Literature mining discerns latent disease-gene relationships.

MOTIVATION: Dysregulation of a gene's function, either due to mutations or impairments in regulatory networks, often triggers pathological states in the affected tissue. Comprehensive mapping of these apparent gene-pathology relationships is an ever-daunting task, primarily due to genetic pleiotropy and lack of suitable computational approaches. With the advent of high throughput genomics platforms and community scale initiatives such as the Human Cell Landscape project, researchers have been able to create gene expression portraits of healthy tissues resolved at the level of single cells. However, a similar wealth of knowledge is currently not at our finger-tip when it comes to diseases. This is because the genetic manifestation of a disease is often quite diverse and is confounded by several clinical and demographic covariates. RESULTS: To circumvent this, we mined ∼18 million PubMed abstracts published till May 2019 and automatically selected ∼4.5 million of them that describe roles of particular genes in disease pathogenesis. Further, we fine-tuned the pretrained bidirectional encoder representations from transformers (BERT) for language modeling from the domain of natural language processing to learn vector representation of entities such as genes, diseases, tissues, cell-types, etc., in a way such that their relationship is preserved in a vector space. The repurposed BERT predicted disease-gene associations that are not cited in the training data, thereby highlighting the feasibility of in silico synthesis of hypotheses linking different biological entities such as genes and conditions. AVAILABILITY AND IMPLEMENTATION: PathoBERT pretrained model: https://github.com/Priyadarshini-Rai/Pathomap-Model. BioSentVec-based abstract classification model: https://github.com/Priyadarshini-Rai/Pathomap-Model. Pathomap R package: https://github.com/Priyadarshini-Rai/Pathomap.

Implications of delayed reopening in controlling the COVID-19 surge in Southern and West-Central USA

1In the wake of the rapid surge in the Covid-19 infected cases seen in Southern and West-Central USA in the period of June-July 2020, there is an urgent need to develop robust, data-driven models to quantify the effect which early reopening had on the infected case count increase. In particular, it is imperative to address the question: How many infected cases could have been prevented, had the worst affected states not reopened early? To address this question, we have developed a novel Covid-19 model by augmenting the classical SIR epidemiological model with a neural network module. The model decomposes the contribution of quarantine strength to the infection timeseries, allowing us to quantify the role of quarantine control and the associated reopening policies in the US states which showed a major surge in infections. We show that the upsurge in the infected cases seen in these states is strongly co-related with a drop in the quarantine/lockdown strength diagnosed by our model. Further, our results demonstrate that in the event of a stricter lockdown without early reopening, the number of active infected cases recorded on 14 July could have been reduced by more than 40% in all states considered, with the actual number of infections reduced being more than 100, 000 for the states of Florida and Texas. As we continue our fight against Covid-19, our proposed model can be used as a valuable asset to simulate the effect of several reopening strategies on the infected count evolution; for any region under consideration.

Safe Blues: A Method for Estimation and Control in the Fight Against COVID-19

How do fine modifications to social distancing measures really affect COVID-19 spread? A major problem for health authorities is that we do not know. In an imaginary world, we might develop a harmless biological virus that spreads just like COVID-19, but is traceable via a cheap and reliable diagnosis. By introducing such an imaginary virus into the population and observing how it spreads, we would have a way of learning about COVID-19 because the benign virus would respond to population behaviour and social distancing measures in a similar manner. Such a benign biological virus does not exist. Instead, we propose a safe and privacy-preserving digital alternative. Our solution is to mimic the benign virus by passing virtual tokens between electronic devices when they move into close proximity. As Bluetooth transmission is the most likely method used for such inter-device communication, and as our suggested "virtual viruses" do not harm individuals software or intrude on privacy, we call these Safe Blues. In contrast to many app-based methods that inform individuals or governments about actual COVID-19 patients or hazards, Safe Blues does not provide information about individuals locations or contacts. Hence the privacy concerns associated with Safe Blues are much lower than other methods. However, from the point of view of data collection, Safe Blues has two major advantages: O_LIData about the spread of Safe Blues is uploaded to a central server in real time, which can give authorities a more up-to-date picture in comparison to actual COVID-19 data, which is only available retrospectively. C_LIO_LISampling of Safe Blues data is not biased by being applied only to people who have shown symptoms or who have come into contact with known positive cases. C_LI These features mean that there would be real statistical value in introducing Safe Blues. In the medium term and end game of COVID-19, information from Safe Blues could aid health authorities to make informed decisions with respect to social distancing and other measures. In this paper we outline the general principles of Safe Blues and we illustrate how Safe Blues data together with neural networks may be used to infer characteristics of the progress of the COVID-19 pandemic in real time. Further information is on the Safe Blues website: https://safeblues.org/.