like receptor 3 activation selectively reverses HIV latency in microglial cells.
2017, Pubmed
Alvarez-Carbonell,
Toll-like receptor 3 activation selectively reverses HIV latency in microglial cells.
2017,
Pubmed
Brenes,
Transmission of ranavirus between ectothermic vertebrate hosts.
2014,
Pubmed
Chen,
Antiviral immunity in amphibians.
2011,
Pubmed
,
Xenbase
Chinchar,
Family Iridoviridae: poor viral relations no longer.
2009,
Pubmed
Chinchar,
Ranaviruses: not just for frogs.
2014,
Pubmed
Coutermarsh-Ott,
Beyond the inflammasome: regulatory NOD-like receptor modulation of the host immune response following virus exposure.
2016,
Pubmed
Daszak,
Emerging infectious diseases and amphibian population declines.
1999,
Pubmed
Duncan,
Viral determinants of HIV-1 macrophage tropism.
2011,
Pubmed
Flajnik,
Evolution of the MHC: antigenicity and unusual tissue distribution of Xenopus (frog) class II molecules.
1990,
Pubmed
,
Xenbase
Gargano,
Signaling through Toll-like receptors induces murine gammaherpesvirus 68 reactivation in vivo.
2009,
Pubmed
Grayfer,
Amphibian macrophage development and antiviral defenses.
2016,
Pubmed
,
Xenbase
Grayfer,
Colony-stimulating factor-1-responsive macrophage precursors reside in the amphibian (Xenopus laevis) bone marrow rather than the hematopoietic subcapsular liver.
2013,
Pubmed
,
Xenbase
Gregory,
Toll-like receptor signaling controls reactivation of KSHV from latency.
2009,
Pubmed
Hayashi,
The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5.
2001,
Pubmed
Hoverman,
Phylogeny, life history, and ecology contribute to differences in amphibian susceptibility to ranaviruses.
2011,
Pubmed
Huang,
The plasticity of dendritic cell responses to pathogens and their components.
2001,
Pubmed
Hyatt,
First identification of a ranavirus from green pythons (Chondropython viridis).
2002,
Pubmed
Iwakiri,
Epstein-Barr virus (EBV)-encoded small RNA is released from EBV-infected cells and activates signaling from Toll-like receptor 3.
2009,
Pubmed
Ji,
Thoroughly Remold the Localization and Signaling Pathway of TLR22.
2019,
Pubmed
Johnson,
Ranavirus infection of free-ranging and captive box turtles and tortoises in the United States.
2008,
Pubmed
Krah,
A simplified multiwell plate assay for the measurement of hepatitis A virus infectivity.
1991,
Pubmed
Leifer,
Molecular mechanisms of regulation of Toll-like receptor signaling.
2016,
Pubmed
Lester,
Toll-like receptors in antiviral innate immunity.
2014,
Pubmed
Li,
Molecular characterization of a fish-specific toll-like receptor 22 (TLR22) gene from common carp (Cyprinus carpio L.): Evolutionary relationship and induced expression upon immune stimulants.
2017,
Pubmed
Maclaine,
Pathogenesis of Bohle Iridovirus (Genus Ranavirus) in Experimentally Infected Juvenile Eastern Water Dragons ( Intellagama lesueurii lesueurii).
2019,
Pubmed
Morales,
Innate immune responses and permissiveness to ranavirus infection of peritoneal leukocytes in the frog Xenopus laevis.
2010,
Pubmed
,
Xenbase
Paria,
Toll-like receptor (TLR) 22, a non-mammalian TLR in Asian seabass, Lates calcarifer: Characterisation, ontogeny and inductive expression upon exposure with bacteria and ligands.
2018,
Pubmed
Price,
Collapse of amphibian communities due to an introduced Ranavirus.
2014,
Pubmed
Robert,
Xenopus laevis: a possible vector of Ranavirus infection?
2007,
Pubmed
,
Xenbase
Robert,
Inflammation-induced reactivation of the ranavirus Frog Virus 3 in asymptomatic Xenopus laevis.
2014,
Pubmed
,
Xenbase
Robert,
Xenopus as an experimental model for studying evolution of hsp--immune system interactions.
2004,
Pubmed
,
Xenbase
Schloegel,
Two amphibian diseases, chytridiomycosis and ranaviral disease, are now globally notifiable to the World Organization for Animal Health (OIE): an assessment.
2010,
Pubmed
Storfer,
Phylogenetic concordance analysis shows an emerging pathogen is novel and endemic.
2007,
Pubmed
Stöhr,
Ranavirus infections associated with skin lesions in lizards.
2013,
Pubmed
Teacher,
Evidence for directional selection at a novel major histocompatibility class I marker in wild common frogs (Rana temporaria) exposed to a viral pathogen (Ranavirus).
2009,
Pubmed
,
Xenbase
Widziolek,
Type I interferon-dependent response of zebrafish larvae during tilapia lake virus (TiLV) infection.
2021,
Pubmed
de Vries,
The pathogenesis of measles.
2012,
Pubmed
