The COVID-19 B.1.617 variant, which originated in India can infect certain lung and intestinal cell lines more efficiently than the original virus, German research has found.
Scientists at the German Primate Centre (DPZ) – Leibniz Institute for Primate Research in Göttingen – say their cell culture investigation into the B.1.617 variant has found it is less sensitive to inhibition by antibodies present in the blood of convalescent or vaccinated individuals, It is also resistant to a therapeutic antibody used for COVID-19 treatment.
B.1.617 originated in India and the Delta variant is a subtype, B.1.617.2 is a subtype.
Writing in Cell Reports, they warn these properties may enable B.1.617 and its subtypes to spread rapidly in the human population, increasing the risk of incompletely vaccinated individuals and those with declining immune protection to become infected.
A team led by infection researchers Dr Markus Hoffmann and Dr Stefan Pöhlmann, from the German Primate Centre, with colleagues from the University Hospital of Göttingen, the University of Erlangen and the Hannover Medical School, investigated how the mutations impact the ability of the B.1.617 variant to enter host cells and how efficiently the antibody response in vaccinated and recovered individuals inhibits this variant.
They analysed entry of the B.1.617 variant into different human cell lines and found that in two cell lines derived from lung and colon, respectively, there was a 50% increase in the virus’ entry efficiency.
When they examined the efficacy of four different therapeutic antibodies that have been approved for the treatment of COVID-19 patients, the B.1.617 variant was found to be completely resistant against one of them and slightly less inhibited by another antibody.
After testing the efficacy of antibodies from the blood of recovered and vaccinated individuals, there was a two- to threefold reduction in protection against the B.1.617 variant.
Lead author Dr Hoffmann said: “Our study shows that this virus variant can infect lung and intestinal cells more efficiently, suggesting increased viral fitness.
“In addition, the protective effect of antibodies is limited because they block the cell entry of B.1.617 less efficiently than that of the original virus. As a result, individuals who are not fully vaccinated or were infected a long time ago and thus produce low amounts of antibodies, may be poorly protected against infection with the B.1.617 variant.”
Booster vaccines
Dr Pöhlmann, head of the Infection Biology Unit at the DPZ, added: “In order to prevent further spread of the B.1.617 variant, especially its subtype Delta, and to prevent the emergence of new virus variants it is advisable to quickly achieve full immunisation of all people that are willing to be vaccinated.
“It is also necessary to investigate whether booster vaccinations with existing vaccines or vaccines optimised to target variants provide long-lasting and broad protection."
* A British study, published last night, has found that the alpha (Kent) variant of the virus was not unusually transmissible – but spread rapidly through “super seeding.”
Researchers at the Universities of Oxford and Edinburgh, UK, and the Northeastern University, Massachusetts, USA, say that population mobility “significantly” affected its spread from the south of England.
Hoffmann M, Hofmann-Winkler H, Krüger N, et al. SARS-CoV-2 variant B.1.617 is resistant to Bamlanivimab and evades antibodies induced by infection and vaccination. Cell Reports 21 July 2021
Spatio-temporal invasion dynamics of SARS-CoV-2 lineage B.1.1.7 emergence combined large-scale well-sampled genomic surveillance data from the COVID-19 Genomics UK (COG-UK) consortium with anonymised, aggregated human mobility data to get an accurate picture of the geographic spread of the Alpha variant. Science 22 July 2021
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