Ranavirus Host Immunity and Immune Evasion

Grayfer, Leon; Edholm, Eva-Stina; Andino, Francisco De Jesús; Chinchar, V. Gregory; Robert, Jacques

doi:10.1007/978-3-319-13755-1_6

Cited by 29 publications

(35 citation statements)

References 141 publications

(192 reference statements)

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“…Ranaviruses persist and propagate through complex interactions between host cells and immune responses (Grayfer et al 2015). Cotter et al (2008) reported >100 up-and down-regulated genes in A. mexicanum following exposure to ATV.…”

Section: Figurementioning

confidence: 99%

“…Cotter et al (2008) reported >100 up-and down-regulated genes in A. mexicanum following exposure to ATV. Some proteins that are encoded by FV3 immune evasion genes include vIF-2a, vCARD, and dUPTase (Grayfer et al 2015). Temperaturedependent synthesis of the immune evasion proteins has not been investigated for FV3; however, it is known to occur in other pathogens (Loh et al 2013).…”

Section: Figurementioning

confidence: 99%

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Water Temperature Affects Susceptibility to Ranavirus

et al. 2016

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The occurrence of emerging infectious diseases in wildlife populations is increasing, and changes in environmental conditions have been hypothesized as a potential driver. For example, warmer ambient temperatures might favor pathogens by providing more ideal conditions for propagation or by stressing hosts. Our objective was to determine if water temperature played a role in the pathogenicity of an emerging pathogen (ranavirus) that infects ectothermic vertebrate species. We exposed larvae of four amphibian species to a Frog Virus 3 (FV3)-like ranavirus at two temperatures (10 and 25°C). We found that FV3 copies in tissues and mortality due to ranaviral disease were greater at 25°C than at 10°C for all species. In a second experiment with wood frogs (Lithobates sylvaticus), we found that a 2°C change (10 vs. 12°C) affected ranaviral disease outcomes, with greater infection and mortality at 12°C. There was evidence that 10°C stressed Cope's gray tree frog (Hyla chrysoscelis) larvae, which is a species that breeds during summer-all individuals died at this temperature, but only 10% tested positive for FV3 infection. The greater pathogenicity of FV3 at 25°C might be related to faster viral replication, which in vitro studies have reported previously. Colder temperatures also may decrease systemic infection by reducing blood circulation and the proportion of phagocytes, which are known to disseminate FV3 through the body. Collectively, our results indicate that water temperature during larval development may play a role in the emergence of ranaviruses.

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Section: Figurementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Water Temperature Affects Susceptibility to Ranavirus

et al. 2016

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“…This is consistent with an active involvement bone marrow in X. laevis monopoiesis. The robust upregulation of CSF-1R mRNA levels in the bone marrow, induced by stimulation with heat-killed E. coli further substantiates this possibility (Grayfer et al, 2015). Based on the literature and our recent studies, we predict that several adult X. laevis organs including the spleen, liver and bone marrow are involved in monopoiesis.…”

Section: Monopoiesis In Anuramentioning

confidence: 80%

“…Interestingly, upon infection with the ranavirus Frog Virus 3 (FV3, discussed in detail in section 4), X. laevis adults exhibit increased CSF-1R gene expression in kidneys, which is consistent with the recruitment of mononuclear phagocytes (bearing the CSF-1R) to this site of prominent FV3 replication (Grayfer et al, 2015). Moreover, while FV3-infected X. laevis tadpoles increase their splenic and hepatic CSF-1R gene expression, the FV3-challenged adult frogs do not (Grayfer et al, 2015), suggesting that these tadpole and adult organs have distinct roles in monopoiesis.…”

Section: Monopoiesis In Anuramentioning

confidence: 84%

“…Moreover, while FV3-infected X. laevis tadpoles increase their splenic and hepatic CSF-1R gene expression, the FV3-challenged adult frogs do not (Grayfer et al, 2015), suggesting that these tadpole and adult organs have distinct roles in monopoiesis. Indeed, although FV3 does not substantially disseminate into the bone marrow (Grayfer and Robert, 2013), CSF-1R gene expression significantly increases within this site during infection (Grayfer et al, 2015). This is consistent with an active involvement bone marrow in X. laevis monopoiesis.…”

Section: Monopoiesis In Anuramentioning

confidence: 99%

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Amphibian macrophage development and antiviral defenses

Grayfer

Robert

2016

Developmental & Comparative Immunology

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Macrophage lineage cells represent the cornerstone of vertebrate physiology and immune defenses. In turn, comparative studies using non-mammalian animal models have revealed that evolutionarily distinct species have adopted diverse molecular and physiological strategies for controlling macrophage development and functions. Notably, amphibian species present a rich array of physiological and environmental adaptations, not to mention the peculiarity of metamorphosis from larval to adult stages of development, involving drastic transformation and differentiation of multiple new tissues. Thus it is not surprising that different amphibian species and their respective tadpole and adult stages have adopted unique hematopoietic strategies. Accordingly and in order to establish a more comprehensive view of these processes, here we review the hematopoietic and monopoietic strategies observed across amphibians, describe the present understanding of the molecular mechanisms driving amphibian, an in particular Xenopus laevis macrophage development and functional polarization, and discuss the roles of macrophage-lineage cells during ranavirus infections.

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Introduction: History and Future of Ranaviruses

Gray¹,

Chinchar

2015

Ranaviruses

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What a wonderful bird the frog areWhen he stand he sit almost ; When he hop , he fl y almost . He ain ' t got no sense hardly ; He ain ' t got no tail hardly either . When he sit , he sit on what he ain ' t got almost . AnonymousAllan Granoff (1923Granoff ( -2012 serendipitously isolated the fi rst ranaviruses (Granoff et al. 1966 ) while attempting to generate cell lines that would support the replication of Lucke herpesvirus. Although one of Allan's isolates, Frog virus 3 (FV3), subsequently became the best-characterized member of both the genus ( Ranavirus ) and the family ( Iridoviridae ); the impact of that discovery was not fully appreciated at the time. FV3 was neither the fi rst iridovirus to be recognized as a pathogen of lower vertebrates or the fi rst isolated. Those honors belonged to lymphocystis disease virus (LCDV) and invertebrate iridovirus 1 (IIV1), respectively (Wissenberg 1965 ;Xeros 1954 ). LCDV is responsible for a generally non-life threatening, but disfi guring, disease in fi sh characterized by the appearance of wartlike growths on the skin and (rarely) internal organs, whereas IIV1 is the causative agent of latent and patent infections in crane fl y larvae. Despite its lack of primacy, FV3 was studied because, in keeping with the mission of St. Jude Hospital, it was initially thought to be linked to adenocarcinoma in frogs and thus could be a useful model of human malignancies. Furthermore, unlike LCDV and IIV1, it could be readily grown in cultured cells and was thus amenable to detailed molecular characterization. Although its role in tumor development was soon proven incorrect, FV3 served as a gateway into understanding the replication strategy of a heretofore poorly studied virus family. Moreover, over the next 20 years, its study led to 2 important insights not only into iridovirus replication, but also eukaryotic biology, virus evolution, and host-virus interactions.Elucidating the molecular and cellular events of FV3 replication occupied Allan, his co-workers, and others in the USA and Europe from the discovery of FV3 in 1965 until the early 1990s (Murti et al. 1985 ;Williams 1996 ). However, despite the molecular insights gained in these studies, investigations of FV3 and other members of the family languished for a variety of reasons. After some initial optimism, it was clear that invertebrate iridoviruses were not suitable, as was baculovirus, as an insect biocontrol agent. Furthermore, FV3 and related vertebrate iridoviruses were initially viewed as minor pathogens, because few outbreaks of ranaviral disease were reported, and those that were, appeared to have minor effects on populations. In addition, unlike LCDV, there was little evidence of infection among ecologically or commercially important fi sh species. Therefore, even before the recent emphasis on "translational research," iridovirus studies took a backseat to more medically and commercially relevant poxviruses and herpesviruses.However, beginning in the mid-1980s and continuing to the present, this sanguine view of...

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Ranavirus Host Immunity and Immune Evasion

Cited by 29 publications

References 141 publications

Water Temperature Affects Susceptibility to Ranavirus

Water Temperature Affects Susceptibility to Ranavirus

Amphibian macrophage development and antiviral defenses

Introduction: History and Future of Ranaviruses

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