Emerging strains of porcine epidemic diarrhoea virus (PEDv) in Mexico

As an emerging disease, the porcine epidemic diarrhoea virus has caused substantial economic losses to the pork industry in Mexico, leading to piglet mortality rates of up to 100%. For detection, sequencing and genetic characterization of the virus, 68 samples of one‐week‐old piglets from pork farms in 17 states of Mexico were analysed. In total, 53 samples were positive by real‐time RT‐PCR, confirming the presence of the virus in 15 states. Twenty‐eight samples from 10 states were amplified by endpoint RT‐PCR, and 20 sequences of the spike gene were obtained. A phylogenetic analysis based on the spike gene demonstrated that all Mexican strains are in Group II and are classified as non‐Indel‐S emerging variants. Three strains showed amino acid insertions: PEDv/MEX/GTO/LI‐DMZC15/2015 and PEDv/MEX/QRO/LI‐DMZC45/2016 showed one amino acid insertion (⁴²⁴Y⁴²⁵ and ⁴⁴⁷D⁴⁴⁸, respectively), and PEDv/MEX/QRO/LI‐DMZC49/2019 showed one and two amino acid insertions (⁴²²C⁴²³ and ⁵³⁷SQ⁵³⁸), with the second insertion in the COE region. These results provide evidence of the prevalence of emerging, non‐Indel‐S strains of the virus are currently circulating in Mexico during 2016–2018, when three of which have amino acid insertions: PEDv/MEX/GTO/IN‐DMZC15/2015 and PEDv/MEX/QRO/IN‐DMZC45/2016 have one amino acid insertion each (⁴²⁴Y⁴²⁵ and ⁴⁴⁷D⁴⁴⁸, respectively), and PEDv/MEX/QRO/IN‐DMZC49/2019 has one (⁴²²C⁴²³) and two amino acid insertions (⁵³⁷SQ⁵³⁸), the latter being in the COE region, which could generate new antigenic variants.     

Imaging in the pre-operative staging of ovarian cancer

Abdominal Radiology - The main prognostic factor in ovarian cancer is the stage of disease at diagnosis. The staging system in use (FIGO classification, updated in 2014) is based on the...     

Genome-wide RNA interference screen identifies previously undescribed regulators of polyglutamine aggregation

Protein misfolding and the formation of aggregates are increasingly recognized components of the pathology of human genetic disease and hallmarks of many neurodegenerative disorders. As exemplified by polyglutamine diseases, the propensity for protein misfolding is associated with the length of polyglutamine expansions and age-dependent changes in protein-folding homeostasis, suggesting a critical role for a protein homeostatic buffer. To identify the complement of protein factors that protects cells against the formation of protein aggregates, we tested transgenic Caenorhabditis elegans strains expressing polyglutamine expansion yellow fluorescent protein fusion proteins at the threshold length associated with the age-dependent appearance of protein aggregation. We used genome-wide RNA interference to identify genes that, when suppressed, resulted in the premature appearance of protein aggregates. Our screen identified 186 genes corresponding to five principal classes of polyglutamine regulators: genes involved in RNA metabolism, protein synthesis, protein folding, and protein degradation; and those involved in protein trafficking. We propose that each of these classes represents a molecular machine collectively comprising the protein homeostatic buffer that responds to the expression of damaged proteins to prevent their misfolding and aggregation.     

The hepcidin gene promoter nc.-1010C > T; −582A > G haplotype modulates serum ferritin in individuals carrying the common H63D mutation in HFE gene

Hereditary hemochromatosis is an autosomal recessive disorder characterized by severe iron overload. It is usually associated with homozygosity for the HFE gene mutation c.845G > A; p.C282Y. However, in some cases, another HFE mutation (c.187C > G; p.H63D) seems to be associated with the disease. Its penetrance is very low, suggesting the possibility of other iron genetic modulators being involved. In this work, we have screened for HAMP promoter polymorphisms in 409 individuals presenting normal or increased serum ferritin levels together with normal or H63D-mutated HFE genotypes. Our results show that the hepcidin gene promoter TG haplotype, originated by linkage of the nc.-1010C > T and nc.-582A > G polymorphisms, is more frequent in the HFE_H63D individuals presenting serum ferritin levels higher than 300 μg/L than in those presenting the HFE_H63D mutation but with normal serum ferritin levels or in the normal control group. Moreover, it was observed that the TG haplotype was associated to increased serum ferritin levels in the overall pool of HFE_H63D individuals. Thus, our data suggest that screening for these polymorphisms could be of interest in order to explain the phenotype. However, this genetic condition seems to have no clinical significance.