Highly motivated scientist with expertise in RNA and genomics seeking a position at a ground-breaking biotech or pharmaceutical company dedicated to solving human health challenges.
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The emergence and spread of SARS-CoV-2 lineage B.1.1.7, first detected in the United Kingdom, has become a global public health concern because of its increased transmissibility. Over 2500 COVID-19 cases associated with this variant have been detected in the US since December 2020, but the extent of establishment is relatively unknown. Using travel, genomic, and diagnostic data, we highlight the primary ports of entry for B.1.1.7 in the US and locations of possible underreporting of B.1.1.7 cases. Furthermore, we found evidence for many independent B.1.1.7 establishments starting in early December 2020, followed by interstate spread by the end of the month. Finally, we project that B.1.1.7 will be the dominant lineage in many states by mid to late March. Thus, genomic surveillance for B.1.1.7 and other variants urgently needs to be enhanced to better inform the public health response.
Sequencing and phylogenetic analysis of SARS-CoV-2 genomes from the beginning of the pandemic show that Connecticut infections resulted from domestic travel from the West Coast, and not from international introductions. While the state and federal government response was focused on travel restrictions, our findings show that local public health measures (such as increased testing capacity, and closure of businesses and social gatherings) would reduce transmission more effectively.
We found that traditional RNA-seq methods can misinterpret transcription dynamics that are revealed by long-read sequencing. Depletion of Nab2, a protein associated with intellectual disability in flies and humans, generated RNA transcripts which overlap multiple genes. Furthermore, we show that these disrupted transcripts are not spliced, highlighting the importance of coordination between RNA synthesis and RNA processing.