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

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The discussion focuses on the increased transmissibility and mutations of various SARS-CoV-2 variants, particularly B.1.1.7 (UK), B.1.351 (South Africa), and B.1.427/B.1.429 (California). The B.1.1.7 variant features mutations such as N501Y, which enhances binding to human ACE2, and deletions that may help evade immune responses. Studies indicate it has a significantly higher reproduction number, suggesting greater transmissibility. The B.1.351 variant also contains mutations like E484K, which may allow it to evade immunity from vaccines and previous infections. The California variant is noted for its potential increased contagiousness and severity, with some evidence suggesting it could lead to higher mortality rates.PCR testing challenges are highlighted, particularly with the B.1.1.7 variant, where specific mutations can lead to false negatives. However, tests are designed to detect multiple viral RNA regions, mitigating this issue.
  • #31
Exonucleases are involved in proofreading replication because they can remove mismatched nucleotides from the end of the nascent RNA molecule. The SARS-CoV-2 Nsp14 gene does encode a protein with exonuclease activity that helps to proofread RNA replication (see https://www.cell.com/molecular-cell/pdf/S1097-2765(20)30518-9.pdf). Maybe this is what you were referring to.
 
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  • #32
Here are the two pre-print articles analyzing infections with the new variants from California, suggesting that the variant may be slightly more transmissible:

Estimation of secondary household attack rates for emergent SARS-CoV-2 variants detected by genomic surveillance at a community-based testing site in San Francisco
https://www.medrxiv.org/content/10.1101/2021.03.01.21252705v1

Transmission, infectivity, and antibody neutralization of an emerging SARS-CoV-2 variant in California carrying a L452R spike protein mutation
https://www.medrxiv.org/content/10.1101/2021.03.07.21252647v1

Popular press summary: https://www.nytimes.com/2021/02/23/health/coronavirus-california-variant.html
 
  • #33
Another observational study published in the peer reviewed journal, Nature, arguing that the B.1.1.7 variant is more deadly than the original SARS-CoV-2 strains. The data are fairly consistent with the findings of the BMJ study I cited earlier:

The B117 COVID-19 variant, which was first identified in the United Kingdom in October 2020, may pose a 61% higher risk of 28-day mortality, according to a study published today in Nature.

The finding is in line with last week's BMJ study that reported B117 had a 64% higher 28-day risk of death among people older than 30, although both studies note absolute 28-day mortality risk remains low for most populations.
https://www.cidrap.umn.edu/news-per...dlier-other-covid-19-strains-more-data-affirm

Here's the study:

Increased mortality in community-tested cases of SARS-CoV-2 lineage B.1.1.7
https://www.nature.com/articles/s41586-021-03426-1

Abstract:
SARS-CoV-2 lineage B.1.1.7, a variant first detected in the UK in September 20201, has spread to multiple countries worldwide. Several studies have established that B.1.1.7 is more transmissible than preexisting variants, but have not identified whether it leads to any change in disease severity2. Here we analyse a dataset linking 2,245,263 positive SARS-CoV-2 community tests and 17,452 COVID-19 deaths in England from 1 September 2020 to 14 February 2021. For 1,146,534 (51%) of these tests, the presence or absence of B.1.1.7 can be identified because of mutations in this lineage preventing PCR amplification of the spike gene target (S gene target failure, SGTF1). Based on 4,945 deaths with known SGTF status, we estimate that the hazard of death associated with SGTF is 55% (95% CI 39–72%) higher after adjustment for age, sex, ethnicity, deprivation, care home residence, local authority of residence and test date. This corresponds to the absolute risk of death for a 55–69-year-old male increasing from 0.6% to 0.9% (95% CI 0.8–1.0%) within 28 days after a positive test in the community. Correcting for misclassification of SGTF and missingness in SGTF status, we estimate a 61% (42–82%) higher hazard of death associated with B.1.1.7. Our analysis suggests that B.1.1.7 is not only more transmissible than preexisting SARS-CoV-2 variants, but may also cause more severe illness.
 
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  • #34
Reuters - Virus variants found to be deadlier, more contagious; some may thwart vaccines
https://www.msn.com/en-us/health/medical/virus-variants-found-to-be-deadlier-more-contagious-some-may-thwart-vaccines/ar-BB1eGYzs?li=BBnbfcL
Antibodies induced by the Moderna Inc and Pfizer Inc/BioNTech SE vaccines are dramatically less effective at neutralizing some of the most worrying Coronavirus variants, a new study suggests. Researchers obtained blood samples from 99 individuals who had received one or two doses of either vaccine and tested their vaccine-induced antibodies against virus replicas engineered to mimic 10 globally circulating variants. Five of the 10 variants were "highly resistant to neutralization," even when volunteers had received both doses of the vaccines, the researchers reported on Friday in Cell. All five highly resistant variants had mutations in the spike on the virus surface - known as K417N/T, E484K, and N501Y - that characterize a variant rampant in South Africa and two variants spreading rapidly in Brazil.
 
  • #36
Astronuc said:
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).
 
  • #37
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
 
  • #39
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."
 
  • #40
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.
 
  • #41
Astronuc said:
B.1.617, first identified in India
Wrichik Basu said:
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.
 
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  • #42
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).
 
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  • #43
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
 
  • #44
Astronuc said:
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.
 
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  • #45
Astronuc said:
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
 
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  • #46
pinball1970 said:
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.
 
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  • #47
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
 
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  • #48
pinball1970 said:
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) ...
 
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  • #49
atyy said:
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.
 
  • #50
Astronuc said:
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.
 
  • #51
Rive said:
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...
 
  • #52
Rive said:
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.
 
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  • #53
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/
 
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  • #54
pinball1970 said:
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 said:
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.
 
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  • #55
pinball1970 said:
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.
 
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  • #56
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
 
  • #59
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​

 
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  • #60
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?
 
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