It was barely a week ago that the Sars-Cov-2 variant B.1.1.529 from southern Africa became known.
The World Health Organization (WHO) is looking at her for the first time today, Friday.
And yet the variant already protrudes far beyond the hundreds of other officially listed pathogens.
The reason: B.1.1.529, first described in Botswana, contains more than thirty mutations on the virus “spines” alone, i.e. the spike proteins on the surface with which the pathogen gains access to the human body.
However, it is not just the number, but above all the combination of mutations that worries many virologists.
And: In South Africa, the new variant attracted attention due to its rapid spread.
Editor in the features section, responsible for the “Nature and Science” section.
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In the Gauteng region with the cities of Pretoria and Johannesburg, the number of newly registered infections has risen exponentially and already accounts for 90 percent of the most recently discovered viruses.
However, with around a thousand B.1.1.529 genomes recorded, the total number is still relatively small.
With the new gene sequencing work, scientists are now discovering new variants much faster.
It could therefore also be a "founder effect" - that is, that the viruses have so far mainly spread in areas with few people who have not been vaccinated.
New temporary entry restrictions
In any case, it is not yet clear whether the new variant is actually more dangerous than Delta or Alpha. Nonetheless, Israel and Great Britain have ordered at least temporary entry restrictions from the countries in which the variant is suspected. EU Commission President Ursula von der Leyen also said on Friday morning that the EU Commission would propose, in close consultation with the member states, to stop air travel in South Africa at short notice. When and where exactly the outbreak took place is still unclear. An infected person who had stayed in South Africa for some time until mid-November was identified in Hong Kong.
If the variant is officially included in the list of “interesting” or “worrying” variants by the WHO today, it should be given the designation “Nu”. The WHO arranges the worrying corona variants according to the Greek alphabet. The last detected pathogens - such as "Mu" - were descendants of the now globally dominant delta variant. Delta already contains some mutations that have significantly increased their transferability and also reduced the effectiveness of vaccines and some drugs. The changes in the spike protein are decisive for this.
If the structure of this protein changes, triggered by the changes in the blueprint in the virus genome, and the shape of the spike on the virus increases, two things can happen: the virus becomes more resistant to the antibody drugs administered by the immune system or therapeutically administered - or the pathogen can become lighter penetrate human cells and become more infectious. It is also conceivable - depending on how serious the mutation-related spike changes are - that the virus affects other organs more heavily or spreads more aggressively in the body and thus triggers dangerous immune overreactions.
After previous experience with Sars-CoV-2, none of this would be a big surprise. Jesse Bloom, one of the leading American virus genome researchers, speaks of "a lot of changes in the antigenic properties" after the first computer analyzes of the genome sequence. Of 36 tested antibodies that are already used therapeutically against Sars-CoV-2, many could lose their effectiveness, speculated the Bloom Laboratory on Twitter. However, that does not mean that vaccines or drugs suddenly lose their protective effect in an instant.
Laboratory tests must first show how exactly the virus is to be assessed in terms of infectivity and immune escape. For virologists, for example, a combination of three known mutations (H655Y, N679K, P681H), which are located directly next to the furin cleavage site in the prickly protein, which is extremely important for Sars-Cov-2, is worrying. In addition, some mutations in both the spike protein and the virus envelope suggest that the immune response could be significantly weakened. It is therefore possible that “Nu” actually came into the world, which was dubbed a “completely new pathogen” in earlier Sars-CoV-2 variants.
How it came about cannot be deduced from the mutations. As a rule, such highly mutated variants arise because they multiply and recombine for weeks or months in the body of immunocompromised corona patients. Genome egg demiologist Trevor Bedford considers it very unlikely that mass vaccinations could have promoted the emergence of the mutation-rich variant. It is much more likely that weak-acting antiviral drugs such as remdesivir are often unable to stop an infection quickly if given too late.
It is still completely open whether the new variant has the potential to spread worldwide, displace Delta and possibly further exacerbate the pandemic.
The decisive factor is likely to be how the transferability changes with the mutations.
Most mutations have the opposite effect: the viruses weaken or at least not both - increased risk of infection and immune defense escape - occur at the same time.
Even the beta variant, which also appeared for the first time in southern Africa last year and became virulent, had many fatal properties for undermining the immune system.
Nevertheless, it did not prevail against the delta variant that appeared a little later and is much easier to transfer.Keywords: