SARS-CoV-2 Mutations: B.1.1.7, B.1.351 & D614G Research

[Ygggdrasil]

Apparently a new variant (double mutation) in India.
https://www.bbc.com/news/world-asia-india-56507988

Here's the relevant information about the mutants from a press release from the Indian government:

The analysis of samples from Maharashtra has revealed that compared to December 2020, there has been an increase in the fraction of samples with the E484Q and L452R mutations. Such mutations confer immune escape and increased infectivity. These mutations have been found in about 15-20% of samples and do not match any previously catalogued VOCs. These have been categorized as VOCs but require the same epidemiological and public health response of “increased testing, comprehensive tracking of close contacts, prompt isolation of positive cases & contacts as well as treatment as per National Treatment Protocol” by the States/UTs.

From Kerala 2032 samples (from all 14 districts) have been sequenced. The N440K variant that is associated with immune escape has been found in 123 samples from 11 districts. This variant was earlier found in 33% of samples from Andhra Pradesh, and in 53 of 104 samples from Telangana. This variant has also been reported from 16 other countries including UK, Denmark, Singapore, Japan and Australia. As of now these can be at best said to be variant under investigation.

https://pib.gov.in/PressReleaseIframePage.aspx?PRID=1707177

Mutations in E484 are also found in the variants from South Africa (B.1.351) and Brazil (P.1) that could be involved in decreasing the virus' susceptibility to neutralizing antibodies. The L452R mutation has also been found in the variants from California (B.1.427/B.1.429), where preliminary work suggests that the variants are slightly more transmissible (though not to the same extent at B.1.1.7).

 

[Astronuc]

Four virus variants are spreading in the US, and studies suggest they can make people sicker, evade the immune response, or spread faster.
https://www.businessinsider.com/cor...south-africa-brazil-us-facts-questions-2021-1

Four "Variants of concern" to the Centers for Disease Control and Prevention (CDC), which are found in the US and which differ from the original virus strain in a number of key ways.
B.1.1.7, first found in the UK
B.1.351, first identified in South Africa
P.1, first identified in Brazil
B.1.427/B.1.429, first identified in California

"Variants of interest" have potentially worrisome mutations, but how they affect the virus' behavior is not yet known.
B.1.526/ B.1.525, first identified in New York
P.2, first identified in Brazil
B.1.617, first identified in India

 

[Wrichik Basu]

Apparently a new variant (double mutation) in India.
https://www.bbc.com/news/world-asia-india-56507988

A new triple mutation has been discovered in West Bengal: B.1.618. It contains the E484K mutation.

 

[Astronuc]

Add a new variant to the list. This one, BV-1, was discovered by Texas A&M and is named BV for Brazos Valley, where it seems to have developed. "The official name of the BV-1 variant is hCoV-19/USA/TX-GHRC-BV1-EQ4526591/2021. It is among thousands of variants scientists have found worldwide."
https://today.tamu.edu/2021/04/19/texas-a-genome-suggests-potential-resistance-to-antibodies/

There is a concern that it may be more resistant to antibodies. ". . . cell culture-based experiments from other labs have shown several neutralizing antibodies are ineffective in controlling other variants with the same genetic markers as BV-1."

 

[Laroxe]

I think we need to be careful about assuming too much about new variants, really because of the rate of mutations and the individual variations in the people infected it could be argued that every infected person is carrying their own individual variant. This is one of the reasons for classifying certain variants as "of concern" when the mutations affect areas of the virus known to be important in the infection and the response to infection.
It's actually surprisingly difficult to be confident that such variants have much of an effect, its only now that people are fairly confident that the so-called UK variant is more infectious, though by how much is still an issue. It's certainly the case that some variants have effected the viruses' ability to avoid at least part of the antibody response to the original strain, that can be checked using the available monoclonal antibodies. Whether any of the variants cause more severe disease is still debated, the populations suffering the highest infection rates keep changing and this introduces extra problems in trying to make comparisons. It is still thought that natural selection would favour viruses' with high infectivity and low severity, something that's suggested might have happened with other human Coronaviruses'.
They are already looking at modified vaccines to address the variants that avoid antibody neutralization, but mutation is an ongoing process and someone will need to decide when the need justifies their production, new variants will continue to arise quickly, until the pandemic is controlled. People talk about the vaccination program as a race, and it is really, but by necessity, the testing of new vaccines has become much more difficult, and we may need to accept studies that use marginally less reliable methods like non inferiority trial rather than placebo controlled.

 

[Astronuc]

B.1.617, first identified in India

A new triple mutation has been discovered in West Bengal: B.1.618. It contains the E484K mutation.

https://www.dnaindia.com/health/rep...ur-indian-states-all-you-need-to-know-2887254

The Indian-origin double mutant strain of the coronavirus, B.1.167, that many experts say could be behind the rapid climb of the second COVID-19 wave, was first detected way back on October 5, last year through genome sequencing of a virus sample.

Now, a third mutation in the B.1.167 has been identified and experts are hoping that this time, given the alarm bells ringing all around, the pace of intervention and follow-up picks up.
. . .
A triple mutant refers to variants that have three different strains that have combined together to form a new variant. As of now, multiple SARS-CoV-2 variants are circulating globally and a triple mutant strain could be the next challenge for India.

 

[Ygggdrasil]

A paper published today in the New England Journal of Medicine provides real world data showing that the Pfizer-BioNTech mRNA vaccine is effective against the B.1.1.7 (originally identified in the UK) and B.1.351 (originally identified in South Africa) variants. Previous studies had confirmed the effectiveness of the vaccine against the B.1.1.7 variant, but evidence of effectiveness against the B.1.351 variant is new and especially notable because this variant contains the E484K mutation that likely decreases the effectiveness of some antibodies against the virus.

The data come from examining health data in Qatar. The study was not a randomized clinical trial, but a case-control study.

The estimated effectiveness of the vaccine against any documented infection with the B.1.1.7 variant was 89.5% (95% confidence interval [CI], 85.9 to 92.3) at 14 or more days after the second dose (Table 1 and Table S2). The effectiveness against any documented infection with the B.1.351 variant was 75.0% (95% CI, 70.5 to 78.9). Vaccine effectiveness against severe, critical, or fatal disease due to infection with any SARS-CoV-2 (with the B.1.1.7 and B.1.351 variants being predominant within Qatar) was very high, at 97.4% (95% CI, 92.2 to 99.5).

https://www.nejm.org/doi/full/10.1056/NEJMc2104974

While the vaccine is slighly less effective against the B.1.351 variant at preventing infection (75% effectiveness vs 90% for B.1.1.7), the vaccine is still very effective (97%) at preventing severe, critical or fatal disease.

These data are consistent with the spike protein mutations impairing the antibody response to the virus (allowing the virus to break through immunity in some cases), but not allowing the virus to escape cellular immunity from the T-cell response (which prevents infections from resulting in severe disease).

 

[pinball1970]

This is probably the most relevant thread for this article?

https://www.sciencealert.com/we-hav...-sars-cov-2-can-insert-itself-into-our-genome

Paper here

https://www.pnas.org/content/118/21/e2105968118

A part of our genome is already ERV remnants, about 5%?

Transposons 17%

I have read about these (on a pretty pop level) for Evolution links with other primates

These sequences can do nothing, make copies of themselves, code for “something” or be involved in a regulatory role.

https://www.frontiersin.org/articles/10.3389/fchem.2016.00021/full (or do this)

COVID is not retrovirus and I do not know what consequences this could have if the findings hold up.

ERV sequences are ancient this is be new
Is something our genome just coped with in the past? Without much ado?
Do we know when the last big event was? In terms of this sort of viral insertion?

Some general stuff on ancient ERVs, transposons and epigenetics but it would be nice to get a view from the cell biology guys if they have time

 

[Astronuc]

B.1.1.7, first found in the UK
. . . .
B.1.617, first identified in India

Vietnam detects hybrid of Indian and UK COVID-19 variants
https://www.reuters.com/world/asia-...hybrid-indian-uk-covid-19-variant-2021-05-29/

Vietnam had previously detected seven virus variants: B.1.222, B.1.619, D614G, B.1.1.7 - known as the UK variant, B.1.351, A.23.1 and B.1.617.2 - the "Indian variant".

Long said Vietnam would soon publish genome data of the newly identified variant, which he said was more transmissible than the previously known types.

I believe the UK and Indian variants were more transmissible than the original or earlier variants, and now the new variant is even more transmissible.

The country of about 98 million people has so far received 2.9 million doses and aims to secure 150 million this year.

 

[pinball1970]

Vietnam detects hybrid of Indian and UK COVID-19 variants
https://www.reuters.com/world/asia-...hybrid-indian-uk-covid-19-variant-2021-05-29/

I believe the UK and Indian variants were more transmissible that the original or earlier variants, and now the new variant is even more transmissible.

Cases slowly increasing again in the UK, it's not quite a spike but we went over 4000 cases in 24 hours first time since early April.
Several days over 3000 before that when we had been bubbling along for weeks at 2500.
Approx 60% of the population first jab, a third both
https://coronavirus.data.gov.uk/details/vaccinations

The Indian is 60% more transmissible and the vaccines are also a lot less effective. As low as 33%.
https://www.bmj.com/content/373/bmj.n1346

@PeroK has a handle on UK @Ygggdrasil and Atty

 

[atyy]

Cases slowly increasing again in the UK, it's not quite a spike but we went over 4000 cases in 24 hours first time since early April.
Several days over 3000 before that when we had been bubbling along for weeks at 2500.
Approx 60% of the population first jab, a third both
https://coronavirus.data.gov.uk/details/vaccinations

The Indian is 60% more transmissible and the vaccines are also a lot less effective. As low as 33%.
https://www.bmj.com/content/373/bmj.n1346

@PeroK has a handle on UK @Ygggdrasil and Atty

Any idea whether this is what they expected from the partial relaxation of rules? Probably some would prefer to have a higher percentage with 2 jabs, but 30% with 2 jabs might be ok if coverage in the vulnerable population is 90% or better.

 

[pinball1970]

I think the scientists expected an increase due to lifting of restrictions but with cases a lot less likely to end up in ICU because of Vaccine protection.
The BMJ publication mentions 'symptomatic' disease.
That could include serious/hospital?
So we can expect this scenario will be mimicked anywhere we have the Indian variant despite high vaccine numbers? @atyy

 

[atyy]

I think the scientists expected an increase due to lifting of restrictions but with cases a lot less likely to end up in ICU because of Vaccine protection.
The BMJ publication mentions 'symptomatic' disease.
That could include serious/hospital?
So we can expect this scenario will be mimicked anywhere we have the Indian variant despite high vaccine numbers? @atyy

Yes, symptomatic disease includes both mild and severe cases. Vaccines are generally expected to have higher effectiveness against severe disease, so for example if the second dose effectivess against variants for both mild and severe cases is 88%, maybe it's 95% effective against severe disease. Overall, we expect declining vaccine effectiveness as more variants inevitably arise. Hopefully at least the vulnerable population can get a booster early next year (ok I know it sounds terrible to say hopefully some people in the UK will get a third dose in early 2022, when most of the world might still not even have had one dose) ...

 

[pinball1970]

Yes, symptomatic disease includes both mild and severe cases. Vaccines are generally expected to have higher effectiveness against severe disease, so for example if the second dose effectivess against variants for both mild and severe cases is 88%, maybe it's 95% effective against severe disease. Overall, we expect declining vaccine effectiveness as more variants inevitably arise. Hopefully at least the vulnerable population can get a booster early next year (ok I know it sounds terrible to say hopefully some people in the UK will get a third dose in early 2022, when most of the world might still not even have had one dose) ...

Yes we are in a privileged position in the UK unlike India Mexico Brazil Africa...

One thing the government has done that was a smart move was to offer vaccines to those with no ID, no papers/NHS number etc. 'no questions asked vaccine.' In London but I hope they offer the same in other cities.

 

[Rive]

I believe the UK and Indian variants were more transmissible that the original or earlier variants, and now the new variant is even more transmissible.

I really wonder how does this calculated. Regarding an effective R the rate of immunity within the population has really remarkable effect: so a slightly immunity-bypassing variant with an actually lower (!) R0 might spread with higher R in a population which had a bad wave previously - or was thoroughly vaccinated.

 

[pinball1970]

I really wonder how does this calculated. Regarding an effective R the rate of immunity within the population has really remarkable effect: so a slightly immunity-bypassing variant with an actually lower (!) R0 might spread with higher R in a population which had a bad wave previously - or was thoroughly vaccinated.

Probably a lot of factors, how viable the virus is on fomites, how long, in droplets/air how effective it is at entering cells, how many copies, where in the respiratory system, antibody evasion...

 

[atyy]

I really wonder how does this calculated. Regarding an effective R the rate of immunity within the population has really remarkable effect: so a slightly immunity-bypassing variant with an actually lower (!) R0 might spread with higher R in a population which had a bad wave previously - or was thoroughly vaccinated.

Tweet by Jeffery Barrett
"It's clear that B.1.617.2 has been growing faster than B.1.1.7 in UK for a few weeks. Key question for policy, not yet fully answered, is how much due to:
1. vaccine efficacy
2. intrinsic transmissibility
3. human epidemiological factors"

He has follow up posts discussing data from many sources, but not yet giving a clear picture.

 

[Ygggdrasil]

The WHO has announced new nomenclature for some of the variants of concern:

Each variant will be given a name from the Greek alphabet, in a bid to both simplify the public discussion and to strip some of the stigma from the emergence of new variants. A country may be more willing to report it has found a new variant if it knows the new version of the virus will be identified as Rho or Sigma rather than with the country’s name, Maria Van Kerkhove, the WHO’s Coronavirus lead, told STAT in an interview.

Under the new scheme, B.1.1.7, the variant first identified in Britain, will be known as Alpha and B.1.351, the variant first spotted in South Africa, will be Beta. P.1, the variant first detected in Brazil, will be Gamma and B.1.671.2, the so-called Indian variant, is Delta.

https://www.statnews.com/2021/05/31/the-name-game-for-coronavirus-variants-just-got-a-little-easier/

Here's the WHO's official page on variants of concern/variants of interest:
https://www.who.int/en/activities/tracking-SARS-CoV-2-variants/

 

[Ygggdrasil]

Cases slowly increasing again in the UK, it's not quite a spike but we went over 4000 cases in 24 hours first time since early April.
Several days over 3000 before that when we had been bubbling along for weeks at 2500.
Approx 60% of the population first jab, a third both
https://coronavirus.data.gov.uk/details/vaccinations

The Indian is 60% more transmissible and the vaccines are also a lot less effective. As low as 33%.
https://www.bmj.com/content/373/bmj.n1346

@PeroK has a handle on UK @Ygggdrasil and Atty

Tweet by Jeffery Barrett
"It's clear that B.1.617.2 has been growing faster than B.1.1.7 in UK for a few weeks. Key question for policy, not yet fully answered, is how much due to:
1. vaccine efficacy
2. intrinsic transmissibility
3. human epidemiological factors"

He has follow up posts discussing data from many sources, but not yet giving a clear picture.

It's worth noting the current COVID-19 outbreak in India (presumably driven by the delta variant, B.1.617) has been occurring in some areas that were estimated to have high (~50%) exposure rates earlier in the pandemic:

Studies that tested for SARS-CoV-2 antibodies — an indicator of past infection — in December and January estimated that more than 50% of the population in some areas of India’s large cities had already been exposed to the virus, which should have conferred some immunity, says Manoj Murhekar, an epidemiologist at the National Institute of Epidemiology in Chennai, who led the work. The studies also suggested that, nationally, some 271 million people had been infected1 — about one-fifth of India’s population of 1.4 billion.

These figures made some researchers optimistic that the next stage of the pandemic would be less severe, says Ramanan Laxminarayan, an epidemiologist in Princeton University, New Jersey, who is based in New Delhi. But the latest eruption of COVID-19 is forcing them to rethink.

One explanation might be that the first wave primarily hit the urban poor. Antibody studies might not have been representative of the entire population and potentially overestimated exposure in other groups, he says.

https://www.nature.com/articles/d41586-021-01059-y

Similarly, Manaus and other regions of Brazil were estimated to have very high rates of exposure to the virus earlier in the pandemic yet also suffered major new waves in Jan 2021, likely driven by the gamma variant P.1 (https://www.thelancet.com/article/S0140-6736(21)00183-5/fulltext). Like the delta variant B.1.617 from India, the gamma variant also has a mutation at position E484 of the spike protein, which is thought to help the variant evade antibody-based immunity.

Of course, there are other non-mutually exclusive factors that could potentially explain some of these resurgences, including overestimation of prior immunity. For example, research has shown that the epsilon variants (B.1.427/B.1.429) from California are more transmissible than the original SARS-CoV-2 strain (Deng et al 2021 and Peng et al 2021), and the delta variant from India shares the L452R spike protein mutation with the epsilon variant, so increased transmissibility is also likely an issue.

Given that it seems like the vaccines protect against severe disease from the variants (even if they are less effective at preventing symptomatic disease and transmission), it will be interesting to see if the current resurgence of COVID-19 in the UK continues, will we still see large new waves of hospitalizations and deaths associated with the new wave of infections.

 

[Ygggdrasil]

This is probably the most relevant thread for this article?

https://www.sciencealert.com/we-hav...-sars-cov-2-can-insert-itself-into-our-genome

Paper here

https://www.pnas.org/content/118/21/e2105968118

A part of our genome is already ERV remnants, about 5%?

Transposons 17%

I have read about these (on a pretty pop level) for Evolution links with other primates

These sequences can do nothing, make copies of themselves, code for “something” or be involved in a regulatory role.

https://www.frontiersin.org/articles/10.3389/fchem.2016.00021/full (or do this)

COVID is not retrovirus and I do not know what consequences this could have if the findings hold up.

ERV sequences are ancient this is be new
Is something our genome just coped with in the past? Without much ado?
Do we know when the last big event was? In terms of this sort of viral insertion?

Some general stuff on ancient ERVs, transposons and epigenetics but it would be nice to get a view from the cell biology guys if they have time

It's worth noting that the PNAS paper used a somewhat artificial system in which they boosted the expression of some of the ERV elements to get SARS-CoV-2 to integrate into the genome. Whether this happens under more normal cellular conditions is still not clear.

A recent pre-print paper argues that integration of the SARS-CoV-2 genome is likely to be rare in the absence of the artificial system used in the PNAS paper:

Human genome integration of SARS-CoV-2 contradicted by long-read sequencing
Smits et al. bioRxiv 2021
https://www.biorxiv.org/content/10.1101/2021.05.28.446065v1

Abstract:

A recent study proposed severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) hijacks the LINE-1 (L1) retrotransposition machinery to integrate into the DNA of infected cells. If confirmed, this finding could have significant clinical implications. Here, we applied deep (>50x) long-read Oxford Nanopore Technologies (ONT) sequencing to HEK293T cells infected with SARS-CoV-2, and did not find any evidence of the virus existing as DNA. By examining ONT data from separate HEK293T cultivars, we resolved the complete sequences of 78 L1 insertions arising in vitro in the absence of L1 overexpression systems. ONT sequencing applied to hepatitis B virus (HBV) positive liver cancer tissues located a single HBV insertion. These experiments demonstrate reliable resolution of retrotransposon and exogenous virus insertions via ONT sequencing. That we found no evidence of SARS-CoV-2 integration suggests such events in vivo are highly unlikely to drive later oncogenesis or explain post-recovery detection of the virus.

 

[Astronuc]

The B.1.1.7 is now being called 'Alpha' coronavirus, or Alpha SARS-Cov-2?

According to an article in NY Times,

Alpha has 23 mutations that set it apart from other coronaviruses. When the variant started to surge in Britain, researchers began inspecting these genetic tweaks to look for explanations as to why it was spreading faster than other variants.

To investigate how Alpha achieved this invisibility, the researchers looked at how the Coronavirus replicated inside of infected cells. They found that Alpha-infected cells make a lot of extra copies — some 80 times more than other versions of the virus — of a gene called Orf9b.

https://www.nytimes.com/2021/06/07/health/covid-alpha-uk-variant.html

 

[pinball1970]

The B.1.1.7 is now being called 'Alpha' coronavirus, or Alpha SARS-Cov-2?

According to an article in NY Times,

https://www.nytimes.com/2021/06/07/health/covid-alpha-uk-variant.html

Yeah they have been given Greek letters. Indian is Delta

 

[Ygggdrasil]

The B.1.1.7 is now being called 'Alpha' coronavirus, or Alpha SARS-Cov-2?

Yes, see post #53 from last week for more information: https://www.physicsforums.com/threads/sars-cov-2-mutations.998345/post-6498262

 

[Phil Core]

While not a scientific journal or peer reviewed I found this article on the B.1.1.7 variant to be well done -

Inside the B.1.1.7 Coronavirus Variant​

https://www.nytimes.com/interactive/2021/health/coronavirus-mutations-B117-variant.html

1. It mentions that this variant contains more mutations than would be expected.
2. It reports on the increased bonding affinity of this variant. This article, as well as ever other article I have seen, does not report a measure for the binding strength of B.1.1.7
3. Prior articles on the increased binding strength of the original SARS-CoV-2 offer an increase in the positive charge of the surface area where the spike interfaces with the ACE2. This article stress changes in the shape of the B.1.1.7 variant. No mention is made of surface charge.

4. What I found to be the most interesting is this statement - "A number of researchers suspect that People with weakened immune systems can remain infected with replicating coronaviruses for several months, allowing the virus to accumulate many extra mutations."

Here is an example of the claim - https://jamanetwork.com/journals/jama/fullarticle/2779850 -

Researchers Tie Severe Immunosuppression to Chronic COVID-19 and Virus Variants​

 

[Astronuc]

Co-infection with two variants of SARS-Cov-2
https://www.independent.co.uk/news/health/covid-variant-cases-infection-mutation-b1881309.html

A 90-year-old woman in Belgium was infected with Alpha and Beta variants of the Covid-19 virus at the same time.

The unvaccinated woman was admitted to hospital in the Belgian city of Aalst on 3 March of this year following a number of falls and was confirmed as being Covid positive on the same day.

Despite showing no initial signs of respiratory distress, she soon deteriorated and died five days after her admission.

When the patient’s respiratory sample was processed for genomic sequencing, researchers discovered that she had been infected by the Alpha and Beta variants, which first emerged in the UK and South Africa respectively.

“This is one of the first documented cases of co-infection with two Sars-CoV-2 variants of concern,” said molecular biologist Dr Anne Vankeerberghen, who helped write a study on the woman.

Since both Alpha and Beta variants were circulating in Belgium at the time, it is expected that the lady was co-infected with different viruses from two different people. How the woman was infected, i.e., from what contacts, is unknown.

The Independent reports that in January 2021, scientists in Brazil reported that two people had been simultaneously infected with two different coronavirus variants, though research into these cases has yet to be published in a scientific journal.

Do superspreader events typically involve a single variant?

 

[atyy]

Co-infection with two variants of SARS-Cov-2
https://www.independent.co.uk/news/health/covid-variant-cases-infection-mutation-b1881309.html

Not quite the same, but about mutations arising in one person.
https://www.scientificamerican.com/...se-in-people-with-compromised-immune-systems/

 

[Laroxe]

Co-infection with two variants of SARS-Cov-2
https://www.independent.co.uk/news/health/covid-variant-cases-infection-mutation-b1881309.html

A 90-year-old woman in Belgium was infected with Alpha and Beta variants of the Covid-19 virus at the same time.Since both Alpha and Beta variants were circulating in Belgium at the time, it is expected that the lady was co-infected with different viruses from two different people. How the woman was infected, i.e., from what contacts, is unknown.

The Independent reports that in January 2021, scientists in Brazil reported that two people had been simultaneously infected with two different coronavirus variants, though research into these cases has yet to be published in a scientific journal.

Do superspreader events typically involve a single variant?

I imagine this should be quite rare, an infection with one virus puts the immune system on alert and makes infection with a new virus less likely. Activation of the immune system is metabolically quite costly, it can also be risky, so it isn't the normal state. This is suggested as an explanation as to why epidemics of viral diseases, "do the rounds," one at a time. This is a general response of the innate immune system to virus attacks rather than anything specific to Covid 19. Presumably, if exposure to both was around the same time, or if the infection was so advanced as to inhibit immunity, something Covid is quite good at, this effect would be less likely. Selective pressure tends to mean that, eventually, one variant will come to predominate in any given population.
Genomic analysis suggests that superspreading evens can usually be traced back to a single individual, they tend to occur in specific environments that limit the number of possible sources of infection, like cruise ships or institutions. They are referred to as "events" in order to avoid demonising specific individuals and attributions of blame. Identification of the source is only possible because the virus adapts to its host, this means that every individual has some changes to its genome, in effect a personal variant, though one only really of "concern" to the infected individual. It may be that certain individuals shed more virus particles than others, so are more infectious. It's thought that the majority of people who act as the source are asymptomatic or in the prodromal phase of infection. This means that these events almost inevitably involve a specific variant of concern but in theory a single event, at which there are several sources of infection, might lead to several clusters of infection. The effect on immune surveillance, combined with the probability of multiple exposure to different variants, would work against the likelihood of dual infections These events are particularly important early in an epidemic and make predictions about how the disease will spread, very difficult.

 

[Astronuc]

A new variant of SARS-Cov-2, B.1.621, evolved in Colombia and is now in Florida, US. This is why wearing a mask on a plane and in public is important.

Characterization of the emerging B.1.621 variant of interest of SARS-CoV-2
https://www.medrxiv.org/content/10.1101/2021.05.08.21256619v1.full.pdf

Abstract

SARS-CoV-2 genetic diversity has the potential to impact the virus transmissibility and the escape from natural infection- or vaccine-elicited neutralizing antibodies. Here, we report the emergence of the B.1.621 lineage, considered a variant of interest (VOI) with the accumulation of several mutations affecting the Spike protein, including the amino acid changes I95I, Y144T, Y145S and the insertion 146N in the N-terminal domain, R346K, E484K and N501Y in the Receptor Binding Domain and P681H in the S1/S2 cleavage site of the Spike protein. The rapid increase in frequency and fixation in a relatively short time in some cities that were near the theoretical herd immunity suggests an epidemiologic impact. Further studies will be required to assess the biological and epidemiologic roles of the substitution pattern found in the B.1.621 lineage.

It doesn't have a greek letter yet.

In Colombia, the National Genomic Characterization Program led by the Instituto Nacional de Salud has carried out real-time monitoring of the SARS-CoV-2 lineages since the beginning of the pandemic (7,8).Until December 2020, over thirty lineages were circulating inside the country without evidence of VOC and VOI importation. However, a lineage turnover accompanied the third epidemic peak during March and April 2021, involving the emergence of B.1 lineage descendants with high mutation accumulation (B.1.621 and the provisionally assigned B.1+L249S+E484K) (9), as well as the introduction of the B.1.1.7, P.1 and VOI in some cities.

In this study, we reported the emergence and spread of the novel B.1.621 lineage of SARS-CoV-2, a new VOI with the insertion 146N and several amino acid substitutions in the Spike protein (Y144T, Y145S, R346K, E484K, N501Y and P681H).

 

[Ygggdrasil]

Here's a nice graph from nextstrain.org showing the emergence of delta:

https://nextstrain.org/ncov/gisaid/global

At its peak in April 2021, Alpha made up ~ 46% of sequences submitted to GISAID. Delta now makes up ~73% of sequences submitted to GISAID.

 

[Astronuc]

I was talking with a family member and doctor, who mentioned they are dealing with Delta, Delta-plus, Epsilon and Lambda.

At the end of June, Delta was not as dominant in the US, and Delta-plus was just taking off in India. I hadn't heard much about Epsilon or Lambda then either.

I think we covered Delta very well, but now Delta Plus is surging in parts of the US and world.

The Delta Plus variant – also known as B.1.617.2.1 or AY.1 – contains a new mutation in the spike protein the virus uses to enter human cells, called K417N. As it’s still closely linked to Delta, it’s been called Delta Plus rather than another letter in the Greek alphabet, according to WHO’s naming system for COVID-19 variants. So far, Delta Plus has been found in relatively low numbers.

https://www.gavi.org/vaccineswork/theres-now-delta-plus-variant-covid-19-what-does-mean

Both Epsilon (B.1.427/B.1.429) and Lambda variants may have some immunity to vaccines, but it's not clear which vaccines.
https://science.sciencemag.org/content/373/6555/648 (I noticed a type in B1.1.427, so there may be others)

A novel variant of concern (VOC) named CAL.20C (B.1.427/B.1.429), which was originally detected in California, carries spike glycoprotein mutations S13I in the signal peptide, W152C in the N-terminal domain (NTD), and L452R in the receptor-binding domain (RBD).

https://en.wikipedia.org/wiki/SARS-CoV-2_Epsilon_variant
https://www.cdc.gov/coronavirus/2019-ncov/variants/variant-info.html
https://gvn.org/covid-19/epsilon-b-1-427-b-1-429/https://en.wikipedia.org/wiki/SARS-CoV-2_Lambda_variant

The Lambda genome has the following amino acid mutations, all of which are in the virus's spike protein code: G75V, T76I, Δ246-252, L452Q, F490S, D614G and T859N.

https://www.news-medical.net/news/2...s-potential-to-become-variant-of-concern.aspx

Then there is the Colombia variant (B.1.621), considered a variant of interest (VOI), which . . .

. . . has the accumulation of several substitutions affecting the Spike protein, including the amino acid changes T95I, Y144T, Y145S and the insertion 146N in the N-terminal domain, R346K, E484K and N501Y in the Receptor-binding Domain (RBD) and P681H1 in the S1/S2 cleavage site of the Spike protein. The rapid increase in frequency and fixation in a relatively short time in Magdalena, Atlántico, Bolivar, Bogotá D.C, and Santander that were near the theoretical herd immunity suggests an epidemiologic impact.

https://www.newsweek.com/colombian-covid-variant-spreading-areas-florida-1613503

The B.1.621 variant, which is being commonly referred to as the Colombian Variant, is responsible for 10 percent of COVID patients at one Miami hospital, according to a health official's report on Monday.

August 2 - https://coronavirus.nautil.us/colombian-covid-variant/

A variant of COVID-19 that first originated in Colombia is now spreading in south Florida, and one health official said the Colombian strain has accounted for about 10% of the positive cases being sequenced at the University of Miami’s pathology lab.

Edit/update - related discussion
https://www.physicsforums.com/threa...coronavirus-different-from-the-others.985500/

 

[Ygggdrasil]

I was talking with a family member and doctor, who mentioned they are dealing with Delta, Delta-plus, Epsilon and Lambda.

Here's a nice figure from the CDC showing the prevalence of the different variants in the US:

https://covid.cdc.gov/covid-data-tracker/#variant-proportions

Currently, the Delta variants make up a huge proportion of cases in the US, with other variants contributing only a few percent of cases at most. Lambda has not yet shown up in the US, so it's not known how well that would spread in the US yet.

However, Epsilon, which the WHO no longer classifies as a variant of interest, shows a different story. This variant was first detected in California, and researchers found that the variant spread much faster than the original strain of SARS-CoV-2. During the Winter surge in California, Epsilon went from ~3% of cases in October 2020 to ~60% of cases in Feb 2021 (CDPH data). However, since then, the prevalence of Epsilon has steadily decreased down to 0.1% of cases in July 2021. This decrease likely suggests that the Epsilon variant was outcompeted by more transmissible variants, first Alpha and later Delta.

 

[Astronuc]

A month later (almost), the Delta variant dominates

Parts of Texas have no ICU beds, and I heard reports that Alabama has no ICU beds left, and apparently similar shortages are occurring in Louisiana and Mississippi.

 

[Astronuc]

I heard a presentation (unpublished) the other day on the sequencing of a group of SARS-Cov-2 specimens taken from a select population, with 2 Alpha variant and the rest Delta variant as I recall. Each sample had a unique set of mutations, which made me wonder with the Delta virus spread, it seems a new subvariant is available from each person who becomes infected. A term used was non-synonomous mutations, and there were about 16 (+/-) mutations in each specimen.

From last year, Investigating the genomic landscape of novel Coronavirus (2019-nCoV) to identify non-synonymous mutations for use in diagnosis and drug design - Journal of Clinical Virology, July 2020
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7227581/

 

[atyy]

A term used was non-synonomous mutations, and there were about 16 (+/-) mutations in each specimen.

A synonymous mutation is a mutation in the RNA sequence that does not affect the amino acid sequence of a protein (because more than one RNA sequence can correspond to a particular amino acid). Since the amino acid sequence (not the RNA sequence) determines how the virus interacts with cells, synonymous mutations have no effect on whether the virus will more easily evade the vaccine or become more transmissible.

A non-synonymous mutation is a changes the protein, so these can affect immune escape and transmissibility.

 

[Laroxe]

Yes, I heard that discussed on TWiV. The virus adapts to each new host, very specifically apparently, so we all get our own version, given a little time. I expect these changes will be less likely to involve the parts of the virus that get them the label of variants of concern, as the selective pressures will be different and will respond to the intra organism variations. Many of these changes will be lost as the virus makes its way through the population and are replaced, but some will persist, and are still transmissible. This has been suggested as the explanation for the observation that the effects of convalescent plasma is only significant when it's collected from the local population of the recipient's. However, the logistics of the donor plasma schemes, the rather unimpressive results and the development of synthetic monoclonals, means that this was never really tested.

There will of course continue to be mutations that occur that have nothing to do with the host's individual differences, but might still affect the viruses inter-organism behaviours, the risk of these changes is related to the amount of virus circulating in the population.