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A mystery illness that causes people to vomit blood has killed 15 people in Tanzania and hospitalized more than 50 others.
The New York Post reported that the illness killed its mostly male patients within hours of them developing symptoms. The illness is being reported in the southern Mbeya region of the country, according to the U.K. Sun.
Up until the discovery of the new variant, all other variants of interest or concern derive from a common ancestral virus, the B.1 strain that first made its appearance in early 2020. This is not so for the newly described variant. It evolved from an entirely different source, the A lineage, a finding that substantially expands our understanding of the repertoire of mutants we must be prepared to contend with in the months and years ahead.
The difference between the A and B lineages are three mutations that have come to define the B lineage that has displaced almost all others around the world. The common understanding is that a single amino acid change in the spike protein, the D614G mutation, increases both the ability of the virus to bind to the ACE2 receptor and, at the same time, stabilizes the interaction between the S1 and S2 protein of the spike, conferring an increase in transmissibility. I and others have suggested that the D614G substitution may not be all to the story of success for the B.1 variant. The B.1 linage viruses carry two additional mutations: the P323L mutation in the RNA-dependent RNA polymerase (NSP12), which is the key to virus replication and the production of viral mRNA and another mutation in the 5 prime untranslated region of the genome. Although hardly studied, both of these mutations may contribute, along with D614G, to the replication competence and transmissibility in the spike protein.
The Tanzanian variant (which is how I will denote it as it lacks official designation) teaches us that variants of interest and concern may lack all three defining mutations of the B.1 strain. Nonetheless, the new variant is of interest and of possible concern as it carries a number of mutations in the spike protein characteristic of other bonafide variants of concern from the B.1 lineage. Of the 13 mutations that distinguish the spike protein of the Tanzanian variant from the original Wuhan strain, eight are found in the B.1 family of variants. This is a remarkable illustration of convergent evolution. No one B.1 variant carries all these mutations, but each must confer some selective advantage to the A lineage variant. It is worth noting the five spike mutations unique to the Tanzanian virus, as they are likely to appear sooner or later in B.1 linage variants as well.
The observation of greatest concern is that the Tanzanian virus posses the E484K mutation found in many of the B.1 variants of concern. This mutation confers resistance to neutralizing antibodies of convalescent and vaccine plasma and also reduces the activity of some neutralizing monoclonal antibodies. This observation suggests that like other variants, this Tanzanian virus may heed resistant, at least partially, to the current generation of Covid-19 vaccines. The E484K mutation also increases the affinity of the spike protein for the ACE2 receptor, raising the possibility of increased transmissibility.
Another mutation of note in the spike protein is P681H. This change occurs near the cleavage site between the S1 and S2 spike subproteins. We and others speculate that this mutation increases transmissibility by increasing the efficiency of the spike precursor S protein, a requirement for infectivity.
All of the variants of concern carry a number of mutants in the N-terminal domain of the spike protein. Again, in an example of convergent evolution, four of these mutations are present in B.1 lineage variants, but not all together in any other single variant.
As no specific function is attributed as yet to the N-terminal domain, this set of mutations is thought to increase the ability of the virus to escape immune detection. I suspect that is not all there is to the story.
originally posted by: itswhatev
I ended up running out of room lol i guess i probably copy/pasted too much.of the article. To anyone else fascinated by the science around Covid- theres more info in the more recent forbes article linked.
This is not a fear mongering or doom porn thread , imtentionally anyway, but if indeed this is a complete seperate lineage from what we have been focused on it could be something to keep an eye on until we know more about whst exactly the effects off all of these changes are.
Also adding the instability in the region already, politically aswell as socioeconomically, and lack of attention... Theres no telling how far it has spread. We only identify a variant when we test for it, and many places simply arent testing enough. In my state. Of Virginia we are still only checking about 8% of knowm infections to identify the strain present... And some states even less. The same holds true in other countries. Again, not to say it is present elsewhere but the probability of it being likely rises with the more unknowm variables introduced.
Just found it interesting and though I would share
Premier Medical Laboratory Services announces their launch of one of the nation's largest variant surveillance initiatives. Now conducting genomic sequencing of 6,000 specimens per day, PMLS plans to increase that number to 12,000 by May.
originally posted by: itswhatev
To me I find this fascinatingly worrying. Not only is this an apparently seperate lineage, suggesting it had evolved alongside the strains currently known independently starting very early one, but it ALSO happened to evolve a combination of practcially all the major changes we HAVE seen thus far combined...independently.
The scientists analyzed a total of 118 nasopharyngeal samples collected between June 2020 and February 2021. Using these samples, they generated 73 high-quality SARS-CoV-2 genomes; of which, 14 were from B.1.351, B.1.1.7, and B.1.525 lineages; 44 were from C.16 lineage from Portugal; and 12 from other lineages. In addition, they identified a novel variant in three air passengers from Tanzania. Interestingly, three viral genomes isolated from these passengers displayed almost identical sequence. They temporarily designated the novel variant A.VOI.V2.
With further analysis, they observed that the novel variant has a total of 31 amino acid substitution mutations and 3 deletion mutations. Of these mutations, 11 out of 31 substitution mutations and all deletion mutations were found in the spike protein. By specifically analyzing the spike mutations, they identified 3 substitutions in the spike RBD, 2 substitutions nearby S1/S2 cleavage site, and 5 substitutions and 3 deletions in the spike N-terminal domain (NTD). Moreover, they observed that some of the NTD mutations are present in the antigenic supersite.
The study identifies a novel SARS-CoV-2 variant with multiple spike mutations. The majority of these mutations are also present in other VOCs and are known to increase viral infectivity and antibody resistance. These observations indicate that in response to certain selective pressures, these mutations are gradually evolving under positive selection and improving viral fitness.
Although the novel variant is identified only in three passengers from Tanzania, the scientists believe that more investigations are urgently needed to control its transmission within and out of the source country.