Emergence and rapid transmission of SARS-CoV-2 B.1.1.7 in the United States

Washington, Nicole; Gangavarapu, Karthik; Zeller, Mark; Bolze, Alexandre; Cirulli, Elizabeth T.; Barrett, Kelly M Schiabor; Larsen, Brendan B.; Anderson, Catelyn; White, Simon; Cassens, Tyler; Jacobs, Sharoni; Levan, Geraint; Nguyen, Jason; Ramirez, Jimmy M.; Rivera-Garcia, Charlotte; Sandoval, Efren; Wang, Xueqing; Wong, David; Spencer, Emily; Robles‐Sikisaka, Refugio; Kurzban, Ezra; Hughes, Laura D.; Deng, Xianding; Wang, Candace; Servellita, Venice; Valentine, Holly; Hoff, Peter De; Seaver, Phoebe; Sathe, Shashank; Gietzen, Kimberly; Sickler, Brad; Antico, Jay; Hoon, Kelly; Liu, Jianwen; Harding, Aaron; Bakhtar, Omid; Basler, Tracy; Austin, Brett; MacCannell, Duncan; Isaksson, Magnus; Febbo, Phillip G.; Becker, David G.; Laurent, Marc; McDonald, Eric; Yeo, G; Knight, Rob; Laurent, Louise C.; Feo, Eileen de; Worobey, Michael; Chiu, Charles Y.; Suchard, Marc A.; Lu, James T.; Lee, William; Andersen, Kristian G.

doi:10.1016/j.cell.2021.03.052

Cited by 299 publications

(291 citation statements)

References 27 publications

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“…Using our standardized ELISpot assay, we also examined the impact of the emerging SARS-CoV- long after their discovery, these variants were detected globally and stirred concern due to their increased transmissibility and virulence [1][2][3][4][5][6] . There have also been reports of SARS-CoV-2 seropositive individuals becoming reinfected with a new variant [41][42][43][44] .…”

Section: T-cell Immunity To Sars-cov-2 Variants Following Vaccinationmentioning

confidence: 99%

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SARS -CoV-2 T-cell immunity to variants of concern following vaccination

Gallagher

Leick

Larson

et al. 2021

Preprint

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Recently, two mRNA vaccines to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have become available, but there is also an emergence of SARS-CoV-2 variants with increased transmissibility and virulence. A major concern is whether the available vaccines will be equally effective against these variants. The vaccines are designed to induce an immune response against the SARS-CoV-2 spike protein, which is required for viral entry to host cells. Immunity to SARS-CoV-2 is often evaluated by antibody production, while less is known about the T-cell response. Here we developed, characterized, and implemented two standardized, functional assays to measure T-cell immunity to SARS-CoV-2 in uninfected, convalescent, and vaccinated individuals. We found that vaccinated individuals had robust T-cell responses to the wild type spike and nucleocapsid proteins, even more so than convalescent patients. We also found detectable but diminished T-cell responses to spike variants (B.1.1.7, B.1.351, and B.1.1.248) among vaccinated but otherwise healthy donors. Since decreases in antibody neutralization have also been observed with some variants, investigation into the T-cell response to these variants as an alternative means of viral control is imperative. Standardized measurements of T-cell responses to SARS-CoV-2 are feasible and can be easily adjusted to determine changes in response to variants.

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Section: T-cell Immunity To Sars-cov-2 Variants Following Vaccinationmentioning

confidence: 99%

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mentioning

confidence: 99%

SARS -CoV-2 T-cell immunity to variants of concern following vaccination

Gallagher

Leick

Larson

et al. 2021

Preprint

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“…We identified a significantly increased hospitalization rate for patients with B.1.1.7, compared to non-B.1.1.7 patients, but no significant difference in length of hospitalization or 28day mortality (Table 1). Several studies [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] In the UK, at the end of April, the B.1.1.7 variant accounted for 98% of all COVID-19 cases (https://en.wikipedia.org/wiki/Lineage_B.1.1.7). 27 A similar rapid increase in B.1.1.7 and population dominance has been reported in many countries, including Israel, France, Denmark, Norway, Lebanon, Norway, and other countries (https://en.wikipedia.org/wiki/Lineage_B.1.1.7).…”

Section: Discussionmentioning

confidence: 99%

“…In particular, VOC UK B.1.1.7 is of special interest because it has the ability to transmit very effectively, spread through populations rapidly, and has been reported to have a significantly higher mortality rate than non-B.1.1.7 infections (https://virological.org/t/preliminary-genomic-characterisation-of-anemergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations/563, last accessed: May 17, 2020, https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file /947048/Technical_Briefing_VOC_SH_NJL2_SH2.pdf, last accessed: May 17, 2020, https://app.box.com/s/3lkcbxepqixkg4mv640dpvvg978ixjtf/file/756963730457, last accessed: May 17, 2020, https://cmmid.github.io/topics/covid19/uk-novel-variant.html, last accessed: May 17, 2020, https://virological.org/t/lineage-specific-growth-of-sars-cov-2-b-1-1-7-during-theenglish-national-lockdown/575, last accessed: May 17, 2020). [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] VOCs known as B.1.351 and P.1, found to cause widespread disease in South Africa and Brazil, respectively, have sequence changes in spike protein that make them less susceptible to host and some therapeutic antibodies. [38][39][40][41] "California" VOC.…”

Section: [Introduction]mentioning

confidence: 99%

Trajectory of Growth of SARS-CoV-2 Variants in Houston, Texas, January through May 2021 Based on 12,476 Genome Sequences

Olsen

Christensen

Long

et al. 2021

Preprint

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Genetic variants of the SARS-CoV-2 virus are of substantial concern because they can detrimentally alter the trajectory of the ongoing pandemic, and disease course in individual patients. Here we report genome sequences from 11,568 COVID-19 patients in the Houston Methodist healthcare system dispersed throughout the metroplex that were diagnosed from January 1, 2021 through April 30, 2021. This sample represents 94% of Houston Methodist cases and 4.6% of all reported cases in the metropolitan area during this period. The SARS-CoV-2 variant designated UK B.1.1.7 increased very rapidly, and now causes 75%-90% of all new cases in the Houston area. Five of the 2,543 B.1.1.7 genomes had an E484K change in spike protein. Compared with non-B.1.1.7 patients, individuals infected with B.1.1.7 had a significantly lower cycle threshold value (considered to be a proxy for higher virus load) and higher rate of hospitalization. Other variants (e.g., B.1.429, B.1.427, P.1, P.2, and R.1) also increased rapidly in frequency, although the magnitude was less than for B.1.1.7. We also identified 42 patients with a recently described R.1 variant that has an E484K amino acid replacement, and seven patients with the B.1.617 "India" variants. In the aggregate, our study shows the occurrence of a diverse array of concerning SARS-CoV-2 variants circulating in a major metropolitan area, documents B.1.1.7 as the major cause of new cases in Houston and heralds the arrival and spread of B.1.617 variants in the metroplex.

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“…Fortunately, effective vaccines have been developed, and a global vaccination programme is underway (Mahase, 2021). New SARS-CoV-2 variants of concern are emerging that are making containment of the pandemic more difficult, by increasing transmissivity of the virus (Davies and Edmunds, 2021; Korber et al, 2020; Volz et al, 2021a, 2021b; Washington et al, 2021) and/or its resistance to protective immunity induced by previous infection or vaccines (Darby and Hiscox, 2021; Dejnirattisai et al, 2021; Garcia-Beltran et al, 2021; Madhi et al, 2021a, 2021b; Mahase, 2021). (Volz et al, 2021a, 2021b)…”

Section: Introductionmentioning

confidence: 99%

Effects of common mutations in the SARS-CoV-2 Spike RBD domain and its ligand the human ACE2 receptor on binding affinity and kinetics

Barton

MacGowan

Kutuzov

et al. 2021

Preprint

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The interaction between the SARS-CoV-2 virus Spike protein receptor binding domain (RBD) and the ACE2 cell surface protein is required for viral infection of cells. Mutations in the RBD domain are present in SARS-CoV-2 variants of concern that have emerged independently worldwide. For example, the more transmissible B.1.1.7 lineage has a mutation (N501Y) in its Spike RBD domain that enhances binding to ACE2. There are also ACE2 alleles in humans with mutations in the RBD binding site. Here we perform a detailed affinity and kinetics analysis of the effect of five common RBD mutations (K417N, K417T, N501Y, E484K and S477N) and two common ACE2 mutations (S19P and K26R) on the RBD/ACE2 interaction. We analysed the effects of individual RBD mutations, and combinations found in new SARS-CoV-2 variants first identified in the UK (B.1.1.7), South Africa (B.1.351) and Brazil (P1). Most of these mutations increased the affinity of the RBD/ACE2 interaction. The exceptions were mutations K417N/T, which decreased the affinity. Taken together with other studies, our results suggest that the N501Y and S477N mutations primarily enhance transmission, the K417N/T mutations facilitate immune escape, and the E484K mutation facilitates both transmission and immune escape.

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Emergence and rapid transmission of SARS-CoV-2 B.1.1.7 in the United States

Cited by 299 publications

References 27 publications

SARS -CoV-2 T-cell immunity to variants of concern following vaccination

SARS -CoV-2 T-cell immunity to variants of concern following vaccination

Trajectory of Growth of SARS-CoV-2 Variants in Houston, Texas, January through May 2021 Based on 12,476 Genome Sequences

Effects of common mutations in the SARS-CoV-2 Spike RBD domain and its ligand the human ACE2 receptor on binding affinity and kinetics

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