US CDC latest guidance on Covid variant B117

A new variant strain of SARS-CoV-2 that contains a series of mutations has been described in the United Kingdom (UK) and become highly prevalent in London and southeast England. Based on these mutations, this variant strain has been predicted to potentially be more rapidly transmissible than other circulating strains of SARS-CoV-2. Although a variant may predominate in a geographic area, that fact alone does not mean that the variant is more infectious. Scientists are working to learn more about this variant to better understand how easily it might be transmitted and whether currently authorized vaccines will protect people against it. At this time, there is no evidence that this variant causes more severe illness or increased risk of death. Information regarding the virologic, epidemiologic, and clinical characteristics of the variant are rapidly emerging. CDC, in collaboration with other public health agencies, is monitoring the situation closely. CDC will communicate new information as it becomes available.

Does this variant have a name?
At present, the variant is referred to as “SARS-CoV-2 VOC 202012/01” (i.e., the first variant of concern from 2020, December), or “B.1.1.7.” The press often uses the terms “variant,” “strain,” “lineage,” and “mutant” interchangeably. For the time being in the context of this variant, the first three of these terms are generally being used interchangeably by the scientific community as well.

Why has this variant been in the news recently?
Since November 2020, a variant strain of SARS-CoV-2 has become prevalent in the southeast of England, reportedly accounting for 60% of recent infections in London. This variant has a mutation in the receptor binding domain (RBD) of the spike protein at position 501, where amino acid asparagine (N) has been replaced with tyrosine (Y). The shorthand for this mutation is N501Y, sometimes noted as S:N501Y to specify that it is in the spike protein. This variant carries many other mutations, including a double deletion (positions 69 and 70).

Why has this variant emerged in the UK?
We do not know. By chance alone, viral variants often emerge or disappear, and that may be the case here. Alternatively, it may be emerging because it is better fit to spread in humans. This rapid change from being a rare strain to becoming a common strain has concerned scientists in the UK, who are urgently evaluating the characteristics of the variant strain and of the illness that it causes.

Have we seen this variant in the United States?
The VOC 202012/01 variant has not been identified through sequencing efforts in the United States, although viruses have only been sequenced from about 51,000 of the 17 million US cases. Ongoing travel between the United Kingdom and the United States, as well as the high prevalence of this variant among current UK infections, increase the likelihood of importation. Given the small fraction of US infections that have been sequenced, the variant could already be in the United States without having been detected.

What do we know already about variants containing N501Y?
Prior work on variants with N501Y suggests they may bind more tightly to the human angiotensin-converting enzyme 2 (ACE2) receptor. It is unknown whether that tighter binding, if true, translates into any significant epidemiological or clinical differences. In one laboratory study of transmission of the virus between ferrets, this mutation (and one other) spontaneously arose in the ferrets during the experiment. The significance of this observation remains to be elucidated. VOC 202012/01 so far has no known association with animals or animal contact.

What about the other mutations in this variant of SARS-CoV-2?
SARS-CoV-2 mutates regularly, acquiring about one new mutation in its genome every two weeks. Many mutations are silent (i.e., cause no change in the structure of the proteins they encode) because they produce a three-letter codon that translates to the same amino acid (i.e., they are “synonymous”). Other mutations may change the codon in a way that leads to an amino acid change (i.e., they are “non-synonymous”), but this amino acid substitution does not impact the protein’s function.

VOC 202012/01 has 14 non-synonymous (amino acid [AA] altering) mutations, 6 synonymous (non-AA altering), and 3 deletions, notably including

69/70 deletion: this double deletion has occurred spontaneously many times, and likely leads to a change in the shape of (i.e., a conformational change in) the spike protein.
P681H: near the S1/S2 furin cleavage site, a site with high variability in coronaviruses. This mutation has also emerged spontaneously multiple times.
ORF8 stop codon (Q27stop): This mutation is not in the spike protein but in a different gene (in open reading frame 8), the function of which is unknown. Similar mutations have occurred in the past. In Singapore, one strain with this type of mutation emerged and disappeared.
What implications could the emergence of new variants have?
Among the potential consequences of these mutations are the following:

Ability to spread more quickly in humans. There is already evidence that one mutation, D614G, has this property to spread more quickly. In the lab, G614 variants propagate more quickly in human respiratory epithelial cells, out-competing D614 viruses. There also is evidence that the G614 variant spreads more quickly than viruses without the mutation.
Ability to cause either milder or more severe disease in humans. There is no evidence that VOC 202012/01 produces more severe illness than other SARS-CoV-2 variants.
Ability to evade detection by specific diagnostic tests. Most commercial polymerase chain reaction (PCR) tests have multiple targets to detect the virus, such that even if a mutation impacts one of the targets, the other PCR targets will still work.
Decreased susceptibility to therapeutic agents such as monoclonal antibodies.
Ability to evade vaccine-induced immunity. FDA-authorized vaccines are “polyclonal,” producing antibodies that target several parts of the spike protein. The virus would likely need to accumulate multiple mutations in the spike protein to evade immunity induced by vaccines or by natural infection.
Among these possibilities, the last—the ability to evade vaccine-induced immunity—would likely be the most concerning because once a large proportion of the population is vaccinated, there will be immune pressure that could favor and accelerate emergence of such variants by selecting for “escape mutants.” There is no evidence that this is occurring, and most experts believe escape mutants are unlikely to emerge because of the nature of the virus.

Is this new variant related to the newly emergent variant in South Africa?
On December 18, 2020, the South African government announced that it had also seen the emergence of a new strain in a scenario similar to that in the UK. The South African variant also has the N501Y mutation and several other mutations but emerged completely independently of the UK strain and is not related to it.

What is CDC doing to track emerging variants of SARS-CoV-2?
In November 2020, CDC officially launched the National SARS-CoV-2 Strain Surveillance (NS3) program to increase the number and representativeness of viruses undergoing characterization. When fully implemented in January 2021, each state will send CDC at least 10 samples biweekly for sequencing and further characterization. In addition, CDC’s COVID-19 response is actively seeking samples of interest, such as samples associated with animal infection and, in the future, samples from vaccine-breakthrough infections. Data from these efforts are continuously analyzed at CDC, and genomic data are rapidly uploaded to public databases for use by researchers, public health agencies, and industry. To coordinate US sequencing efforts outside of CDC, since early in the pandemic, CDC has led a national coalition of laboratories sequencing SARS-CoV-2 (SPHERES). The SPHERES coalition consists of more than 160 institutions, including academic centers, industry, non-governmental organizations, and public health agencies. Of the approximately 275,000 full-genome sequences currently in public databases, 51,000 are from the United States. (The UK currently has the most sequences, with 125,000). more  

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And what do you think every day person should do? worry and fear 24/7?? Stop this sort of idiotic nonsense. more  
VIRUSES reproduce abundantly, and with imperfect fidelity, so mutations are commonplace among them. Most such mutations, though, have little or no effect on how a virus spreads or how deadly it is. And, until recently, SARS-CoV-2, the covid-19 virus, has been no exception to that rule. Regrettably, this seems to be changing. A new variant of the virus, known as B.1.1.7, is spreading rapidly through Britain, and local scientists estimate that it is about 50% more transmissible than other variants currently in circulation. The British authorities are therefore rushing into action to try to limit its spread. Those parts of the country where B.1.1.7 is most prevalent, including London, went into lockdown on December 20th. But cases have been turning up elsewhere, and more areas will be locked down from December 26th. More than 50 countries, moreover, have closed their borders to arrivals from Britain. Some parts of Europe are admitting only those who can show evidence of a recent negative test. At the moment, only a few cases of B.1.1.7 are known from places other than Britain—though it has turned up in Australia, Denmark, Iceland and the Netherlands. Many experts think, however, that it is already circulating more widely than that. It is likely Britain rang the alarm bell first because it has a well-organised system for sequencing the genes of viral samples taken from patients. About 10% of virus-positive samples are so sequenced, compared with either about 1%, or none at all, in most other European countries. According to Thomas Connor of Cardiff University, in the past week alone more samples have been sequenced in Wales (population 3m) than in France (67m) during the entire pandemic. Similarly, one estimate suggests that America has sequenced only about 40 samples since the beginning of December, compared with more than 3,700 in Britain. It is not yet clear whether B.1.1.7 causes symptoms that are any more severe than those induced by its longer-established cousins. Studies to answer this question are under way, but encouragingly hospital-admission data in B.1.1.7 hotspots do not imply that the new variant is making people more ill. Researchers in Britain are also looking for further evidence that B.1.1.7 is more contagious than previous strains—and, if so, why. The two factors which currently suggest its greater contagiousness are its speed of spread and the details of its mutations. That B.1.1.7 has spread faster than older versions of SARS-CoV-2 in those parts of Britain where infections have been rising unusually rapidly seems certain. It accounted, for example, for 62% of new infections in London in the week ending December 9th, up from 28% in early November. It has also accumulated an exceptionally large number of mutations—23 of them, only six of which are silent (meaning they make no difference to the final composition of the proteins encoded by their parts of the virus’s genome). Yet more worryingly, both laboratory and animal studies have found that some of the 17 non-silent mutations in the new variant make it better at infecting cells, at making more copies of itself once it enters those cells, and at evading antibodies originally generated by the immune system during infections with other variants. Perhaps the best evidence that B.1.1.7 is more contagious, though, is that those infected by it have higher viral loads—that is, they have more virus particles in their throat and nose swabs—than people infected by other variants. The role of viral load in contagiousness was, until recently, based on supposition rather than evidence. But a new study in Britain of about 30,000 infected people and their close contacts shows that the likelihood of someone with SARS-CoV-2 infecting others increases steadily with viral load. Reinforcing this point, researchers from South Africa, which also has an efficient covid-19 genome-sequencing programme, have found that a fast-spreading variant detected there also has an unusually high number of mutations and shares one in particular with B.1.1.7. The South African variant is also linked to higher viral load, and has been suggested by researchers as a reason why the epidemic there has accelerated. Several countries have also banned travellers from South Africa. A big worry with the emergence of B.1.1.7 and similar variants is whether they may reduce the effectiveness of covid-19 vaccinations. Several of the changes in B.1.1.7 are in the gene that encodes “spike”, a protein found on the surfaces of coronavirus particles which they use to enter cells. Spike is the target of the first covid-19 vaccines. But these vaccines stimulate immune reactions to parts of the protein not affected by those mutations. There is a broad consensus among experts that vaccines already in use against SARS-CoV-2 will be effective against the B.1.1.7 variant, at least until large numbers of people are vaccinated. At that point, however, natural selection will begin to favour mutations which evade the vaccine’s effects. In the meantime, a lurking fear is that far stricter measures than have been employed previously will be needed to slow the spread of covid-19 wherever B.1.1.7 lands. All eyes are on Britain, where results from the current lockdown in London and other hotspots will provide, over the next couple of weeks, a rough idea of how much such lockdowns can achieve. If these measures fail to bend the epidemic curve downward, hospitals everywhere may have to brace themselves for yet another wave of covid-19 patients. more  
Exhaustive information on virus and it's variant. Why should common people bother about it? Take the required precautions to avoid spreading/catching the virus. That's it. more  
Let us be careful and track emerging variants of SARS-CoV-2. more  
The UK Strain New Carona Virus :: Proteins are the real Virus-machinators : My Point of Research . Proteins & Genes could change over time at a steady rate and thus act as Virus- machinators for a virus-clock. The research on genetic material, the mitochondrial DNA proved that that is passed only from Females to Offsprings and further showed that the mitochondrion is an energy-producing organ inside every living cell and contains its own complement of genes separate from the genes in the cell nucleus. After examining mitochondrial DNA from people of various races, the Scientists said that all humans living today have mitochondria traceable to a common ancestor, a female who was common to every body while made out as the Mother of us all . Also that that consequent descendants, called the humans beings, did and have been spreading out on the Globe called the Mother Earth , for all types of Air +Water dependent livings in the life-beings . Reconciliation between the Mother of us all and the Mother Earth should put an end to the Carona Virus , a parental-China-strain and its UK-Cosiness-Strain, the newer Carona with formidable transmissibilitity. Let me see what is going to happen for our betterment in the hands of Mother of us all and the Mother Earth . more  
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