It is clear that SARS-CoV-2, the agent of the Covid-19 epidemic, is here to stay. Like the flu, a respiratory virus that transmits smoothly, SARS-CoV-2 mutates to evade the immune systems of those who suffer from it. you have already been vaccinated, infected, or both. The question remains: how harmful is each new edition of SARS-CoV-2?Again, as with the flu, if you’ve already been vaccinated, infected, or both, the new variants of SARS-CoV-2 can be life-threatening, if they’re not.
As summer approaches, a number of new types are on the horizon. While they are derived from the original Omicron and feature many similarities, they are different enough to cause a new wave of Covid-19 cases.
A new variant, KP. 2, could lead the wave over the next summer. This newly known variant is basically spreading in the United States, Canada, and the United Kingdom, with degrees expanding in Singapore, New Zealand, and Australia. Currently, 1,816 cases of KP. 2 have been reported in the GISAID SARS-CoV-2 database, indicating that potentially thousands, if not tens of thousands, of Americans have already been infected with this variant, as sequencing efforts have done. significantly limited in recent years.
KP. 2 belongs to an organization recently characterized as FLiRT variants. This call is derived from the technical designations of two mutations in their spike proteins: the F456L mutation and the R346T mutation.
The FLiRT group is a subset of variants of the Omicron tree, which has primarily driven SARS-CoV-2 infections over the past two years. KP. 2 is structured based on previous Omicron primary variants, adding BA. 2. 86, JN. 1, and XBB. 1. 5.
Omicron’s variability is extensive. As with the flu for many years, the afterlife is a prologue with the SARS-CoV-2 virus. Over time, new variants appear to contain unique mutations, not only in the Spike protein, but also in the virus’s genome. Below is a diagram illustrating the network of Omicron variants that have emerged in recent months. KP. 2 and its FLiRT variant organization are located in the upper right corner, shaded in soft green.
As JN. 1 is the newer dominant variant, we’ll compare it to KP. 2 in this article to demonstrate how KP. 2 can differentiate itself from previous variants and hint at why it could lead to an additional surge in cases this summer.
FIGURE 2: Phased construction of KP. 2 replacing JN. 1 as the dominant variant in the United States.
SARS-CoV-2 will have to bind the ACE2 receptor to human mobiles, fuse its membrane with the host’s mobile membrane, and eventually access it to initiate infection and replicate in human mobiles. It is important to note that this protein is at the heart of vaccines, antibodies and antiviral remedies against Covid-19.
As with JN. 1, many spike protein mutations in KP. 2 are also provided in earlier variants of concern, E484K and N501Y. These variants, known as the Alpha and Beta variants of SARS-CoV-2, were first detected in early 2021.
In fact, there are 3 differences in spike proteins between KP. 2 and JN. 1. Two of them are named after KP. 2’s FLiRT organization.
There is only one mutational variation in the N-terminal region, which is related to the access of the virus after infection. In KP. 2, R346T is present, which may limit the potency of viral access and allow antibody evasion through the introduction of N-glycosylation. sites.
In the receptor-binding domain, a single JN. 1 update could have a significant effect on F456L, which could improve ACE2 binding affinity or minimize antibody binding efficiency.
Finally, V1104L was added to the S2 subunit of the spike protein, which has the power to fuse the viral envelope with the host’s cell membrane, allowing the viral genome to enter the cell.
FIGURE 3: Mutational profile of the Spike protein from KP. 2 to JN. 1.
I would like to highlight mutations that occur outside the main region, which can have a significant effect on the virus’s ability to cause disease and spread. In various parts of the genetic material, there is a wide diversity of mutations. in the replication-transcription complex Orf1ab (NSP1-16), some in structural proteins (E, M and N) and some in accessory proteins (Orf3a-8). We draw attention to these mutations because adjustments in the expressed proteins, especially the N protein, can especially favor the replication of the virus.
Below is the full catalog of discovered mutations of the virus.
FIGURE 4: KP. 2 mutation spike.
There is only one spikeless mutational difference of JN. 1 in KP. 2. It belongs to the Orf1a collection, which includes 11 proteins involved in various replication processes. This mutation is NSP3 T1465I.
Non-structural protein 3 is one of the most complex proteins of the SARS-CoV-2 virus. Among its many functions are proteolytic activity, the formation of replication-transcription complexes, the antagonism of the host immune response, and the regulation of viral translation. , and the induction of mobile death. The T1465I can improve on any of those features, it’s tricky to determine which ones or to what extent.
I saw that the N protein was widely mutated. Mutations in R203K and G204R have been provided in most viral variants during the pandemic and are more likely to increase the rate of viral replication. Although those mutations are the same as those in JN. 1, the N protein continues to play a very important role. in the pathogenicity of the virus.
Changes in mutations, whether internal or external to the spike protein, have several reasons: the first reason is to adapt to increased infectivity; The moment consists of evading neutralizing antibodies; the third is to adapt for more effective post-infectious development, which includes replication supported by mutations in the N protein; and the fourth is popularity through T cells.
Also, it is worth mentioning that this virus, as well as most of the sequenced variants of the Covid-19 outbreak, features 3 mutations with the first variant emerging from the original Wuhan virus. These are D614G at the peak, P323L at NSP12. and the synonymous C241U mutation at the 5′ end of the virus.
In fact, there are many synonymous mutations scattered around KP. 2, but gathering knowledge about those mutations is much more complex than gathering knowledge about amino acid mutations.
Synonymous mutations do not replace the amino acid sequence of the virus, but they do influence the tertiary arrangement of its RNA. Research indicates that this would possibly contribute to the adaptation of the virus to the human host environment. These mutations also have an effect on viral protein abundance and immune responses in the inflamed individual.
It remains to be seen whether KP. 2 will cause a new wave of Covid cases similar to Alpha or Omicron in previous years. In addition, existing knowledge cannot verify whether this variant is more pathogenic or viral than JN. 1, especially for in the past inflamed or vaccinated people. For those who have not been inflamed or vaccinated, KP. 2 infection can be very serious and they should be careful.
It is very important to be aware of those threats before they spread, not after. As we head into the summer months, another wave of cases will most likely occur, and KP. 2 is a clue.
To learn more about my work, visit www. williamhaseltine. com.
A community. Lots of voices. Create a free account to share your thoughts.
Our network aims to connect other people through open and thoughtful conversations. We need our readers to share their perspectives and exchange ideas and facts in one space.
To do so, please comply with the posting regulations in our site’s terms of use. Below we summarize some of those key regulations. In short, civilians.
Your message will be rejected if we notice that it appears to contain:
User accounts will be blocked if we become aware of or if users are concerned about:
So how can you become a user?
Thank you for reading our Community Standards. Read the full list of publishing regulations discovered in our site’s terms of use.