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 dealing with it for the first time today, Friday, and yet it is already a long way off out over the hundreds of other officially listed pathogens.

The reason: B.1.1.529, first described in Botswana, contains more than thirty mutations in the virus "spines" alone, 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 puzzles many virologists.

And: In South Africa, the new variant attracted attention due to its rapid spread.

Joachim Müller-Jung

Editor in the features section, responsible for the “Nature and Science” section.

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In regions like Gauteng with Pretoria and Johannesburg, the number of newly registered infections has risen exponentially and already accounts for ninety percent of the viruses discovered.

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 the viruses have so far mainly spread in areas with few people who have not been vaccinated.

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. 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 most recently recorded pathogens were, like "Mu", descendants of the now globally dominant delta variant. Delta already contains some mutations that have significantly increased their transferability and have 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 is more resistant to the antibody drugs administered by the immune system or by thrapeutic methods - or the pathogen can more easily penetrate human cells and become more infectious. It is also conceivable, depending on how serious the mutation-related spike changes are, that the virus attacks 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 no time at all.

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 in no time at all what was actually called the world in earlier Sars-CoV-2 variants as a "completely new pathogen". How it came about cannot be deduced from the mutations. As a rule, such highly mutated variants arise fromthat they multiply and recombine for weeks or months in the body of immunocompromised corona patients. The genome egg demiologist Trevor Bedford considers it very unlikely that the 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 capable of doing so, which often fail to stop an infection quickly if given too late.which most often do not stop an infection quickly if given too late.which most often do not 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.