scholarly journals Identification of Reptarenaviruses, Hartmaniviruses, and a Novel Chuvirus in Captive Native Brazilian Boa Constrictors with Boid Inclusion Body Disease

2020 ◽  
Vol 94 (11) ◽  
Author(s):  
Fernando Froner Argenta ◽  
Jussi Hepojoki ◽  
Teemu Smura ◽  
Leonora Szirovicza ◽  
Márcia Elisa Hammerschmitt ◽  
...  

ABSTRACT Boid inclusion body disease (BIBD) is a transmissible viral disease of captive snakes that causes severe losses in snake collections worldwide. It is caused by reptarenavirus infection, which can persist over several years without overt signs but is generally associated with the eventual death of the affected snakes. Thus far, reports have confirmed the existence of reptarenaviruses in captive snakes in North America, Europe, Asia, and Australia, but there is no evidence that it also occurs in wild snakes. BIBD affects boa species within the subfamily Boinae and pythons in the family Pythonidae, the habitats of which do not naturally overlap. Here, we studied Brazilian captive snakes with BIBD using a metatranscriptomic approach, and we report the identification of novel reptarenaviruses, hartmaniviruses, and a new species in the family Chuviridae. The reptarenavirus L segments identified are divergent enough to represent six novel species, while we found only a single novel reptarenavirus S segment. Until now, hartmaniviruses had been identified only in European captive boas with BIBD, and the present results increase the number of known hartmaniviruses from four to six. The newly identified chuvirus showed 38.4%, 40.9%, and 48.1% amino acid identity to the nucleoprotein, glycoprotein, and RNA-dependent RNA polymerase, respectively, of its closest relative, Guangdong red-banded snake chuvirus-like virus. Although we cannot rule out the possibility that the found viruses originated from imported snakes, the results suggest that the viruses could circulate in indigenous snake populations. IMPORTANCE Boid inclusion body disease (BIBD), caused by reptarenavirus infection, affects captive snake populations worldwide, but the reservoir hosts of reptarenaviruses remain unknown. Here, we report the identification of novel reptarenaviruses, hartmaniviruses, and a chuvirus in captive Brazilian boas with BIBD. Three of the four snakes studied showed coinfection with all three viruses, and one of the snakes harbored three novel reptarenavirus L segments and one novel S segment. The samples originated from collections with Brazilian indigenous snakes only, which could indicate that these viruses circulate in wild snakes. The findings could further indicate that boid snakes are the natural reservoir of reptarena- and hartmaniviruses commonly found in captive snakes. The snakes infected with the novel chuvirus all suffered from BIBD; it is therefore not possible to comment on its potential pathogenicity and contribution to the observed changes in the present case material.

Author(s):  
Fernando Froner Argenta ◽  
Jussi Hepojoki ◽  
Teemu Smura ◽  
Leonora Szirovicza ◽  
Márcia Elisa Hammerschmitt ◽  
...  

ABSTRACTBoid Inclusion Body Disease (BIBD) is a transmissible viral disease of captive snakes that causes severe losses in snake collections worldwide. It is caused by reptarenavirus infection, which can persist over several years without overt signs, but is generally associated with the eventual death of the affected snakes. Thus far, reports have confirmed existence of reptarenaviruses in captive snakes in North America, Europe, and Australia, but there is no evidence that it also occurs in wild snakes. BIBD affects both boas and pythons, the habitats of which do not naturally overlap. Herein, we studied Brazilian captive snakes with BIBD using a metatranscriptomic approach, and report the identification of novel reptarenaviruses, hartmaniviruses, and a new species in the family Chuviridae. The reptarenavirus L segments identified represent six novel species, while we only found a single novel reptarenavirus S segment. Until now, hartmaniviruses had been identified only in European captive boas with BIBD, and the present results increase the number of known hartmanivirus species from four to six. The newly identified chuvirus showed 38.4%, 40.9%, and 48.1% amino acid identity to the nucleoprotein, glycoprotein, and RNA-dependent RNA polymerase of its closest relative, Guangdong red-banded snake chuvirus-like virus. Although we cannot rule out the possibility that the found viruses originated from imported snakes, the results suggest that the viruses would circulate in indigenous snake populations.IMPORTANCEBoid Inclusion Body Disease (BIBD) caused by reptarenavirus infection affects captive snake populations worldwide, but the reservoir hosts of reptarenaviruses remain unknown. Herein, we report the identification of novel reptarenavirus and hartmanivirus species, and a chuvirus in captive Brazilian boas with BIBD. Three of the four snakes studied showed co-infection with all three viruses, and one of the snakes harbored three novel reptarenavirus L and one novel S segment. The samples originated from collections with Brazilian indigenous snakes only, which could indicate that these viruses circulate in wild snakes. The findings could further indicate that boid snakes are the natural reservoir of reptarena- and hartmaniviruses commonly found in captive snakes. The snakes infected with the novel chuvirus all suffered from BIBD; it is therefore not possible to comment on its potential pathogenicity and contribution to the observed changes in the present case material.


2015 ◽  
Vol 89 (16) ◽  
pp. 8657-8660 ◽  
Author(s):  
J. Hepojoki ◽  
P. Salmenperä ◽  
T. Sironen ◽  
U. Hetzel ◽  
Y. Korzyukov ◽  
...  

Recently, novel arenaviruses were found in snakes with boid inclusion body disease (BIBD); these form the new genusReptarenaviruswithin the familyArenaviridae. We used next-generation sequencing andde novosequence assembly to investigate reptarenavirus isolates from our previous study. Four of the six isolates and all of the samples from snakes with BIBD contained at least two reptarenavirus species. The viruses sequenced comprise four novel reptarenavirus species and a representative of a new arenavirus genus.


2021 ◽  
Author(s):  
Sanghwa Park ◽  
JaYoung Cho ◽  
Dong-Hyun Jung ◽  
SeokWon Jang ◽  
JungHye Eom ◽  
...  

Abstract An aerobic, gram-negative, pink-colored, non-motile, rod-shaped algicidal bacterium, designated JA-25T was isolated from the freshwater of the Geumgang River, Republic of Korea. It grew at 15–30°C, 6.0–9.0 pH, and in the presence of 0–1% (w/v) NaCl. Phylogenetic analysis based on 16S rRNA gene sequences revealed that strain JA-25T belongs to the Family ‘Spirosomaceae’ and is most closely related to Fibrella aestuarina BUZ 2T (93.6%). The strain JA-25T showed < 90% sequence similarity to other members of the Family ‘Spirosomaceae’. The average nucleotide identity(ANI), in silico DNA-DNA hybridization and the average amino acid identity(AAI) values based on the genomic sequences of JA-25T and F. aestuarina BUZ 2T were 74.4, 20.5 and 73.6 %, respectively. The genomic DNA G + C content was 52.5mol %. The major cellular fatty acids were Summed feature 3 (C16:1 ω6c/C16:1 ω7c), C16:1 ω5c, C16:0 (> 10%). The genomic DNA G + C content was 52.5 mol %. The major respiratory quinone was MK-7 and the polar lipids were phosphatidylethanolamine, two unidentified aminolipids, two phospholipids and five unidentified lipids. Considering the phylogenetic inference, phenotypic and chemotaxonomic data, strain JA-25T should be classified as a novel species of the novel genus Fibrivirga, with the proposed name Fibrivirga algicola sp. nov. The type strain is JA-25T (= KCCM 43334T = NBRC 114259T).


2014 ◽  
Vol 89 (2) ◽  
pp. 1119-1128 ◽  
Author(s):  
Jussi Hepojoki ◽  
Anja Kipar ◽  
Yegor Korzyukov ◽  
Lesley Bell-Sakyi ◽  
Olli Vapalahti ◽  
...  

ABSTRACTBoid inclusion body disease (BIDB) is a fatal disease of boid snakes, the etiology of which has only recently been revealed following the identification of several novel arenaviruses in diseased snakes. BIBD-associated arenaviruses (BIBDAV) are genetically divergent from the classical Old and New World arenaviruses and also differ substantially from each other. Even though there is convincing evidence that BIBDAV are indeed the etiological agent of BIBD, the BIBDAV reservoir hosts—if any exist besides boid snakes themselves—are not yet known. In this report, we use University of Helsinki virus (UHV; a virus that we isolated from aBoa constrictorwith BIBD) to show that BIBDAV can also replicate effectively in mammalian cells, including human cells, provided they are cultured at 30°C. The infection induces the formation of cytoplasmic inclusion bodies (IB), comprised mainly of viral nucleoprotein (NP), similar to those observed in BIBD and in boid cell cultures. Transferring infected cells from 30°C to 37°C ambient temperature resulted in progressive declines in IB formation and in the amounts of viral NP and RNA, suggesting that BIBDAV growth is limited at 37°C. These observations indirectly indicate that IB formation is linked to viral replication. In addition to mammalian and reptilian cells, UHV infected arthropod (tick) cells when grown at 30°C. Even though our findings suggest that BIBDAV have a high potential to cross the species barrier, their inefficient growth at mammalian body temperatures indicates that the reservoir hosts of BIBDAV are likely species with a lower body temperature, such as snakes.IMPORTANCEThe newly discovered boid inclusion body disease-associated arenaviruses (BIBDAV) of reptiles have drastically altered the phylogeny of the familyArenavirus. Prior to their discovery, known arenaviruses were considered mainly rodent-borne viruses, with each arenavirus species having its own reservoir host. BIBDAV have so far been demonstrated in captive boid snakes, but their possible reservoir host(s) have not yet been identified. Here we show, using University of Helsinki virus as a model, that these viruses are able to infect mammalian (including human) and arthropod cells. Our results providein vitroproof of the considerable ability of arenaviruses to cross species barriers. However, our data indicate that BIBDAV growth occurs at 30°C but is inhibited at 37°C, implying that crossing of the species barrier would be hindered by the body temperature of mammalian species.


2020 ◽  
Vol 70 (8) ◽  
pp. 4432-4450 ◽  
Author(s):  
Ainsley C. Nicholson ◽  
Christopher A. Gulvik ◽  
Anne M. Whitney ◽  
Ben W. Humrighouse ◽  
Melissa E. Bell ◽  
...  

The genus Chryseobacterium in the family Weeksellaceae is known to be polyphyletic. Amino acid identity (AAI) values were calculated from whole-genome sequences of species of the genus Chryseobacterium, and their distribution was found to be multi-modal. These naturally-occurring non-continuities were leveraged to standardise genus assignment of these species. We speculate that this multi-modal distribution is a consequence of loss of biodiversity during major extinction events, leading to the concept that a bacterial genus corresponds to a set of species that diversified since the Permian extinction. Transfer of nine species ( Chryseobacterium arachidiradicis , Chryseobacterium bovis, Chryseobacterium caeni, Chryseobacterium hispanicum, Chryseobacterium hominis, Chryseobacterium hungaricum,, Chryseobacterium pallidum and Chryseobacterium zeae ) to the genus Epilithonimonas and eleven ( Chryseobacterium anthropi , Chryseobacterium antarcticum , Chryseobacterium carnis , Chryseobacterium chaponense , Chryseobacterium haifense, Chryseobacterium jeonii, Chryseobacterium montanum , Chryseobacterium palustre , Chryseobacterium solincola , Chryseobacterium treverense and Chryseobacterium yonginense ) to the genus Kaistella is proposed. Two novel species are described: Kaistella daneshvariae sp. nov. and Epilithonimonas vandammei sp. nov. Evidence is presented to support the assignment of Planobacterium taklimakanense to a genus apart from Chryseobacterium, to which Planobacterium salipaludis comb nov. also belongs. The novel genus Halpernia is proposed, to contain the type species Halpernia frigidisoli comb. nov., along with Halpernia humi comb. nov., and Halpernia marina comb. nov.


Author(s):  
Shingo Kato ◽  
Masafumi Ohnishi ◽  
Mai Nagamori ◽  
Masahiro Yuki ◽  
Tomonori Takashina ◽  
...  

A thermoacidophilic, anaerobic, and iron- and sulfur-reducing archaeon, strain NAS-02T, was isolated from a terrestrial hot spring in Japan, as previously reported. This organism is the first non-ammonia-oxidizing isolate in the phylum Thaumarchaeota . Here, we propose Conexivisphaera calida gen. nov., sp. nov. to accommodate this strain. The type strain of the type species is NAS-02T (=JCM 31663T=DSM 105898T). The values of 16S rRNA gene similarity and average amino acid identity between NAS-02T and its closest relatives are <86 and <42 %, respectively. Based on the phylogeny and physiology, we propose the family Conexivisphaeraceae fam. nov., the order Conexivisphaerales ord. nov. and the class Conexivisphaeria class. nov. to accommodate the novel genus.


Author(s):  
W.L. Steffens ◽  
M.B. Ard ◽  
C.E. Greene ◽  
A. Jaggy

Canine distemper is a multisystemic contagious viral disease having a worldwide distribution, a high mortality rate, and significant central neurologic system (CNS) complications. In its systemic manifestations, it is often presumptively diagnosed on the basis of clinical signs and history. Few definitive antemortem diagnostic tests exist, and most are limited to the detection of viral antigen by immunofluorescence techniques on tissues or cytologic specimens or high immunoglobulin levels in CSF (cerebrospinal fluid). Diagnosis of CNS distemper is often unreliable due to the relatively low cell count in CSF (<50 cells/μl) and the binding of blocking immunoglobulins in CSF to cell surfaces. A more reliable and definitive test might be possible utilizing direct morphologic detection of the etiologic agent. Distemper is the canine equivalent of human measles, in that both involve a closely related member of the Paramyxoviridae, both produce mucosal inflammation, and may produce CNS complications. In humans, diagnosis of measles-induced subacute sclerosing panencephalitis is through negative stain identification of whole or incomplete viral particles in patient CSF.


Author(s):  
Anton Wahyudi

The novel Sepertiga Malam di Manhattan by Arumi E is very interesting to study. This novel is a novel about the struggle of a family to get happiness. This novel is the Arumi E's 27th newest novel. The struggle in this novel is to make the family happy, expecting for the baby. Before writing the novel, Arumi E did a research in the places written in the novel to achieve a very interesting fictional story and most of this story was taken from the traveling results so it was so interesting. The objective of this research is to describe (1) the Autopoetic System in the novel Sepertiga MalamdiManhattan by Arumi E. (2) The differentiation system in the Novel Sepertiga Malamdi Manhattan by Arumi E.The research method used is in the form of a descriptive qualitative method that uses a social system approach. The method used by the researcher is the dialectical method. The data source used in this research is the novel Sepertiga Malamdi Manhattan by Arumi E, published by Gramedia publisher in 2018. The data collection in this study uses the steps of reading the novel. To collect data, the researcher use any instrument.There are two results of the study: (1) The autopoetic system in the novel Sepertiga MalamdiManhattan by Arumi E. is concerning to some characters who have their own beliefs or rules in their lives who do not want to follow the rules of others, they are more confident in their own way to success and purpose of life. (2) The system of differentiation in the novel Sepertiga Malamdi Manhattan by Arumi E. is covering the handling of changes in the environment, the characters are able to adapt to the new environment, which has a different culture from the original culture. This shows evidence of the system autopoetic and differentiation in the novel Sepertiga MalamdiManhattan by Arumi E.


2018 ◽  
Vol 8 (3) ◽  
pp. 247-266
Author(s):  
Michelle L. Wilson

Initially, Oliver Twist (1839) might seem representative of the archetypal male social plot, following an orphan and finding him a place by discovering the father and settling the boy within his inheritance. But Agnes Fleming haunts this narrative, undoing its neat, linear transmission. This reconsideration of maternal inheritance and plot in the novel occurs against the backdrop of legal and social change. I extend the critical consideration of the novel's relationship to the New Poor Law by thinking about its reflection on the bastardy clauses. And here, of course, is where the mother enters. Under the bastardy clauses, the responsibility for economic maintenance of bastard children was, for the first time, legally assigned to the mother, relieving the father of any and all obligation. Oliver Twist manages to critique the bastardy clauses for their release of the father, while simultaneously embracing the placement of the mother at the head of the family line. Both Oliver and the novel thus suggest that it is the mother's story that matters, her name through which we find our own. And by containing both plots – that of the father and the mother – Oliver Twist reveals the violence implicit in traditional modes of inheritance in the novel and under the law.


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