Since January, several studies have claimed that the ‘British’ coronavirus variant is more deadly than the original virus (“Kent Covid is up to 100% deadlier than original virus”). Almost all media and almost all supposed experts have amplified this claim. In contrast, SPR and a few other independent research groups noted that these claims were based on very weak evidence.
A new study by Public Health England now confirms that the British variant is not deadlier than the original virus. The study claims, however, that the British variant increases the risk of hospitalization by 30%. But this figure, too, is based on poor evidence and is most likely a statistical artifact, as the influence of age, comorbidities and seasonal effects is much larger.
(Update: A second study, published in the Lancet, confirmed this finding: “We found no evidence of an association between severe disease and death and lineage (B.1.1.7 vs non-B.1.1.7) in unadjusted analyses, or in analyses adjusted for hospital, sex, age, comorbidities, and ethnicity.”)
It is true that new variants of the novel coronavirus are replacing previous variants in most countries (see covariants.org), but this effect is well known from seasonal influenza viruses, and it requires neither increased virulence nor increased intrinsic infectiousness of the virus: otherwise, seasonal influenza would get more infectious and more deadly in every season (which it doesn’t). Moreover, this effect is independent of any measures, including masks.
Nevertheless, some of the new coronavirus variants – most notably the ‘South African’ variant – are beginning to show partial immune evasion, as was to be expected. Some monoclonal antibodies already fail to neutralize some of the new variants, and most vaccines achieve lower neutralization, too. Pharmaceutical companies will respond to this by creating new therapeutic antibody combinations and by updating their coronavirus vaccines (a multi-billion dollar business).
In fact, by March 2021, the novel coronavirus has managed to escape two out of three major antibody classes. If a new strain manages to escape all three major antibody classes, this “would be a worrying development, and should be monitored closely”. (Greaney et al.) This is one more reason why progress in early and prophylactic treatment is so very important.
To be sure, antibody immune evasion doesn’t necessarily mean complete immune evasion, as the immune system has additional means to fight off infections, including the famed T cells.
Figure 1: Coronavirus escape mutations in new virus variants
Coronavirus escape mutations against major antibody classes 1 to 3 in new coronavirus variants. Currently, no variant combines all three escape mutations (Greaney et al, page 22).
Lineages: B.1.1.7 is British, B.1.351 is South Africa, P.1-2 is Brazil, B.1.429 is California, B.1.526 is New York. RBD: receptor binding domain.
Figure 2: Coronavirus mutations and their effect on ACE2 receptor binding affinity
Coronavirus mutations and their effect on ACE2 receptor binding affinity (Starr et al.). It is possible that higher binding affinity may increase virulence or infectiousness, but it may also decrease it. x is SARS-CoV-2 (original variant), o is SARS-CoV-1. The British variant, for instance, has a mutation from amino acid 501N to 501Y, which increases receptor binding affinity (blue field).
Figure 3: RNA vaccines: Reduced neutralization against new virus variants
Covid RNA vaccines: reduction in neutralization of variants (x-fold reduction). P.1/P.2: “Brazilian” variants; B.1.351.V1-3: “South African” variants (Source: Garcia-Beltran).
Figure 4: Reduced effectiveness of some monoclonal antibodies
Reduced effectiveness of monoclonal antibodies casirivimab, bamlanivimab and REGN10989 against the South African and Brazilian coronavirus variants (Hoffmann et al)