Search results
Items: 12
1. Orthocoronavirinae, Alphacoronavirus,Tegacovirus, Feline coronaviruses (FCoV) , Canine coronaviruses
Paul A, Stayt J.
Aust Vet J. 2019 Oct;97(10):418-421. doi: 10.1111/avj.12867.
Abstract
This study reports the prevalence of potential faecal pathogens in the microbiome
 detected in a cohort of cats and dogs with diarrhoea in Perth, Western 
Australia. Records from a commercial diagnostic laboratory using faecal 
PCR testing between July 2014 and August 2015 were reviewed
Of 289 feline faecal samples reviewed,
Salmonella spp. (1.7%),
Campylobacter spp. (47.6%),
Clostridium perfringens (81.3%),
Giardia spp. (11.1%),
Toxoplasma gondii (1.2%),
Tritrichomonas foetus (4.8%),
panleukopenia virus (6.5%) and
coronavirus (39.5%) were detected.
In dogs,
Salmonella spp. (5.4%),
Campylobacter spp. (36.3%),
C. perfringens (85.4%),
Giardia spp. (6.2%),
parvovirus (9.4%),
coronavirus (4.7%) and
distemper virus (1.5%) were detected.
Of 289 feline faecal samples reviewed,
Salmonella spp. (1.7%),
Campylobacter spp. (47.6%),
Clostridium perfringens (81.3%),
Giardia spp. (11.1%),
Toxoplasma gondii (1.2%),
Tritrichomonas foetus (4.8%),
panleukopenia virus (6.5%) and
coronavirus (39.5%) were detected.
In dogs,
Salmonella spp. (5.4%),
Campylobacter spp. (36.3%),
C. perfringens (85.4%),
Giardia spp. (6.2%),
parvovirus (9.4%),
coronavirus (4.7%) and
distemper virus (1.5%) were detected.
© 2019 Australian Veterinary Association.
2.Orthocoronavirinae, Alphacoronavirus, Tegacovirus, FCoV , Feline coronavirus
Meazzi S, Stranieri A, Lauzi S, Bonsembiante F, Ferro S, Paltrinieri S, Giordano A.
Res Vet Sci. 2019 Aug;125:272-278. doi: 10.1016/j.rvsc.2019.07.003. Epub 2019 Jul 9.
Feline coronaviruses (FCoV) colonize
 the intestinal tract, however, due to not fully understood mutations (Feline enteric CoV strain, FeCV) , 
they can spread systemically and cause feline infectious peritonitis 
(FIP). Recent studies on human medicine report that gut
 microbiota is involved in the development of systemic disorders and 
could influence the immune response to viral diseases.
The aim of this study was to provide preliminary data on the fecal microbiota composition in healthy cats compared to FCoV-infected cats, with and without FIP. Cats were equally grouped as healthy FCoV-negative, healthy FCoV-positive or FIP affected (total n = 15). Fecal sample were evaluated for the microbiota composition. A total of 3,231,916 sequences were analyzed. The samples' alpha-diversity curves did not reach a proper plateau and, for the beta-diversity, the samples seemed not to group perfectly by category, even if the healthy FCoV-positive group showed a hybrid microbial composition between FCoV-negative and FIP groups. Although there were no taxa significantly linked to the different conditions, some peculiar patterns were recognized:
Firmicutes was always the most represented phylum, followed by
Bacteroidetes and
Actinobacteria.
In FCoV-positive cats, the Firmicutes and Bacteroidetes were respectively over- and under-represented, compared to the other groups.
Among FIP cats, three subjects shared a similar microbiome, one cat showed a different microbial profile and the other one had the lowest number of diverse phyla. Despite the limited number of animals, some differences in the fecal microbiome between the groups were observed, suggesting to further investigate the possible correlation between gut microbiota and FCoV infection in cats.
The aim of this study was to provide preliminary data on the fecal microbiota composition in healthy cats compared to FCoV-infected cats, with and without FIP. Cats were equally grouped as healthy FCoV-negative, healthy FCoV-positive or FIP affected (total n = 15). Fecal sample were evaluated for the microbiota composition. A total of 3,231,916 sequences were analyzed. The samples' alpha-diversity curves did not reach a proper plateau and, for the beta-diversity, the samples seemed not to group perfectly by category, even if the healthy FCoV-positive group showed a hybrid microbial composition between FCoV-negative and FIP groups. Although there were no taxa significantly linked to the different conditions, some peculiar patterns were recognized:
Firmicutes was always the most represented phylum, followed by
Bacteroidetes and
Actinobacteria.
In FCoV-positive cats, the Firmicutes and Bacteroidetes were respectively over- and under-represented, compared to the other groups.
Among FIP cats, three subjects shared a similar microbiome, one cat showed a different microbial profile and the other one had the lowest number of diverse phyla. Despite the limited number of animals, some differences in the fecal microbiome between the groups were observed, suggesting to further investigate the possible correlation between gut microbiota and FCoV infection in cats.
Copyright © 2019 Elsevier Ltd. All rights reserved. KEYWORDS: 
Feline coronavirus; Feline infectious peritonitis; Gut microbiota
Free Article3. Orthocoronavirinae, Alpha coronavirus, Pedacovirus, PDEV, Porcine epidemic diarrhea virus
Tan Z, Dong W, Ding Y, Ding X, Zhang Q, Jiang L.
PLoS One. 2019 Jul 16;14(7):e0219868. doi: 10.1371/journal.pone.0219868. eCollection 2019.
Diarrhea, caused by porcine epidemic diarrhea virus (PEDV), is a catastrophic gastrointestinal
 disease among suckling piglets, with high infectivity, morbidity, and 
mortality, causing huge economic losses to the pig industry. In the 
present study, we investigated the different microbiota from the cecal 
mucosa and cecal contents between healthy and PEDV-infected piglets. 
High-throughput 16S rRNA gene sequencing was performed to explore 
differences. The results revealed that microbial dysbiosis by PEDV 
infection occurred in the cecal mucosa and contents of suckling piglets 
at each microbial taxonomic level. The abundance of pathogenic bacteria 
associated with diseases, including diarrhea, was increased. 
The 
abundance of Fusobacterium was 26.71% and 33.91% in cecal mucosa and 
contents of PEDV-infected group, respectively, whereas that in the 
healthy groups was 17.85% and 9.88%. 
The proportion of Proteobacteria in
 the infected groups was relatively high (24.67% and 22.79%, 
respectively), whereas that in the healthy group was 13.13% and 11.34% 
in the cecal mucosa and contents, respectively.
 Additionally, the 
proportion of Bacteroidetes in the healthy group (29.89%, 37.32%) was 
approximately twice that of the PEDV-infected group (15.50%, 15.39%). 
"Nitrate reduction",
"Human pathogens diarrhea", 
"Human pathogens 
gastroenteritis",
 "Nitrite respiration", and 
"Nitrite ammonification" 
were the enriched functional annotation terms in the PEDV-infected 
groups. Porcine epidemic diarrhea virus infection increased the 
proportion of harmful bacteria and    in the cecal mucosa and contents of suckling 
piglets. Our findings suggest that determining the intestinal microbiota
 might provide a promising method to prevent PEDV and open a new avenue 
for future research.Free PMC Article
4. Orthocoronavirinae, Gammacoronavirus, Igacovirus, Infectious Bronchitis Virus, IBV
Wu C, Yang Z, Song C, Liang C, Li H, Chen W, Lin W, Xie Q.
Poult Sci. 2018 Nov 1;97(11):3837-3846. doi: 10.3382/ps/pey268 Abstract
Yeast nucleotides 
are a fine functional additive in human and animals. The effects of 
dietary yeast nucleotides supplementation on intestinal development, 
expression of intestinal barrier-related genes, intestinal microbiota, 
and infectious bronchitis virus (IBV) antibody titer of specific 
pathogen-free (SPF) chickens were investigated. A total of 60 1-d-old 
chickens were divided into 4 groups, each of which included 3 replicates
 of 5 chickens. Group 1 served as a control that was fed a basal diet. 
Groups 2 to 4 were fed the basal diet supplemented with 0.1%, 0.3% and 
0.5% yeast nucleotides, respectively. All chickens were inoculated 
intranasally with inactivated IBV vaccine at day 1 and day 10. At day 
17, the intestinal development, expression of intestinal barrier-related
 genes and microbiota were evaluated. There was a significant increased 
ileal villus height and villus height to crypt depth ratio in group 2 (P
 < 0.05). Moreover, group 4 exhibited higher expression of zonula 
occludens-1 (ZO-1) and Occludin gene in ileum (P < 0.05), whereas 
groups 2 and 3 exhibited higher expression of Mucin 2 (MUC2) and trefoil
 factor 2 (TFF2) gene (P < 0.05), group 2 showed lower expression of 
IFN-α gene (P < 0.05). Dietary yeast nucleotides increased intestinal
 bacterial diversity (P < 0.05), and the abundance of Lactobacillus 
(P < 0.05). At day 10, 17, 24, 31, 38, and 45, the serum IBV antibody
 titers were tested. Group 2 exhibited higher IBV antibody titer at day 
17 (P < 0.05), furthermore, groups 2 to 4 reached the effective 
levels 1 wk earlier than control group. In conclusion, dietary yeast 
nucleotides supplementation can help birds to mount a faster and 
stronger antibody response to IBV vaccine. In addition, dietary yeast 
nucleotides supplementation can also promote the intestinal development 
and barrier-related genes expression, and diversity and richness of 
intestinal microbiota.
5. Nidovirales, Cornidovirinae, Coronaviridae Orthocoronavirinae, Alphacoronavirus, Tegacovirus, TGEV, Transmissible gastroenteritis virus
Xia L, Yang Y, Wang J, Jing Y, Yang Q.
Virol J. 2018 Jun 19;15(1):102. doi: 10.1186/s12985-018-1012-9.
BACKGROUND: 
Pig diarrhea causes high mortality and large economic losses in the swine industry. Transmissible gastroenteritis virus (TGEV) causes pig diarrhea, with 100% mortality in piglets less than 2 weeks old. No investigation has yet been made of the small intestine of piglets that survived infection by TGEV.
METHODS:
In this study, we evaluated the impact of TGEV infection on the small intestine of recovered pigs.
RESULTS:
Histological analyses showed that TGEV infection led to villi atrophy, and reduced villous height and crypt depth. The number of SIgA positive cells, CD3+T cells, and dendritic cells (DCs) in jejunum decreased after TGEV infection in vivo. In contrast, microfold cell (M cell) numbers and cell proliferation increased in infected pigs. TGEV infection also significantly enhanced the mRNA expression levels of cytokine IL-1β, IL-6, TNF-α, IL-10, and TGF-β. Additionally, lower gene copy numbers of Lactobacillus, and higher numbers of Enterobacteriaceae, were detected in mucosal scraping samples from TGEV-infected pigs.
CONCLUSIONS:
TGEV infection damages the small intestine, impairs immune functions, and increases pathogenic bacterial loading, all of which may facilitate secondary infections by other pathogens. These findings help quantify the impact of TGEV infection and clarify the pathogenic mechanisms underlying its effects in pigs. (Suolistomuutoket ohutsuolessa muistuttavat keliakiamuutoksia, kommenttini. Tämä tutkimus ei paljasta, ovatko muutokset ohimeneviä vai pysyviä)
Free PMC ArticlePig diarrhea causes high mortality and large economic losses in the swine industry. Transmissible gastroenteritis virus (TGEV) causes pig diarrhea, with 100% mortality in piglets less than 2 weeks old. No investigation has yet been made of the small intestine of piglets that survived infection by TGEV.
METHODS:
In this study, we evaluated the impact of TGEV infection on the small intestine of recovered pigs.
RESULTS:
Histological analyses showed that TGEV infection led to villi atrophy, and reduced villous height and crypt depth. The number of SIgA positive cells, CD3+T cells, and dendritic cells (DCs) in jejunum decreased after TGEV infection in vivo. In contrast, microfold cell (M cell) numbers and cell proliferation increased in infected pigs. TGEV infection also significantly enhanced the mRNA expression levels of cytokine IL-1β, IL-6, TNF-α, IL-10, and TGF-β. Additionally, lower gene copy numbers of Lactobacillus, and higher numbers of Enterobacteriaceae, were detected in mucosal scraping samples from TGEV-infected pigs.
CONCLUSIONS:
TGEV infection damages the small intestine, impairs immune functions, and increases pathogenic bacterial loading, all of which may facilitate secondary infections by other pathogens. These findings help quantify the impact of TGEV infection and clarify the pathogenic mechanisms underlying its effects in pigs. (Suolistomuutoket ohutsuolessa muistuttavat keliakiamuutoksia, kommenttini. Tämä tutkimus ei paljasta, ovatko muutokset ohimeneviä vai pysyviä)
6. Nidovirales, Cornidovirinae,Coronaviridae Orthocoronavirinae,Gammacoronavirus, Igacovirus, Duck coronaviruses, Avian coronaviruses
Metagenomics detection and characterisation of viruses in faecal samples from Australian wild birds.
Vibin J, Chamings A, Collier F, Klaassen M, Nelson TM, Alexandersen S.
Sci Rep. 2018 Jun 6;8(1):8686. doi: 10.1038/s41598-018-26851-1.
We present an optimised metagenomics method for detection and 
characterisation of all virus types including single and double stranded
 DNA/RNA and enveloped and non-enveloped viruses. Initial evaluation 
included both spiked and non-spiked bird faecal samples as well as 
non-spiked human faecal samples. From the non-spiked bird samples 
(Australian Muscovy duck and Pacific black ducks) we detected 21 
viruses, and we also present a summary of a few viruses detected in 
human faecal samples. We then present a detailed analysis of selected 
virus sequences in the avian samples that were somewhat similar to known
 viruses, and had good quality (Q20 or higher) and quantity of 
next-generation sequencing reads, and was of interest from a virological
 point of view, for example, avian coronavirus
 and avian paramyxovirus 6. Some of these viruses were closely related 
to known viruses while others were more distantly related with 70% or 
less identity to currently known/sequenced viruses. Besides detecting 
viruses, the technique also allowed the characterisation of host 
mitochondrial DNA present and thus identifying host species, while 
ribosomal RNA sequences provided insight into the "ribosomal activity microbiome"; of gut parasites; and of food eaten such as plants or insects, which we correlated to non-avian host associated viruses.Free PMC Article
7. Nidovirales, Cornidovirinae,Coronaviridae Orthocoronavirinae, Alphacoronavirus, Pedacovirus, PEDV, Porcine epidemic diarrhea virus
Huang MZ, Wang SY, Wang H, Cui DA, Yang YJ, Liu XW, Kong XJ, Li JY.
PLoS One. 2018 Feb 15;13(2):e0192992. doi: 10.1371/journal.pone.0192992. eCollection 2018.
Porcine epidemic diarrhea, a disastrous gastrointestinal
 disease, causes great financial losses due to its high infectivity, 
morbidity and mortality in suckling piglets despite the development and 
application of various vaccines. In this study, high-throughput 
sequencing was used to explore differences in the intestinal microbiota 
between uninfected piglets and piglets infected with porcine epidemic 
diarrhea virus (PEDV). The results revealed that the small intestinal 
microbiota of suckling piglets infected with PEDV showed low diversity 
and was dominated by Proteobacteria (49.1%). Additionally, the 
composition of the small intestinal microbiota of sucking piglets 
infected with PEDV showed marked differences from that of the uninfected
 piglets. Some of the taxa showing differences in abundance between 
uninfected piglets and piglets infected with PEDV were associated with 
cellular transport and catabolism, energy metabolism, the biosynthesis 
of other secondary metabolites, and amino acid metabolism as determined 
through the prediction of microbial function based on the bacterial 16S 
rRNA gene. Therefore, adjusting the intestinal microbiota might be a 
promising method for the prevention or treatment of PEDV.Free PMC Article
8. Nidovirales, Cornidovirinae,Coronaviridae, Orthocoronavirinae, Alphacoronavirus, Tegacovirus, Swine enteric CoV, Pedacovirus PEDV,  Procine epidemic diarrhea virus 
Song D, Peng Q, Chen Y, Zhou X, Zhang F, Li A, Huang D, Wu Q, Ye Y, He H, Wang L, Tang Y.
Sci Rep. 2017 Dec 12;7(1):17439. doi: 10.1038/s41598-017-17830-z.
Porcine epidemic diarrhea virus (PEDV) is a devastating cause of 
diarrhea in pigs worldwide. Most of studies have focused on molecular 
and pathogenic characterization of PEDV, whereas there were limited 
studies in understanding the role of gut
 microbiota (GM) in viral-associated diarrhea. Here, using the Illumina 
MiSeq platform, we examined and compared the impact of PEDV infection on
 the GM of sows and their piglets less than 10 days old. Our results 
showed that PEDV caused alternations in the structure and abundance of 
GM from levels of phylum to genus, and even species. For sows, a 
significant decrease of observed species was found in diarrheal sows 
than that in healthy sows (p < 0.05). The unweighted and weighted 
UniFrac distances also revealed considerable segregations of GM 
structure among healthy, asymptomatic, and diarrheal sows.
 For piglets, 
Bacteroidetes, the dominant bacteria in healthy piglets, were replaced 
by Firmicutes in asymptomatic and diarrheal piglets. The abundances of 
Fusobacteria and Proteobacteria were also remarkably increased in 
asymptomatic piglets and diarrheal piglets when compared to those of the
 healthy piglets. Our findings demonstrated that PEDV infection caused 
severe perturbations of GM, reduced probiotic bacteria, and enriched 
pathogenic bacteria.Free PMC Article
9. Nidovirales, Tornidovirinae, Tobaniviridae, Torovirinae, Renitovirus, Bovine Torovirus
Gomez DE, Weese JS.
Can Vet J. 2017 Dec;58(12):1267-1274. Review.
A complex community of bacteria, viruses, fungi, protists, and other microorganisms inhabit the gastrointestinal tract of calves and play important roles in gut health and disease. The viral component of the microbiome (the virome) is receiving increasing attention for its role in neonatal calf diarrhea (NCD). Rotavirus and coronavirus 
(Cornidovirinae, Nidovirales)  have for a long time been associated with NCD and commercial vaccines 
have been produced against these agents. Recently, several other viruses
 which may play a role in diarrhea have been discovered in calf fecal 
samples, mostly by sequence-based methods. These viruses include 
torovirus (Tornidovirinae, Nidovirales), norovirus, nebovirus, astrovirus, kobuvirus, and enterovirus.
 Most studies have involved epidemiologic investigations seeking to show
 association with diarrhea for each virus alone or in combination with 
potential pathogens. However, determining the contribution of these 
viruses to calf diarrhea has been challenging and much uncertainty 
remains concerning their roles as primary pathogens, co-infection 
agents, or commensals.
Free PMC Article
10.
Liu S, Zhao L, Zhai Z, Zhao W, Ding J, Dai R, Sun T, Meng H.
Curr Microbiol. 2015 Dec;71(6):643-9. doi: 10.1007/s00284-015-0895-6. Epub 2015 Aug 29.
.. A little was known regarding the status of gut microbiota after piglets infected by PEDV. In this study, aided by metagenome sequencing technology, gut
 microbiota profiles in feces of viral diarrhea (VD) and viral control 
(VC) piglets were investigated. 
The results showed that the abundance of
 four dominant phyla (Fusobacteria, Actinobacteria, Verrucomicrobia, and
 Proteobacteria) in feces was affected greatly by porcine epidemic 
diarrhea. Especially, the abundance of Fusobacteria was higher in VD 
piglets (36%) than in VC piglets (5%). On the contrary, the 
Verrucomicrobia was detected in lower distribution proportion in VD 
piglets (around 0%) than in VC piglets (20%). Furthermore, 25 genera 
were significantly different between VC and VD piglets at the genus 
level. Among the 25 genera, Leptotrichia belonging to Fusobacteria was 
remarkably lower in VC piglets than in VD piglets. Akkermansia belonging
 to Verrucomicrobia was higher in VC piglets than in VD piglets. Our 
findings implicated that the gut microbiota associated with PED significantly provided an insight into the pathology and physiology of PED.
11. (PED vaikutus pitemmällä ajalla: dysbioosi  heijastumaa). 
Koh HW, Kim MS, Lee JS, Kim H, Park SJ.
Microbes Environ. 2015;30(3):284-7. doi: 10.1264/jsme2.ME15046. Epub 2015 Jul 25.
The gastrointestinal
 tract of mammals is a complex ecosystem with distinct environments and 
comprises hundreds of different types of bacterial cells. The gut microbiota may play a critical role in the gut
 health of the host. We herein attempted to identify a microbiota shift 
that may be affected by porcine epidemic diarrhea (PED). We observed 
significant differences in microbiota between the control and PED virus 
(PEDV)-infected groups at both the phylum and genus level. Most 
commensal bacteria (i.e. Psychrobacter, Prevotella, and 
Faecalibacterium) in the healthy gastrointestinal tract were decreased due to dysbiosis induced by PEDV infection.Free PMC Article
12.
Kuba K, Imai Y, Penninger JM.
Circ J. 2013;77(2):301-8. Epub 2013 Jan 18. Revie  Abstract
Angiotensin-converting enzyme 2 (ACE2) is a negative regulator of the renin-angiotensin system, and functions as the key SARS coronavirus
 receptor and stabilizer of neutral amino acid transporters. ACE2 
catalyzes the conversion of angiotensin II to angiotensin 1-7, thereby 
counterbalancing ACE activity. Accumulating evidence indicates that the 
enzymatic activity of ACE2 has a protective role in cardiovascular 
diseases. Loss of ACE2 can be detrimental, as it leads to functional 
deterioration of the heart and progression of cardiac, renal, and 
vascular pathologies. Recombinant soluble human ACE2 protein has been 
demonstrated to exhibit beneficial effects in various animal models, 
including cardiovascular diseases. ACE2 is a multifunctional enzyme and 
thus potentially acts on other vasoactive peptides, such as Apelin, a 
vital regulator of blood pressure and myocardium contractility. In 
addition, ACE2 is structurally a chimeric protein that has emerged from 
the duplication of 2 genes: homology with ACE at the carboxypeptidase 
domain and homology with Collectrin in the transmembrane C-terminal 
domain. ACE2 has been implicated in the pathology of Hartnup's disease, a
 disorder of amino acid homeostasis, and, via its function in amino acid
 transport, it has been recently revealed that ACE2 controls intestinal 
inflammation and diarrhea, thus regulating the gut microbiome.
 This review summarizes and discusses the structure and multiple 
functions of ACE2 and the relevance of this key enzyme in disease 
pathogenesis.
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