PT  - JOURNAL ARTICLE
AU  - S. Wesley Long
AU  - Randall J. Olsen
AU  - Paul A. Christensen
AU  - David W. Bernard
AU  - James R. Davis
AU  - Maulik Shukla
AU  - Marcus Nguyen
AU  - Matthew Ojeda Saavedra
AU  - Concepcion C. Cantu
AU  - Prasanti Yerramilli
AU  - Layne Pruitt
AU  - Sishir Subedi
AU  - Heather Hendrickson
AU  - Ghazaleh Eskandari
AU  - Muthiah Kumaraswami
AU  - Jason S. McLellan
AU  - James M. Musser
TI  - Molecular Architecture of Early Dissemination and Evolution of the SARS-CoV-2 Virus in Metropolitan Houston, Texas
AID  - 10.1101/2020.05.01.072652
DP  - 2020 Jan 01
TA  - bioRxiv
PG  - 2020.05.01.072652
4099  - http://biorxiv.org/content/early/2020/05/03/2020.05.01.072652.short
4100  - http://biorxiv.org/content/early/2020/05/03/2020.05.01.072652.full
AB  - We sequenced the genomes of 320 SARS-CoV-2 strains from COVID-19 patients in metropolitan Houston, Texas, an ethnically diverse region with seven million residents. These genomes were from the viruses causing infections in the earliest recognized phase of the pandemic affecting Houston. Substantial viral genomic diversity was identified, which we interpret to mean that the virus was introduced into Houston many times independently by individuals who had traveled from different parts of the country and the world. The majority of viruses are apparent progeny of strains derived from Europe and Asia. We found no significant evidence of more virulent viral types, stressing the linkage between severe disease, underlying medical conditions, and perhaps host genetics. We discovered a signal of selection acting on the spike protein, the primary target of massive vaccine efforts worldwide. The data provide a critical resource for assessing virus evolution, the origin of new outbreaks, and the effect of host immune response.Significance COVID-19, the disease caused by the SARS-CoV-2 virus, is a global pandemic. To better understand the first phase of virus spread in metropolitan Houston, Texas, we sequenced the genomes of 320 SARS-CoV-2 strains recovered from COVID-19 patients early in the Houston viral arc. We identified no evidence that a particular strain or its progeny causes more severe disease, underscoring the connection between severe disease, underlying health conditions, and host genetics. Some amino acid replacements in the spike protein suggest positive immune selection is at work in shaping variation in this protein. Our analysis traces the early molecular architecture of SARS-CoV-2 in Houston, and will help us to understand the origin and trajectory of future infection spikes.Competing Interest StatementThe authors have declared no competing interest.