First report and genomic characterization of a bovine‐like coronavirus causing enteric infection in an odd‐toed non‐ruminant species (Indonesian tapir, Acrocodia indica ) during an outbreak of winter dysentery in a zoo

Author(s):  
Christian Savard ◽  
Chantale Provost ◽  
Olivier Ariel ◽  
Samuel Morin ◽  
Richard Fredrickson ◽  
...  
2020 ◽  
Vol 22 ◽  
pp. 54-56
Author(s):  
Suchanda Dey ◽  
Mahendra Gaur ◽  
Rajesh Kumar Sahoo ◽  
Aradhana Das ◽  
Bhawana Jain ◽  
...  

2019 ◽  
Vol 91 (6) ◽  
pp. 928-934
Author(s):  
Franck‐Martin Obam Mekanda ◽  
Chavely Gwladys Monamele ◽  
Frédy Brice Simo Nemg ◽  
Francine Berlange Sado Yousseu ◽  
Dieudonné Ndjonka ◽  
...  

Author(s):  
John R. White ◽  
David T. Williams ◽  
Kelly Davies ◽  
Jianning Wang ◽  
Honglei Chen ◽  
...  

Bluetongue virus (BTV) is an arbovirus (genus: Orbivirus) that occurs worldwide. It infects domestic and wild ruminant species and can cause disease in livestock, producing high economic impact. Recently, it gained extra prominence throughout Europe, with disease occurring in regions traditionally free of BTV. BTV enters Australia from Southeast Asia via wind-borne infected Culicoides spp. The first Australian isolation was 1975 (BTV-20) and further serotypes were isolated between 1979–86 (BTV-1, -3, -9, -15, -16, -21, -23). Despite increased, more sensitive, monitoring, no more were detected in over two decades, implying a stable BTV episystem of eastern ancestry. Isolations of BTV-2, -7 and -5 then occurred between 2007–15, with the latter two possessing genome segments with high sequence identity to western isolates. We report on the first isolation and genomic characterization of BTV-12, which revealed that three more novel western topotype gene segments have entered northern Australia.


Planta Medica ◽  
2011 ◽  
Vol 77 (12) ◽  
Author(s):  
AS Lima ◽  
B Lukas ◽  
J Novak ◽  
AC Figueiredo ◽  
LG Pedro ◽  
...  

2020 ◽  
Vol 20 (7) ◽  
pp. 490-500 ◽  
Author(s):  
Justin S. Becker ◽  
Amir T. Fathi

The genomic characterization of acute myeloid leukemia (AML) by DNA sequencing has illuminated subclasses of the disease, with distinct driver mutations, that might be responsive to targeted therapies. Approximately 15-23% of AML genomes harbor mutations in one of two isoforms of isocitrate dehydrogenase (IDH1 or IDH2). These enzymes are constitutive mediators of basic cellular metabolism, but their mutated forms in cancer synthesize an abnormal metabolite, 2- hydroxyglutarate, that in turn acts as a competitive inhibitor of multiple gene regulatory enzymes. As a result, leukemic IDH mutations cause changes in genome structure and gene activity, culminating in an arrest of normal myeloid differentiation. These discoveries have motivated the development of a new class of selective small molecules with the ability to inhibit the mutant IDH enzymes while sparing normal cellular metabolism. These agents have shown promising anti-leukemic activity in animal models and early clinical trials, and are now entering Phase 3 study. This review will focus on the growing preclinical and clinical data evaluating IDH inhibitors for the treatment of IDH-mutated AML. These data suggest that inducing cellular differentiation is central to the mechanism of clinical efficacy for IDH inhibitors, while also mediating toxicity for patients who experience IDH Differentiation Syndrome. Ongoing trials are studying the efficacy of IDH inhibitors in combination with other AML therapies, both to evaluate potential synergistic combinations as well as to identify the appropriate place for IDH inhibitors within existing standard-of-care regimens.


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