On December 14, 2020, the United Kingdom reported a SARS-CoV-2 variant of concern (VOC), lineage B.1.1.7,also referred to as VOC 202012/01 or 20I/501Y.V1.* The B.1.1.7 variant is estimated to have emerged in September 2020 and has quickly become the dominant circulating SARS-CoV-2 variant in England (1). B.1.1.7 has been detected in over 30 countries, including the United States. As of January 13, 2021, approximately 76 cases of B.1.1.7 have been detected in 12 U.S. states. Multiple lines of evidence indicate that B.1.1.7 is more efficiently transmitted than are other SARS-CoV-2 variants (1–3). The modeled trajectory of this variant in the U.S. exhibits rapid growth in early 2021,becoming the predominant variant in March. IncreasedSARS-CoV-2 transmission might threaten strained health care resources, require extended and more rigorous implementation of public health strategies (4), and increase the percentage of population immunity required for pandemic control. Taking measures to reduce transmission now can lessen the potential impact of B.1.1.7 and allow critical time to increase vaccination coverage. Collectively, enhanced genomic surveillance combined with continued compliance with effective public health measures, including vaccination, physical distancing,use of masks, hand hygiene, and isolation and quarantine, will be essential to limiting the spread of SARS-CoV-2, the virus that causes coronavirus disease 2019 (COVID-19). Strategic testing of persons without symptoms but at higher risk of infection, such as those exposed to SARS-CoV-2 or who have frequent unavoidable contact with the public, provides another opportunity to limit ongoing spread.

Global genomic surveillance and rapid open-source sharing of viral genome sequences have facilitated near real-time detection, comparison, and tracking of evolving SARS-CoV-2 variants that can inform public health efforts to control the pandemic. Whereas some mutations in the viral genome emerge and then recede, others might confer a selective advantage to the variant, including enhanced transmissibility, so thatsuch a variant can rapidly dominate other circulating variants.

    Early in the pandemic, variants of SARS-CoV-2 containing the D614G mutation in the spike (S) protein that increases receptor binding avidity rapidly became dominant in many geographic regions (5,6).In late fall 2020, multiple countries reported detecting SARS-CoV-2 variants that spread more efficiently. In addition to the B.1.1.7 variant, notable variants include the B.1.351 lineage first detected in South Africa and the recently identified B.1.1.28 subclade (renamed “P.1”) detected in four travelers from Brazil during routine screening at the Haneda (Tokyo)  airport. § These variants carry a constellation of genetic mutations, including in the S protein receptor-binding domain,which is essential for binding to the host cell angiotensin-converting enzyme-2 (ACE-2) receptor to facilitate virus  entry. Evidence suggests that other mutations found in these variants might confer not only increased transmissibility but might also affect the performance of some diagnostic real-time  reverse transcription–polymerase chain reaction (RT-PCR) assays ¶ and reduce susceptibility to neutralizing antibodies(2,3,5–10). A recent case report documented the first case of SARS-CoV-2 reinfection in Brazil with a SARS-CoV-2 variant  that contained the E484K mutation,** which has been shown to reduce neutralization by convalescent sera and monoclonal antibodies (9,10).

     This report focuses on the emergence of the B.1.1.7 variant in the United States. As of January 12, 2021, neither the B.1.351 nor the P.1 variants have been detected in the United States. For information about emerging SARS-CoV-2 variants of concern, CDC maintains a webpage dedicated to providing information on emerging SARS-CoV-2 variants. ††

 B.1.1.7 lineage (20I/501Y.V1)

The B.1.1.7 variant carries a mutation in the S protein (N501Y) that affects the conformation of receptor-binding domain. This variant has 13 other B.1.1.7 lineage-definingmutations (Table), several of which are in the S protein,including a deletion at positions 69 and 70 (del69–70) that evolved spontaneously in other SARS-CoV-2 variants and is hypothesized to increase transmissibility (2,7). The deletion at positions 69 and 70 causes S-gene target failure (SGTF) in at least one RT-PCR–based diagnostic assay (i.e., with the ThermoFisher Taq Path COVID-19 assay, the B.1.1.7 variant and other variants with the del69–70 produce a negative result for S-gene target and a positive result for the other two targets); SGTF has served as a proxy in the United Kingdom for identifying B.1.1.7 cases (1).Multiple lines of evidence indicate that B.1.1.7 is more efficiently transmitted compared with other SARS-CoV-2 variants circulating in the United Kingdom. U.K. regions with a higher proportion of B.1.1.7 sequences had faster epidemic growth than did other areas, diagnoses with SGTF increased faster than did non-SGTF diagnoses in the same areas, and a higher proportion of contacts were infected by index patients with B.1.1.7 infections than by index patients infected with other variants (1,3). Variant B.1.1.7 has the potential to increase the U.S. pandemic trajectory in the coming months. To illustrate this effect,a simple, two-variant compartmental model was developed.The current U.S. prevalence of B.1.1.7 among all circulating viruses is unknown but is thought to be <0.5% based on the limited number of cases detected and SGTF data (8). For the model, initial assumptions included a B.1.1.7 prevalence of 0.5% among all infections, SARS-CoV-2 immunity from previous infection of 10%–30%, a time-varying reproductive number (R t ) of 1.1 (mitigated but increasing transmission)or 0.9 (decreasing transmission) for current variants, and areported incidence of 60 cases per 100,000 persons per day on January 1, 2021. These assumptions do not precisely represent any single U.S. location, but rather, indicate a generalization of conditions common across the country. The change in R t over time resulting from acquired immunity and increasing prevalence of B.1.1.7, was modeled, with the B.1.1.7 R t assumed to be a constant 1.5 times the R t of current variants, based on initial estimates from the United Kingdom (1,3).Next, the potential impact of vaccination was modeled assuming that 1 million vaccine doses were administered per day beginning January 1, 2021, and that 95% immunity was achieved 14 days after receipt of 2 doses. Specifically, immunity against infection with either current variants or the B.1.1.7 variant was assumed, although the effectiveness and duration of protection against infection remains uncertain, because these were not the primary endpoint of clinical trials for initial vaccines.In this model, B.1.1.7 prevalence is initially low, yet because it is more transmissible than are current variants, it exhibits rapid growth in early 2021, becoming the predominant variant in March (Figure 1). Whether transmission of current variants is increasing (initial R t  = 1.1) or slowly decreasing(initial R t  = 0.9) in January, B.1.1.7 drives a substantial change in the transmission trajectory and a new phase of exponential growth. With vaccination that protects against infection, the early epidemic trajectories do not change and B.1.1.7 spread still occurs (Figure 2). However, after B.1.1.7 becomes the dominant variant, its transmission was substantially reduced. The effect of vaccination on reducing transmission in the near term was greatest in the scenario in which transmission was already decreasing (initial R t = 0.9) (Figure 2). Early efforts that can limit the spread of the B.1.1.7 variant, such as universal and increased compliance with public health mitigation strategies,will allow more time for ongoing vaccination to achieve higher population-level immunity.

Discussion

   Currently, there is no known difference in clinical outcomes associated with the described SARS-CoV-2 variants; however,a higher rate of transmission will lead to more cases, increasing the number of persons overall who need clinical care, exacerbating the burden on an already strained health care system,and resulting in more deaths. Continued genomic surveillance to identify B.1.1.7 cases, as well as the emergence of other variants of concern in the United States, is important for the COVID-19 public health response. Whereas the SGTF results can help identify potential B.1.1.7 cases that can be confirmed by sequencing, identifying priority variants that do not exhibit SGTF relies exclusively on sequence-based surveillance.