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BackgroundThe aquatic pulmonate snail Biomphalaria glabrata is a significant vector and laboratory host for the parasitic flatworm Schistosoma mansoni, an etiological agent for the neglected tropical disease schistosomiasis. Much is known regarding the host-parasite interactions of these two organisms, and the B. glabrata embryonic (Bge) cell line has been an invaluable resource in these studies. The B. glabrata BB02 genome sequence was recently released, but nothing is known of the sequence variation between this reference and the Bge cell genome, which has likely accumulated substantial genetic variation in the ~50 years since its isolation.ResultsHere, we report the genome sequence of our laboratory subculture of the Bge cell line (designated Bge3), which we mapped to the B. glabrata BB02 reference genome. Single nucleotide variants (SNVs) were predicted and focus was given to those SNVs that are most likely to affect the structure or expression of protein-coding genes. Furthermore, we have highlighted and validated high-impact SNVs in genes that have often been studied using Bge cells as an in vitro model, and other genes that may have contributed to the immortalization of this cell line. We also resolved representative karyotypes for the Bge3 subculture, which revealed a mixed population exhibiting substantial aneuploidy, in line with previous reports from other Bge subcultures.ConclusionsThe Bge3 genome differs from the B. glabrata BB02 reference genome in both sequence and structure, and these are likely to have significant biological effects. The availability of the Bge3 genome sequence, and an awareness of genomic differences with B. glabrata, will inform the design of experiments to understand gene function in this unique in vitro snail cell model. Additionally, this resource will aid in the development of new technologies and molecular approaches that promise to reveal more about this schistosomiasis-transmitting snail vector.Electronic supplementary materialThe online version of this article (10.1186/s13071-018-3059-2) contains supplementary material, which is available to authorized users.

Stroke in patients with COVID-19 has received increasing attention throughout the global COVID-19 pandemic, perhaps due to the substantial disability and mortality that can result when the two conditions co-occur. We reviewed the existing literature and found that the proposed pathomechanism underlying COVID-19-associated ischemic stroke is broadly divided into the following three categories: vasculitis, endothelialitis, and endothelial dysfunction; hypercoagulable state; and cardioembolism secondary to cardiac dysfunction. There has been substantial debate as to whether there is a causal link between stroke and COVID-19. However, the distinct phenotype of COVID-19-associated strokes, with multivessel territory infarcts, higher proportion of large vessel occlusions, and cryptogenic stroke mechanism, that emerged in pooled analytic comparisons with non-COVID-19 strokes is compelling. Further, in this article, we review the various treatment approaches that have emerged as they relate to the proposed pathomechanisms. Finally, we briefly cover the logistical challenges, such as delays in treatment, faced by providers and health systems; the innovative approaches utilized, including the role of tele-stroke; and the future directions in COVID-19-associated stroke research and healthcare delivery.

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