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Wheat streak mosaic virus (WSMV; Tritimovirus tritici) and Triticum mosaic virus (TriMV; Poacevirus tritici), the type members of the genera Tritimovirus and Poacevirus , respectively, in the family Potyviridae , are economically important wheat viruses in the Great Plains region of the USA. Co-infection of wheat by WSMV and TriMV results in disease synergism. Wheat transcriptome from singly (WSMV or TriMV) and doubly (WSMV+TriMV) infected upper uninoculated leaves were analyzed by RNA-Seq at 9, 12, and 21 days postinoculation. A total of 31,754 differentially expressed wheat genes were identified among all comparisons. Weighted gene co-expression network analysis resulted in 11 co-expression modules that broadly indicated gene expression profiles attributable to control, single, and double infections. Gene ontology, protein domain and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis revealed that genes specifically related to photosynthesis, growth, stress, senescence, and defense were differentially enriched. Analyses of transcription factor families indicated that genes encoding MADS-Box and ARFs were strongly enriched in control plants, moderately repressed in TriMV-infected plants, and more strongly repressed in WSMV- and doubly-infected plants, whereas genes encoding WRKYs and NACs were more enriched in WSMV or doubly infected plants. Synergistic interactions between WSMV and TriMV drastically enhanced disease phenotype compared to individual virus infections. The progression of disease phenotype was correlated to transcriptomic changes, indicating the strong disruption to plant metabolism and likely channeling of energy and metabolites for viral replication. There also appeared to be a connection between viral replication and plastid health, with stronger downregulation of genes needed for chloroplast functions and integrity and increased synergism between TriMV and WSMV. This study provides an overview of transcriptomic changes distinctly influenced by TriMV and WSMV either singly or in combination and provides a good correlation between specific transcription factors and genes associated with metabolism to observed phenotypic changes in plant growth and disease synergism. [ABSTRACT FROM AUTHOR]

Wheat streak mosaic virus (WSMV; genus Tritimovirus, family Potyviridae) is the causal agent of the most economically important wheat streak mosaic disease of wheat (Triticum aestivum) in the Great Plains region of the United States. WSMV determinants responsible for wheat streak mosaic disease in wheat are unknown. Triticum mosaic virus (TriMV), a wheat-infecting virus, was used as an expression vector for the transient expression of each of the WSMV-encoded cistrons in wheat. WSMV-encoded 6K1, NIa-VPg, NIa-Pro, and CP cistrons in TriMV elicited symptoms specific to different stages of wheat streak mosaic disease without significantly affecting the genomic RNA accumulation. WSMV 6K1 produced early wheat streak mosaic disease-like symptoms of severe chlorotic streaks and patches. NIa-VPg and CP caused severe chlorotic streaks, followed by moderate stunting (only with NIa-VPg) of wheat, mimicking early- and mid-stage symptoms of wheat streak mosaic disease. WSMV NIa-Pro caused mild chlorotic streaks, followed by dark green leaves with severe stunting, representing the late symptoms of wheat streak mosaic disease. Collectively, these data suggest that cumulative effects of WSMV-encoded 6K1, NIa-VPg, NIa-Pro, and CP are responsible for different stages of wheat streak mosaic disease symptoms in wheat. Furthermore, deletion analysis of wheat streak mosaic disease determinants revealed that complete 6K1 and NIa-Pro, amino acids 3 to 60 and 121 to 197 of NIa-VPg, and amino acids 101 to 294 of CP are responsible for wheat streak mosaic disease-like symptoms in wheat. This study suggests that management strategies for wheat streak mosaic disease in wheat should target WSMV determinants of the disease phenotype. [ABSTRACT FROM AUTHOR]

The mitral valve of the heart regulates the flow of blood from the left atrium to the left ventricle, from where it is pumped to the tissues of the body. When the orifice of the valve is narrowed, restricting the flow of blood from one chamber to the other, the condition is known as mitral stenosis. An increasingly used treatment for mitral stenosis is percutaneous mitral balloon valvuloplasty, in which a balloon-tipped catheter is threaded through the vasculature to the stenotic valve, inflated (distending the opening) and removed. The short-term success rate is about the same as with the more invasive surgical repair techniques. A long-term complication that plagues patients who have undergone valvuloplasty is mitral regurgitation, a condition in which the valve does not close completely during contraction of the ventricle, permitting blood to flow back into the atrium from the ventricle (rather than out through the aorta to the body). This condition is newly seen in about 20 percent of valvuloplasty patients, and pre-existing mitral regurgitation worsens in 35 to 45 percent of the patients. In most cases, severe mitral regurgitation requiring surgical repair is noted fairly soon - within days - after valvuloplasty. A case is reported describing extremely severe mitral regurgitation which was delayed by several months following the performance of uncomplicated valvuloplasty. The patient was a 60-year-old woman with a past history of rheumatic fever, who underwent valvuloplasty to relieve symptoms of mitral stenosis. For six months following the successful procedure, the patient did well, but then the symptoms of cardiac dysfunction began to return. Diagnostic testing revealed mitral regurgitation of such severe nature that valve replacement had to be done with a mechanical prosthesis. The aortic valve (regulating blood flow from the left ventricle to the aorta) was also replaced during the operation. The patient made a full recovery and was discharged. (Consumer Summary produced by Reliance Medical Information, Inc.)