→See accompanying article http://dx.doi.org/10.1002/emmm.201302857 Treatment of inherited protein deficiency may be complicated by pathogenic antibody responses during replacement therapy, highlighting the need for development of suitable immune tolerance protocols.
However, some data suggest that the situation may be more complicated, and that pathogenic mechanisms beyond toxicity or abnormal interactions solely due to the polyQ-containing protein may contribute to polyQ expansion diseases.
Indeed, both the complicated life history of pathogenic yeast strains and adaptation to antifungal drugs (polyenes) might function together to keep this highly mutated PDR5 allele at a certain frequency in pathogenic population of S. cerevisiae.
Both the diagnosis of mitochondrial disease and the molecular characterization of underlying pathogenic mutations are complicated by the variability in penetrance and tissue specificity observed even between close family members, as well as the lack of a consistent genotype phenotype correlation [McFarland et al., 2010; Ylikallio and Suomalainen, 2012].
Here we describe the first case of successfully treated A. haemolyticum infective endocarditis complicated with cerebral emboli and review the features of this rarely pathogenic organism.
As if that were not sufficient enough a challenge, the homeostasis within the intestine is further complicated by the presence of 105 1011 bacteria (pathogenic and non-pathogenic) per gram of mucus and the constant turnover of gut epithelial cells.
To reveal pathogenic mechanism of AD, complicated signaling pathways among neuron, glial cell, microglia, presynaptic cell, postsynaptic cell, astrocyte, and blood brain barrier should be clarified.
In conclusion, we report this case to draw attention that influenza B, which is usually considered less pathogenic, can unexpectedly be complicated by fulminant myocarditis or cardiomyopathy leading to cardiogenic shock in adults.
As is the case here, conclusions regarding the origin of newly emergent pathogens are often complicated by difficulty in discriminating between nonpathogenic progenitors and avirulent mutants of pathogenic strains.
