{I read, copy, cut, paste}
• covid-19 delta variant (sar-covid-2 delta variant) (also known as (SARS‑CoV‑2))
• spreads as easily as chickenpox (internal Centers for Disease Control and Prevention slide presentation)
• officials must "acknowledge the war has changed".
• prevention measures, including mask-wearing
• vaccinated people can spread the virus
• a variant so contagious that it acts almost like a different novel virus
• still-unpublished data from outbreak investigations and outside studies showing that vaccinated individuals infected with delta may be able to transmit the virus as easily as those who are unvaccinated.
• Vaccinated people infected with delta have measurable viral loads similar to those who are unvaccinated and infected with the variant.
• Vaccinated people infected with delta have measurable viral loads similar to those who are unvaccinated and infected with the variant. ([ this one need more explanation: all vaccinated people?, some vaccinated people?, if you have measurable viral loads similar to those who are unvaccinated, then it seems like the vaccine is really not working for the new variant in the people you have tested for the viral load; of course, it does not mean you should not get vaccinated, but if breakthrough cases [where the people who are vaccinated still get infected and spreading the virus] exist, and the new variant is really that different then, maybe you gals and guys need to work on a new vaccine variant?; oh, you are already working on that, but ...; how about working on a vaccine to counter the breakthrough cases; yes, look into those cases ... ])
• conclusion (in my [uneducated] opinion): if all of that is true, then there is a new virus on the scene (SARS‑CoV‑3)(?).
• no, not a new virus, a new strain
• this is a new flu virus (the common cold?) (do not read this) (speculation)
'The War Has Changed': Internal CDC Document Urges New Messaging, Warns Delta Infections Likely More Severe
Posted by msmash • 2021-Jul-30 10:37 • View on SlashDot • Shareable Link
Yasmeen Abutaleb, Carolyn Y. Johnson, and Joel Achenbach, reporting at Washington
Post:
The delta variant of the coronavirus appears to cause more severe illness than earlier variants and spreads as easily as chickenpox, according to an internal federal health document that argues officials must "acknowledge the war has changed." The document is an internal Centers for Disease Control and Prevention slide presentation, shared within the CDC and obtained by The Washington Post. It captures the struggle of the nation's top public health agency to persuade the public to embrace vaccination and prevention measures, including mask-wearing, as cases surge across the United States and new research suggests vaccinated people can spread the virus.
The document strikes an urgent note, revealing the agency knows it must revamp its public messaging to emphasize vaccination as the best defense against a variant so contagious that it acts almost like a different novel virus, leaping from target to target more swiftly than Ebola or the common cold. It cites a combination of recently obtained, still-unpublished data from outbreak investigations and outside studies showing that vaccinated individuals infected with delta may be able to transmit the virus as easily as those who are unvaccinated. Vaccinated people infected with delta have measurable viral loads similar to those who are unvaccinated and infected with the variant.
"I finished reading it significantly more concerned than when I began," Robert Wachter, chairman of the Department of Medicine at the University of California at San Francisco, wrote in an email. CDC scientists were so alarmed by the new research that the agency earlier this week significantly changed guidance for vaccinated people even before making new data public. The data and studies cited in the document played a key role in revamped recommendations that call for everyone -- vaccinated or not -- to wear masks indoors in public settings in certain circumstances, a federal health official said.
source:
https://alterslash.org/day/20210730#article-19444531
https://science.slashdot.org/story/21/07/30/1437244/the-war-has-changed-internal-cdc-document-urges-new-messaging-warns-delta-infections-likely-more-severe#comments
https://www.cdc.gov/mmwr/volumes/70/wr/mm7031e2.htm
https://en.wikipedia.org/wiki/SARS-CoV-2
https://en.wikipedia.org/wiki/SARS-CoV-2_Delta_variant
• do not believe in everything you read
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sar-cov-2 and HIV (immuno compromising conditions)
•••• ••• ••••
During July 3–17, 2021, multiple summer events and large public gatherings were held in a town in Barnstable County, Massachusetts, that attracted thousands of tourists from across the United States. Beginning July 10, the Massachusetts Department of Public Health (MA DPH) received reports of an increase in COVID-19 cases among persons who reside in or recently visited Barnstable County, including in fully vaccinated persons. Persons with COVID-19 reported attending densely packed indoor and outdoor events at venues that included bars, restaurants, guest houses, and rental homes.
•••• ••• ••••
Among the 469 cases in Massachusetts residents, 346 (74%) occurred in persons who were fully vaccinated; of these, 301 (87%) were male, with a median age of 42 years. Vaccine products received by persons experiencing breakthrough infections were Pfizer-BioNTech (159; 46%), Moderna (131; 38%), and Janssen (56; 16%); among fully vaccinated persons in the Massachusetts general population, 56% had received Pfizer-BioNTech, 38% had received Moderna, and 7% had received Janssen vaccine products. Among persons with breakthrough infection, 274 (79%) reported signs or symptoms, with the most common being cough, headache, sore throat, myalgia, and fever.
•••• ••• ••••
Second, asymptomatic breakthrough infections might be underrepresented because of detection bias. Third, demographics of cases likely reflect those of attendees at the public gatherings, as events were marketed to adult male participants; further study is underway to identify other population characteristics among cases, such as additional demographic characteristics and underlying health conditions including immunocompromising conditions.***
•••• ••• ••••
*** A preliminary analysis matching cluster-associated COVID-19 cases with the state HIV case surveillance data identified 30 (6%) cases with verified HIV infection; all were virally suppressed, and none were hospitalized as a result of infection with SARS-CoV-2.
source:
https://www.cdc.gov/mmwr/volumes/70/wr/mm7031e2.htm
• do not believe in everything you read
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breakthrough cases are the vaccinated people who become infected with the virus who still get sick, are hospitalized, or die from COVID-19. Because no vaccines are 100% effective at preventing illness. Vaccinated people can also be infected and show no symptom.
According to the Harvard T.H. Chan School of Public Health's news article:
Fortunately, breakthrough infections are rare, according to the experts quoted in the article. Most vaccinated people who become infected will either be asymptomatic or will experience only mild symptoms. But it’s still important to control outbreaks, said Fortune. That’s because the more that the virus is left to circulate, the more chances it has to mutate in a way that makes it more transmissible, able to cause more severe disease, or more able to evade the protection of vaccines.
source:
https://www.cdc.gov/vaccines/covid-19/health-departments/breakthrough-cases.html
https://www.hsph.harvard.edu/news/hsph-in-the-news/why-breakthrough-covid-19-cases-happen/
• do not believe in everything you read
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1. Delta is more contagious than the other virus strains.
Delta is the name for the B.1.617.2. variant, a SARS-CoV-2 mutation that
([ how did it get into the country if it really did originated from India ])
([ it was [initially identified] in India. ])
([ maybe the mutation happened concurrently in the states ])
source:
https://www.yalemedicine.org/news/5-things-to-know-delta-variant-covid
• do not believe in everything you read
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Variants in the United States
We are monitoring multiple variants; currently there are four notable variants in the United States:
B.1.1.7 (Alpha): This variant was first detected in the United States in December 2020. It was initially detected in the United Kingdom.
B.1.351 (Beta): This variant was first detected in the United States at the end of January 2021. It was initially detected in South Africa in December 2020.
P.1 (Gamma): This variant was first detected in the United States in January 2021. P.1 was initially identified in travelers from Brazil, who were tested during routine screening at an airport in Japan, in early January.
B.1.617.2 (Delta): This variant was first detected in the United States in March 2021. It was initially identified in India in December 2020.
source:
https://www.cdc.gov/coronavirus/2019-ncov/variants/variant.html
• do not believe in everything you read
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GISAID SARS-CoV-2 database
source:
https://scitechdaily.com/tracing-covid-back-to-origin-many-variant-strains-were-already-present-before-the-first-known-cases-identified-in-china/
• do not believe in everything you read
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SARS-CoV-2 Life Cycle: Stages and Inhibition Targets
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) belongs to the enveloped positive-sense RNA viruses. This virus is characterized by club-like spikes on the surface, and a unique replication strategy. Cell entry of coronaviruses depends on binding of the viral spike (S) proteins to cellular receptors and on S protein priming by host cell proteases. Unravelling which cellular factors are used by SARS-CoV-2 for entry might provide insights into viral transmission and reveal therapeutic targets.1
In the following the replication cycle of SARS-CoV-2 is explained together with possible inhibitors and their respective targets. This compilation is based on current literature however we make no claim to accuracy.
Stages of the SARS-CoV-2 Life Cycle:
1. Virus Entry
2. Translation of Viral Replication Machinery
3. Replication
4. Translation of Viral Structure Proteins
5. Virion Assembly
6. Release of Virus
https://www.antibodies-online.com/a0ae968aacd4883458c83e68d2996e8ad1be38cb/resources/images/blog/sars-cov2-replicationcycle-v8.png
•••• ••• ••••
Release of Virus (6)
Virions are then released from the infected cell through exocytosis and search another host cell. Oseltamivir inhibits cleavage of sialic acids by neuroamidase from the cell receptors thus preventing release of newly formed virions from the cell surface (Inhibitor XI). 8
References
(1) Hoffmann et al.: SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor, Cell (2020), PDF
Suprewicz et al.: Vimentin binds to SARS-CoV-2 spike protein and antibodies targeting extracellular vimentin block in vitro uptake of SARS-CoV-2 virus-like particles, BioRxiv preprint (2021), [DOI]
(2) Henderson et al: Controlling the SARS-CoV-2 Spike Glycoprotein Conformation, Nat Struct Mol Biol. (2021), [ DOI]
(3) Shirato, K., Kawase, M. & Matsuyama, S.: Wild-type human coronaviruses prefer cell-surface TMPRSS2 to endosomal cathepsins for cell entry, Virology 517, 9–15 (2018), [ DOI]
(4) Zhavoronkov et al.: Potential COVID-2019 3C-like Protease Inhibitors Designed Using Generative Deep Learning Approaches, ChemRxiv (2020), [ DOI]
(5) Shin et al.: Saracatinib Inhibits Middle East Respiratory Syndrome-Coronavirus Replication In Vitro, Viruses, 10(6):283 (2018), [ DOI]
(6) Lin, S. C., Ho, C. T., Chuo, W. H., Li, S., Wang, T. T., & Lin, C. C. : Effective inhibition of MERS-CoV infection by resveratrol, BMC Infectious Diseases, 17(1)(2017), [ DOI]
(7) McKimm‐Breschkin: Influenza neuraminidase inhibitors: Antiviral action and mechanisms of resistance. Influenza and Other Respiratory Viruses 7(Suppl. 1), 25–36., [ PMC]
source:
https://www.antibodies-online.com/resources/18/5410/sars-cov-2-life-cycle-stages-and-inhibition-targets/
• do not believe in everything you read
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Severe acute respiratory syndrome coronavirus (SARS-CoV or SARS-CoV-1)[2] is a strain of coronavirus that causes severe acute respiratory syndrome (SARS).[3] It is an enveloped, positive-sense, single-stranded RNA virus which infects the epithelial cells within the lungs.[4] The virus enters the host cell by binding to angiotensin-converting enzyme 2.[5] It infects humans, bats, and palm civets.[6][7]
On 16 April 2003, following the outbreak of SARS in Asia and secondary cases elsewhere in the world, the World Health Organization (WHO) issued a press release stating that the coronavirus identified by a number of laboratories was the official cause of SARS. The Centers for Disease Control and Prevention (CDC) in the United States and National Microbiology Laboratory (NML) in Canada identified the SARS-CoV-1 genome in April 2003.[8][9] Scientists at Erasmus University in Rotterdam, the Netherlands, demonstrated that the SARS coronavirus fulfilled Koch's postulates, thereby confirming it as the causative agent. In the experiments, macaques infected with the virus developed the same symptoms as human SARS victims.[10]
A virus very similar to SARS was discovered in late 2019. This virus, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is the causative pathogen of COVID-19, forming the COVID-19 pandemic.[11]
source:
https://en.wikipedia.org/wiki/SARS-CoV-1
• do not believe in everything you read
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Severe acute respiratory syndrome (SARS) is the disease caused by SARS-CoV-1. It causes an often severe illness and is marked initially by systemic symptoms of muscle pain, headache, and fever, followed in 2–14 days by the onset of respiratory symptoms,[12] mainly cough, dyspnea, and pneumonia. Another common finding in SARS patients is a decrease in the number of lymphocytes circulating in the blood.[13]
In the SARS outbreak of 2003, about 9% of patients with confirmed SARS-CoV-1 infection died.[14] The mortality rate was much higher for those over 60 years old, with mortality rates approaching 50% for this subset of patients.[14]
source:
https://en.wikipedia.org/wiki/SARS-CoV-1
• do not believe in everything you read
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flu virus (influenza virus)
source:
https://en.wikipedia.org/wiki/Orthomyxoviridae
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Now we know that it is caused by an RNA virus of the family Orthomyxoviridae (the influenza viruses). In humans, common symptoms of influenza infection are fever, sore throat, muscle pains, severe headache, coughing, and weakness and fatigue.[7] In more serious cases, influenza causes pneumonia, which can be fatal, particularly in young children and the elderly. While sometimes confused with the common cold, influenza is a much more severe disease and is caused by a different type of virus.[8] Although nausea and vomiting can be produced, especially in children,[7] these symptoms are more characteristic of the unrelated gastroenteritis, which is sometimes called "stomach flu" or "24-hour flu."[9]
Typically, influenza is transmitted from infected mammals through the air by coughs or sneezes, creating aerosols containing the virus, and from infected birds through their droppings. Influenza can also be transmitted by saliva, nasal secretions, feces and blood. Healthy individuals can become infected if they breathe in a virus-laden aerosol directly, or if they touch their eyes, nose or mouth after touching any of the aforementioned bodily fluids (or surfaces contaminated with those fluids). Flu viruses can remain infectious for about one week at human body temperature, over 30 days at 0 °C (32 °F), and indefinitely at very low temperatures (such as lakes in northeast Siberia). Most influenza strains can be inactivated easily by disinfectants and detergents.[10][11][12]
Flu spreads around the world in seasonal epidemics.
source:
https://en.wikipedia.org/wiki/Influenza_pandemic
• do not believe in everything you read
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https://www.who.int/news-room/fact-sheets/detail/influenza-(seasonal)
Seasonal influenza is an acute respiratory infection caused by influenza viruses which circulate in all parts of the world.
The pathogen
There are 4 types of seasonal influenza viruses, types A, B, C and D. Influenza A and B viruses circulate and cause seasonal epidemics of disease.
• Influenza A viruses are further classified into subtypes according to the combinations of the hemagglutinin (HA) and the neuraminidase (NA), the proteins on the surface of the virus. Currently circulating in humans are subtype A(H1N1) and A(H3N2) influenza viruses. The A(H1N1) is also written as A(H1N1)pdm09 as it caused the pandemic in 2009 and subsequently replaced the seasonal influenza A(H1N1) virus which had circulated prior to 2009. Only influenza type A viruses are known to have caused pandemics.
• Influenza B viruses are not classified into subtypes, but can be broken down into lineages. Currently circulating influenza type B viruses belong to either B/Yamagata or B/Victoria lineage.
• Influenza C virus is detected less frequently and usually causes mild infections, thus does not present public health importance.
• Influenza D viruses primarily affect cattle and are not known to infect or cause illness in people.
Signs and symptoms
Seasonal influenza is characterized by a sudden onset of fever, cough (usually dry), headache, muscle and joint pain, severe malaise (feeling unwell), sore throat and a runny nose. The cough can be severe and can last 2 or more weeks. Most people recover from fever and other symptoms within a week without requiring medical attention. But influenza can cause severe illness or death especially in people at high risk (see below).
source:
https://www.who.int/news-room/fact-sheets/detail/influenza-(seasonal)
• do not believe in everything you read
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H5N1
H5N1 is a subtype of the influenza A virus, also known as A(H5N1)
H5N1, also known as HPAI A(H5N1), which stands for highly pathogenic, avian influenza ‘A’ virus, subtype H5N1.
influenza A virus
influenza A virus subtype H5N1
influenza A virus, subtype H5N1
influenza A virus of subtype H5N1
a bird-adapted strain of H5N1
a bird-adapted strain of H5N1 (genetic subtype)
HPAI A(H5N1)
HP - highly pathogenic (LP - low pathogenic)
AI - avian influenza (bird-adapted virus strain)
A - influenza A virus, influenza virus of type A
H5N1 - subtype H5N1
H5 - H5 stands for the 5th of several known types of the
protein hemagglutinin.
N1 - N1 stands for the 1st of several known types of the
protein neuraminidase.
H5 - H5 influenza viruses
- H5 viruses
H - hemagglutinin (HA) RNA strands and
N - neuraminidase (NA) RNA strands
RNA strands specify the structure of proteins.
H5N1 - HA subtype (H5) - subtype H5 - RNA strands - RNA segments
NA subtype (N1) - subtype N1 - RNA strands - RNA segments
H5N1 - H - Hemagglutinin protein - RNA strands - RNA genetic strand
N - Neuraminidase protein - RNA strands - RNA genetic strand
H5N1 - H - surface antigen (Hemagglutinin) - gene - RNA
N - secondary surface antigen (Neuraminidase) - gene - RNA
Hemagglutinin - an antigenic glycoprotein found on the surface of
the influenza viruses and is responsible for binding
the virus to the cell that is being infected.
- responsible for binding the virus to the cell
- enable the virus to infect the cell
- to bind and then to infect the cell, in order to replicate
- Hemagglutinin or an antigenic glycoprotein made this binding
possible; the binding thus make it possible for the virus to
infect the cell; the virus must infect the cell, in order to
replicating itself; the virus can not self-replicate and
virus needs the cell as a host for replication.
Neuraminidase - an antigenic glycosylated enzyme found on the surface of
the influenza viruses and facilitates the release of
progeny viruses from infected cells.[34]
- enzyme, glycosylated enzyme
- facilitates the release of viruses from infected cells
- the more Neuraminidases enzyme there is on the surface of the
influenza virus, the easier it is for the virus to spread itself
HA - Hemagglutinin antigen ?
HA - Hemagglutinin antigenic surface ?
surface antigen (Hemagglutinin) - binding - alpha 2-3 sialic acid receptors
Like all other influenza A subtypes, the H5N1 subtype is an RNA virus.
Dr. Daniel Lucey, co-director of the Biohazardous Threats and Emerging Diseases graduate program at Georgetown University has made this point, "There is no H5N1 pandemic so there can be no pandemic vaccine".[43]
humanized influenza A virus (a human flu virus of type A)
The avian influenza hemagglutinin binds alpha 2-3 sialic acid receptors, while human influenza hemagglutinins bind alpha 2-6 sialic acid receptors.[22]
Α α alpha (Greek letter)
hemagglutinin alpha 2-3 sialic acid receptors [α2-3-linkage of sialic acids]
hemagglutinin alpha 2-6 sialic acid receptors [α2-6-linked sialic acids]
//
// In the special mice breed to resemble humans, injecting sialic acids
// antibodies in these mice created a low grade inflammation with the red
// meat sialic acids - and that inflammation causes the tumors to grow
// larger than they would otherwise.
//
// Primate Evolution and Human Disease
//
// Dr. Ajit Varki, Glycobiology research and training center,
// the surface of cells
// the sugar molecules that make up the outside of cell
//
// sialic acids
// sialic quirks
// most of the diseases we loathe are only able to attack humans by
// acting like our sialic acids
// cancerous tumors contain high amounts of this foreign sialic acids
//
// sialic acid is a generic term for neuraminic acid, a monosaccharide
//
// sialic acid are found widely distributed in animal tissues; in other
// organisms, from plants and fungi to yeast and bacteria,
// sialic acid are found in glycoproteins and gangliosides (they occur
// at the end of sugar chains connected to the surfaces of cells and
// soluble proteins).
//
// Neu5Ac is the most common sialic acids in mammals.
// These acidic sugars share a 9-carbon backbone.
//
// non-human sialic acid
// N-glycolylneuraminic acid (Neu5Gc)
//
Α Alpha, uppercase Greek letter alpha
α αlpha, lowercase Greek letter alpha
from the intestine of birds to the airway of humans
from the intestine [α2-3-linkage of sialic acids] of birds
αlpha two dash 3hree linkage
to the airway [α2-6-linked sialic acids] of humans
αlpha two dash 6ix linked
22. Shinya K, Ebina M, Yamada S, Ono M, Kasai N, Kawaoka Y (March 2006). "Avian flu: influenza virus receptors in the human airway". Nature. 440 (7083): 435–6.
There is now evidence that a direct bird to human transfer did occur at least once before, when the infamous 1918 influenza pandemic killed tens of millions of people [83,84].
source: en.wikipedia.org,
The Next Influenza Pandemic Lessons from Hong Kong, 1997 - Volume 5, Number 2 — April 1999 - Emerging Infectious Disease journal - CDC
• do not believe in everything you read
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What is the difference between Influenza (Flu) and COVID-19?
Influenza (flu) and COVID-19 are both contagious respiratory illnesses, but they are caused by different viruses. COVID-19 is caused by infection with a coronavirus first identified in 2019, and flu is caused by infection with influenza viruses.
COVID-19 seems to spread more easily than flu. However, as more people become fully vaccinated against COVID-19, the spread of the virus that causes COVID-19 should slow down. More information about COVID-19 vaccines and how well they work.
Compared to flu, COVID-19 can cause more serious illnesses in some people. COVID-19 can also take longer before people show symptoms and people can be contagious for longer.
Because some of the symptoms of flu, COVID-19, and other respiratory illnesses are similar, the difference between them cannot be made based on symptoms alone.
People can be infected with both flu and the virus that causes COVID-19 at the same time and have symptoms of both influenza and COVID-19.
Overall, COVID-19 seems to cause more serious illnesses in some people.
Compared to young children, teens and adolescents with COVID-19 are more likely to have Multisystem Inflammatory Syndrome in Children (MIS-C), a rare but severe complication of COVID-19. However, for adolescents, the risk of serious COVID-19 illness is less than in children younger than 5.
source:
https://www.cdc.gov/flu/symptoms/flu-vs-covid19.htm
• do not believe in everything you read
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SARS-CoV-2 Delta variant, also known as lineage B.1.617.2, is a variant of lineage B.1.617 of SARS-CoV-2, the virus that causes COVID-19.[1]
It has mutations in the gene encoding the SARS-CoV-2 spike protein[5] causing the substitutions T478K, P681R and L452R,[6] which are known to affect transmissibility of the virus as well as whether it can be neutralised by antibodies for previously circulating variants of the COVID-19 virus.[7][failed verification]
Some evidence suggests vaccinated people are more likely to develop symptoms from Delta than other variants (why?)
because ...
COVID-19 vaccines are effective in preventing severe disease or hospitalisation from infection with the variant, and some evidence suggests vaccinated people are more likely to develop symptoms from Delta than other variants of SARS-CoV-2.[9]
On 7 May 2021, PHE changed their classification of lineage B.1.617.2 from a variant under investigation (VUI) to a variant of concern (VOC) based on an assessment of transmissibility being at least equivalent to B.1.1.7 (Alpha variant);[10] the UK's SAGE subsequently estimated a "realistic" possibility of being 50% more transmissible.[11]
On 15 June 2021, the Centers for Disease Control and Prevention (CDC) declared Delta a variant of concern.[12]
"Delta plus" variant
• people with Delta infection had 1,000 time [1000] more copies of the virus in the respiratory tracts than those with Wuhan strain infection (not peer-reviewed)(Guangdong Provincial Center for Disease Control and Prevention) (transmissibility)
A study[75] published online (not peer-reviewed) by Guangdong Provincial Center for Disease Control and Prevention may partly explain the increased transmissibility: people with Delta infection had 1,000 time [1000] more copies of the virus in the respiratory tracts than those with Wuhan strain infection; and it took on average 4 days for people infected with Delta for the virus to be detectable compared to 6 days with the Wuhan strain.[76][77]
In countries other than India, the first cases of the variant were detected in late February 2021, including the United Kingdom on 22 February, the United States on 23 February and Singapore on 26 February.[156][3][2]
source:
https://en.wikipedia.org/wiki/SARS-CoV-2_Delta_variant
https://en.wikipedia.org/wiki/SARS-CoV-2_lineage_B.1.617
https://en.wikipedia.org/wiki/SARS-CoV-2_Alpha_variant
https://en.wikipedia.org/wiki/Variants_of_SARS-CoV-2
• do not believe in everything you read
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November 2002
On 16 November 2002,[9] an outbreak of severe acute respiratory syndrome (SARS) began in China's Guangdong province, bordering Hong Kong. The first case of infection was traced to Foshan.[10][11] This first outbreak affected people in the food industry, such as farmers, market vendors, and chefs.[12][13] The outbreak spread to healthcare workers after people sought medical treatment for the disease.[13] The People's Republic of China notified the World Health Organization (WHO) about this outbreak on 10 February 2003, reporting 305 cases including 105 health-care workers and five deaths.[14] Later it reported that the outbreak in Guangdong had peaked in mid-February 2003. However, this appears to have been false because subsequently 806 cases of infection and 34 deaths were reported.[15] Italian physician Carlo Urbani was the first to identify SARS as probably a new and dangerously contagious viral disease.[16][17]
Early in the epidemic, the Chinese government discouraged its press from reporting on SARS, delayed reporting to WHO, and initially did not provide information to Chinese outside Guangdong province, where the disease is believed to have originated.[18] Also, a WHO team that travelled to Beijing was not allowed to visit Guangdong province for several weeks.[19] This resulted in international criticism, which seems to have led to a change in government policy in early April.[20][21]
January 2003
The first super-spreader, Zhou Zuofen, a fishmonger, checked in to the Sun Yat-sen Memorial Hospital in Guangzhou on 31 January, where he infected 30 nurses and doctors. The virus soon spread to nearby hospitals.[22]
February 2003
Hong Kong
Ninth floor layout of the Hotel Metropole in Hong Kong, showing where a super-spreading event of the severe acute respiratory syndrome (SARS) occurred
In February 2003, Hong Kong's SARS index patient was Liu Jianlun, who had come to attend a family wedding gathering; Liu was on the staff at Sun Yat-Sen Memorial Hospital in Guangzhou and had treated SARS patients.[23]
On 21 February, Liu and his wife checked into room 911 on the ninth floor of the Metropole Hotel. Despite feeling ill he visited with his family and they traveled around Hong Kong. By the morning of 22 February, he knew he was very sick and walked to nearby Kwong Wah Hospital to seek treatment. He warned staff that he was very sick and to put him in isolation. He never recovered and died in the intensive care unit on 4 March.[citation needed]
Liu is believed to have been a SARS super-spreader: 23 other Metropole guests developed SARS, including seven from the ninth floor. Liu's brother-in-law, who sought treatment in late February, was hospitalized in Kwong Wah Hospital on 1 March and died on 19 March. It is estimated that around 80% of the Hong Kong cases were due to Liu.[24]
source:
https://en.wikipedia.org/wiki/Timeline_of_the_SARS_outbreak
• do not believe in everything you read
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• "GGR," or the law of gradual granularity refinement. [ ]
Written by Bill Buxton
JND significance ~ 1 / familiarity.
JND (just noticeable difference)
"What is the smallest level of differentiation that you can perceive as being significant?"
The tilde character (~) means "varies with."
Hence, the law says that the granularity at which we distinguish meaningful differences gets finer the more our familiarity with a subject grows. Conversely, it also says the less familiar we are with something, the coarser the granularity will be before we can distinguish differences as being significant.
Predictable and Avoidable
Let me tie all of this back to our two scenarios. Each is the result of differences in JND (the granularity of recognizing differences of significance) at play between the two parties involved.
In the first, you had the insight and saw something significant in it because you were immersed in the problem space. The granularity of your analysis was really refined. But the subtlety required to appreciate the essence of the idea fell below the threshold of your audience's ability to see any difference between it and what they had seen before.
In the second, the roles were reversed. Yes, you had all of the data. But what you didn't have was the ability to see the significance buried within. The granularity of your analysis was too coarse compared to that of your competitor. Most likely, despite your hard work, you simply weren't sufficiently familiar with the problem space to fully appreciate the significance of its subtleties.
The reason that I've taken the seemingly pretentious step of declaring the GGR as a law is to help emphasize there are no villains or stupid people in any of this. The behaviors in both scenarios are human nature. But that means they are predictable and avoidable――so there are some lessons that can be drawn from all of this.
source:
gradual granularity refinement
https://www.billbuxton.com/BW%20Assets/02a.%20A%20Familiar%20Problem%20Published.pdf
• do not believe in everything you read
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It takes time to gain experience and familiarity that lead to the fineness of granularity wherein the sweet spots lie. And, no, we haven't found a solution to time travel. But the history of technology is full of discoveries of how to move [slower], finer, smoother. That is the heart of your quest to find ways to [slow down] the rate and quality of gaining experience that get you to the fine level. What all of this says is that to be successful, we need to innovate around the whole package, not just one part.”; ([ you need to work on each part, the interaction between the parts, the whole package, and avoid doing all things at the same time ])
── Bill Buxton, February 06, 2008
Innovation & Design :
A Familiar Problem,
gradual granularity refinement
http://www.bloomberg.com/bw/stories/2008-02-06/a-familiar-problembusinessweek-business-news-stock-market-and-financial-advice
https://www.billbuxton.com/BW%20Assets/02a.%20A%20Familiar%20Problem%20Published.pdf
https://www.billbuxton.com/
https://en.wikipedia.org/wiki/Bill_Buxton
• do not believe in everything you read
____________________________________
Patricia S. Churchland and Terrence J. Sejnowski, The computational brain [ ]
pp.113-114
Following training, the accuracy of the classification of new echoes was very good--as good or better than trained humans and other classification methods. In a network with three hidden units, it was possible to analyze the features discovered by the training procedure (figure 3.35). The most important features of the input signals were the frequency bandwidth, the onset time, and the rate of decay of the signal. These general features, which could have been discovered by data analysis techniques, accounted for about 50% of the successfully classified echoes. The remainder of the echoes were more difficult to classify because they did not follow the general trend. To classify these exceptional cases, the hidden units developed weights that recognized clusters of echoes that shared the same spectral features. The most closely the input resembles the prototype, the more near will be the activation vector to the prototypical activation vector. The two-pronged strategy adopted by the hidden units exploited large-scale regularities and finer scale distinctions in different ways.
p.113
Training of the net correctly to categorize proceeds in the following way. We give the net examples of mine echoes and rock echoes, one by one. For each case, the actual values of the output units is measured against what the values ought to have been, given the input. This difference is a measure of error, which can then be used to compute small changes in the weights of the units in the system. This is a gradient-descent procedure, and slowly the weights of the network are adjusted so that when fed a mine echo, either a familiar old example or a brand new case, it gives a value of <1,0>, or close to that, and when fed a rock echo, it responds with something close to <0,1>. (For a more detailed but still basic account, see P. M. Churchland 1989.)
p.464
gradient descent Procedure for reducing error while training a neural network based on taking the derivative of the error with respect to each parameter, then changing the parameters such that the net moves down the error gradient to an error minimum.
(Churchland, Patricia Smith., The computational brain / Patricia S. Churchland and Terrence J. Sejnowski., 1. brain--computer simulation., 2. neural networks (computer science)., 3. neural circuitry., 4. neurosciences--methods., 1992, 1993, )
____________________________________
SARS-CoV-2 virus (human infection)
(dog infection)
(cat infection)
rate of mutation
____________________________________
molecular biology
constant rate of mutation
mammals
genetic dating
genetic dating using constant rate of mutation in mammals
mitochondrial mutation rate variation
molecular clocks
____________________________________
Abstract
Knowledge of the rate of point mutation is of fundamental importance, because mutations are a vital source of genetic novelty and a significant cause of human diseases. Currently, mutation rate is thought to vary many fold among genes within a genome and among lineages in mammals. We have conducted a computational analysis of 5,669 genes (17,208 sequences) from species representing major groups of placental mammals to characterize the extent of mutation rate differences among genes in a genome and among diverse mammalian lineages. We find that mutation rate is approximately constant per year and largely similar among genes. Similarity of mutation rates among lineages with vastly different generation lengths and physiological attributes points to a much greater contribution of replication-independent mutational processes to the overall mutation rate. Our results suggest that the average mammalian genome mutation rate is 2.2 × 10−9 per base pair per year, which provides further opportunities for estimating species and population divergence times by using molecular clocks.
source:
https://www.pnas.org/content/99/2/803
____________________________________
Also, genetics have revealed other surprises, the total genome size of species does not translate “simple” life from “complex” life as expected. “Molecules to Man” evolution puts bacteria on the bottom and mankind at the top, but it is flowering plants (and not humans) which have the largest genomes.
source:
https://www.evolutionisamyth.com/dating-methods/mutational-molecular-clocks-are-calibrated-by-assumptions/
https://www.evolutionisamyth.com/wp-content/uploads/2019/09/genome-distribution-deceptive-vs-factual-1024x448.png
____________________________________
https://upload.wikimedia.org/wikipedia/commons/thumb/8/80/Genome_Sizes.png/220px-Genome_Sizes.png
source:
https://en.wikipedia.org/wiki/Genome_size
____________________________________
genome size, chromosomes, genes, base pairs
____________________________________
Release of Virus (6)
Virions are then released from the infected cell through exocytosis and search another host cell. Oseltamivir inhibits cleavage of sialic acids by neuroamidase from the cell receptors thus preventing release of newly formed virions from the cell surface (Inhibitor XI). 8
References
(1) Hoffmann et al.: SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor, Cell (2020), PDF
Suprewicz et al.: Vimentin binds to SARS-CoV-2 spike protein and antibodies targeting extracellular vimentin block in vitro uptake of SARS-CoV-2 virus-like particles, BioRxiv preprint (2021), [DOI]
(2) Henderson et al: Controlling the SARS-CoV-2 Spike Glycoprotein Conformation, Nat Struct Mol Biol. (2021), [ DOI]
(3) Shirato, K., Kawase, M. & Matsuyama, S.: Wild-type human coronaviruses prefer cell-surface TMPRSS2 to endosomal cathepsins for cell entry, Virology 517, 9–15 (2018), [ DOI]
(4) Zhavoronkov et al.: Potential COVID-2019 3C-like Protease Inhibitors Designed Using Generative Deep Learning Approaches, ChemRxiv (2020), [ DOI]
(5) Shin et al.: Saracatinib Inhibits Middle East Respiratory Syndrome-Coronavirus Replication In Vitro, Viruses, 10(6):283 (2018), [ DOI]
(6) Lin, S. C., Ho, C. T., Chuo, W. H., Li, S., Wang, T. T., & Lin, C. C. : Effective inhibition of MERS-CoV infection by resveratrol, BMC Infectious Diseases, 17(1)(2017), [ DOI]
(7) McKimm‐Breschkin: Influenza neuraminidase inhibitors: Antiviral action and mechanisms of resistance. Influenza and Other Respiratory Viruses 7(Suppl. 1), 25–36., [ PMC]
source:
https://www.antibodies-online.com/resources/18/5410/sars-cov-2-life-cycle-stages-and-inhibition-targets/
• do not believe in everything you read
___________________________________
Severe acute respiratory syndrome coronavirus (SARS-CoV or SARS-CoV-1)[2] is a strain of coronavirus that causes severe acute respiratory syndrome (SARS).[3] It is an enveloped, positive-sense, single-stranded RNA virus which infects the epithelial cells within the lungs.[4] The virus enters the host cell by binding to angiotensin-converting enzyme 2.[5] It infects humans, bats, and palm civets.[6][7]
On 16 April 2003, following the outbreak of SARS in Asia and secondary cases elsewhere in the world, the World Health Organization (WHO) issued a press release stating that the coronavirus identified by a number of laboratories was the official cause of SARS. The Centers for Disease Control and Prevention (CDC) in the United States and National Microbiology Laboratory (NML) in Canada identified the SARS-CoV-1 genome in April 2003.[8][9] Scientists at Erasmus University in Rotterdam, the Netherlands, demonstrated that the SARS coronavirus fulfilled Koch's postulates, thereby confirming it as the causative agent. In the experiments, macaques infected with the virus developed the same symptoms as human SARS victims.[10]
A virus very similar to SARS was discovered in late 2019. This virus, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is the causative pathogen of COVID-19, forming the COVID-19 pandemic.[11]
source:
https://en.wikipedia.org/wiki/SARS-CoV-1
• do not believe in everything you read
____________________________________
Severe acute respiratory syndrome (SARS) is the disease caused by SARS-CoV-1. It causes an often severe illness and is marked initially by systemic symptoms of muscle pain, headache, and fever, followed in 2–14 days by the onset of respiratory symptoms,[12] mainly cough, dyspnea, and pneumonia. Another common finding in SARS patients is a decrease in the number of lymphocytes circulating in the blood.[13]
In the SARS outbreak of 2003, about 9% of patients with confirmed SARS-CoV-1 infection died.[14] The mortality rate was much higher for those over 60 years old, with mortality rates approaching 50% for this subset of patients.[14]
source:
https://en.wikipedia.org/wiki/SARS-CoV-1
• do not believe in everything you read
____________________________________
flu virus (influenza virus)
source:
https://en.wikipedia.org/wiki/Orthomyxoviridae
____________________________________
Now we know that it is caused by an RNA virus of the family Orthomyxoviridae (the influenza viruses). In humans, common symptoms of influenza infection are fever, sore throat, muscle pains, severe headache, coughing, and weakness and fatigue.[7] In more serious cases, influenza causes pneumonia, which can be fatal, particularly in young children and the elderly. While sometimes confused with the common cold, influenza is a much more severe disease and is caused by a different type of virus.[8] Although nausea and vomiting can be produced, especially in children,[7] these symptoms are more characteristic of the unrelated gastroenteritis, which is sometimes called "stomach flu" or "24-hour flu."[9]
Typically, influenza is transmitted from infected mammals through the air by coughs or sneezes, creating aerosols containing the virus, and from infected birds through their droppings. Influenza can also be transmitted by saliva, nasal secretions, feces and blood. Healthy individuals can become infected if they breathe in a virus-laden aerosol directly, or if they touch their eyes, nose or mouth after touching any of the aforementioned bodily fluids (or surfaces contaminated with those fluids). Flu viruses can remain infectious for about one week at human body temperature, over 30 days at 0 °C (32 °F), and indefinitely at very low temperatures (such as lakes in northeast Siberia). Most influenza strains can be inactivated easily by disinfectants and detergents.[10][11][12]
Flu spreads around the world in seasonal epidemics.
source:
https://en.wikipedia.org/wiki/Influenza_pandemic
• do not believe in everything you read
____________________________________
https://www.who.int/news-room/fact-sheets/detail/influenza-(seasonal)
Seasonal influenza is an acute respiratory infection caused by influenza viruses which circulate in all parts of the world.
The pathogen
There are 4 types of seasonal influenza viruses, types A, B, C and D. Influenza A and B viruses circulate and cause seasonal epidemics of disease.
• Influenza A viruses are further classified into subtypes according to the combinations of the hemagglutinin (HA) and the neuraminidase (NA), the proteins on the surface of the virus. Currently circulating in humans are subtype A(H1N1) and A(H3N2) influenza viruses. The A(H1N1) is also written as A(H1N1)pdm09 as it caused the pandemic in 2009 and subsequently replaced the seasonal influenza A(H1N1) virus which had circulated prior to 2009. Only influenza type A viruses are known to have caused pandemics.
• Influenza B viruses are not classified into subtypes, but can be broken down into lineages. Currently circulating influenza type B viruses belong to either B/Yamagata or B/Victoria lineage.
• Influenza C virus is detected less frequently and usually causes mild infections, thus does not present public health importance.
• Influenza D viruses primarily affect cattle and are not known to infect or cause illness in people.
Signs and symptoms
Seasonal influenza is characterized by a sudden onset of fever, cough (usually dry), headache, muscle and joint pain, severe malaise (feeling unwell), sore throat and a runny nose. The cough can be severe and can last 2 or more weeks. Most people recover from fever and other symptoms within a week without requiring medical attention. But influenza can cause severe illness or death especially in people at high risk (see below).
source:
https://www.who.int/news-room/fact-sheets/detail/influenza-(seasonal)
• do not believe in everything you read
____________________________________
H5N1
H5N1 is a subtype of the influenza A virus, also known as A(H5N1)
H5N1, also known as HPAI A(H5N1), which stands for highly pathogenic, avian influenza ‘A’ virus, subtype H5N1.
influenza A virus
influenza A virus subtype H5N1
influenza A virus, subtype H5N1
influenza A virus of subtype H5N1
a bird-adapted strain of H5N1
a bird-adapted strain of H5N1 (genetic subtype)
HPAI A(H5N1)
HP - highly pathogenic (LP - low pathogenic)
AI - avian influenza (bird-adapted virus strain)
A - influenza A virus, influenza virus of type A
H5N1 - subtype H5N1
H5 - H5 stands for the 5th of several known types of the
protein hemagglutinin.
N1 - N1 stands for the 1st of several known types of the
protein neuraminidase.
H5 - H5 influenza viruses
- H5 viruses
H - hemagglutinin (HA) RNA strands and
N - neuraminidase (NA) RNA strands
RNA strands specify the structure of proteins.
H5N1 - HA subtype (H5) - subtype H5 - RNA strands - RNA segments
NA subtype (N1) - subtype N1 - RNA strands - RNA segments
H5N1 - H - Hemagglutinin protein - RNA strands - RNA genetic strand
N - Neuraminidase protein - RNA strands - RNA genetic strand
H5N1 - H - surface antigen (Hemagglutinin) - gene - RNA
N - secondary surface antigen (Neuraminidase) - gene - RNA
Hemagglutinin - an antigenic glycoprotein found on the surface of
the influenza viruses and is responsible for binding
the virus to the cell that is being infected.
- responsible for binding the virus to the cell
- enable the virus to infect the cell
- to bind and then to infect the cell, in order to replicate
- Hemagglutinin or an antigenic glycoprotein made this binding
possible; the binding thus make it possible for the virus to
infect the cell; the virus must infect the cell, in order to
replicating itself; the virus can not self-replicate and
virus needs the cell as a host for replication.
Neuraminidase - an antigenic glycosylated enzyme found on the surface of
the influenza viruses and facilitates the release of
progeny viruses from infected cells.[34]
- enzyme, glycosylated enzyme
- facilitates the release of viruses from infected cells
- the more Neuraminidases enzyme there is on the surface of the
influenza virus, the easier it is for the virus to spread itself
HA - Hemagglutinin antigen ?
HA - Hemagglutinin antigenic surface ?
surface antigen (Hemagglutinin) - binding - alpha 2-3 sialic acid receptors
Like all other influenza A subtypes, the H5N1 subtype is an RNA virus.
Dr. Daniel Lucey, co-director of the Biohazardous Threats and Emerging Diseases graduate program at Georgetown University has made this point, "There is no H5N1 pandemic so there can be no pandemic vaccine".[43]
humanized influenza A virus (a human flu virus of type A)
The avian influenza hemagglutinin binds alpha 2-3 sialic acid receptors, while human influenza hemagglutinins bind alpha 2-6 sialic acid receptors.[22]
Α α alpha (Greek letter)
hemagglutinin alpha 2-3 sialic acid receptors [α2-3-linkage of sialic acids]
hemagglutinin alpha 2-6 sialic acid receptors [α2-6-linked sialic acids]
//
// In the special mice breed to resemble humans, injecting sialic acids
// antibodies in these mice created a low grade inflammation with the red
// meat sialic acids - and that inflammation causes the tumors to grow
// larger than they would otherwise.
//
// Primate Evolution and Human Disease
//
// Dr. Ajit Varki, Glycobiology research and training center,
// the surface of cells
// the sugar molecules that make up the outside of cell
//
// sialic acids
// sialic quirks
// most of the diseases we loathe are only able to attack humans by
// acting like our sialic acids
// cancerous tumors contain high amounts of this foreign sialic acids
//
// sialic acid is a generic term for neuraminic acid, a monosaccharide
//
// sialic acid are found widely distributed in animal tissues; in other
// organisms, from plants and fungi to yeast and bacteria,
// sialic acid are found in glycoproteins and gangliosides (they occur
// at the end of sugar chains connected to the surfaces of cells and
// soluble proteins).
//
// Neu5Ac is the most common sialic acids in mammals.
// These acidic sugars share a 9-carbon backbone.
//
// non-human sialic acid
// N-glycolylneuraminic acid (Neu5Gc)
//
Α Alpha, uppercase Greek letter alpha
α αlpha, lowercase Greek letter alpha
from the intestine of birds to the airway of humans
from the intestine [α2-3-linkage of sialic acids] of birds
αlpha two dash 3hree linkage
to the airway [α2-6-linked sialic acids] of humans
αlpha two dash 6ix linked
22. Shinya K, Ebina M, Yamada S, Ono M, Kasai N, Kawaoka Y (March 2006). "Avian flu: influenza virus receptors in the human airway". Nature. 440 (7083): 435–6.
There is now evidence that a direct bird to human transfer did occur at least once before, when the infamous 1918 influenza pandemic killed tens of millions of people [83,84].
source: en.wikipedia.org,
The Next Influenza Pandemic Lessons from Hong Kong, 1997 - Volume 5, Number 2 — April 1999 - Emerging Infectious Disease journal - CDC
• do not believe in everything you read
____________________________________
What is the difference between Influenza (Flu) and COVID-19?
Influenza (flu) and COVID-19 are both contagious respiratory illnesses, but they are caused by different viruses. COVID-19 is caused by infection with a coronavirus first identified in 2019, and flu is caused by infection with influenza viruses.
COVID-19 seems to spread more easily than flu. However, as more people become fully vaccinated against COVID-19, the spread of the virus that causes COVID-19 should slow down. More information about COVID-19 vaccines and how well they work.
Compared to flu, COVID-19 can cause more serious illnesses in some people. COVID-19 can also take longer before people show symptoms and people can be contagious for longer.
Because some of the symptoms of flu, COVID-19, and other respiratory illnesses are similar, the difference between them cannot be made based on symptoms alone.
People can be infected with both flu and the virus that causes COVID-19 at the same time and have symptoms of both influenza and COVID-19.
Overall, COVID-19 seems to cause more serious illnesses in some people.
Compared to young children, teens and adolescents with COVID-19 are more likely to have Multisystem Inflammatory Syndrome in Children (MIS-C), a rare but severe complication of COVID-19. However, for adolescents, the risk of serious COVID-19 illness is less than in children younger than 5.
source:
https://www.cdc.gov/flu/symptoms/flu-vs-covid19.htm
• do not believe in everything you read
____________________________________
SARS-CoV-2 Delta variant, also known as lineage B.1.617.2, is a variant of lineage B.1.617 of SARS-CoV-2, the virus that causes COVID-19.[1]
It has mutations in the gene encoding the SARS-CoV-2 spike protein[5] causing the substitutions T478K, P681R and L452R,[6] which are known to affect transmissibility of the virus as well as whether it can be neutralised by antibodies for previously circulating variants of the COVID-19 virus.[7][failed verification]
Some evidence suggests vaccinated people are more likely to develop symptoms from Delta than other variants (why?)
because ...
COVID-19 vaccines are effective in preventing severe disease or hospitalisation from infection with the variant, and some evidence suggests vaccinated people are more likely to develop symptoms from Delta than other variants of SARS-CoV-2.[9]
On 7 May 2021, PHE changed their classification of lineage B.1.617.2 from a variant under investigation (VUI) to a variant of concern (VOC) based on an assessment of transmissibility being at least equivalent to B.1.1.7 (Alpha variant);[10] the UK's SAGE subsequently estimated a "realistic" possibility of being 50% more transmissible.[11]
On 15 June 2021, the Centers for Disease Control and Prevention (CDC) declared Delta a variant of concern.[12]
"Delta plus" variant
• people with Delta infection had 1,000 time [1000] more copies of the virus in the respiratory tracts than those with Wuhan strain infection (not peer-reviewed)(Guangdong Provincial Center for Disease Control and Prevention) (transmissibility)
A study[75] published online (not peer-reviewed) by Guangdong Provincial Center for Disease Control and Prevention may partly explain the increased transmissibility: people with Delta infection had 1,000 time [1000] more copies of the virus in the respiratory tracts than those with Wuhan strain infection; and it took on average 4 days for people infected with Delta for the virus to be detectable compared to 6 days with the Wuhan strain.[76][77]
In countries other than India, the first cases of the variant were detected in late February 2021, including the United Kingdom on 22 February, the United States on 23 February and Singapore on 26 February.[156][3][2]
source:
https://en.wikipedia.org/wiki/SARS-CoV-2_Delta_variant
https://en.wikipedia.org/wiki/SARS-CoV-2_lineage_B.1.617
https://en.wikipedia.org/wiki/SARS-CoV-2_Alpha_variant
https://en.wikipedia.org/wiki/Variants_of_SARS-CoV-2
• do not believe in everything you read
____________________________________
November 2002
On 16 November 2002,[9] an outbreak of severe acute respiratory syndrome (SARS) began in China's Guangdong province, bordering Hong Kong. The first case of infection was traced to Foshan.[10][11] This first outbreak affected people in the food industry, such as farmers, market vendors, and chefs.[12][13] The outbreak spread to healthcare workers after people sought medical treatment for the disease.[13] The People's Republic of China notified the World Health Organization (WHO) about this outbreak on 10 February 2003, reporting 305 cases including 105 health-care workers and five deaths.[14] Later it reported that the outbreak in Guangdong had peaked in mid-February 2003. However, this appears to have been false because subsequently 806 cases of infection and 34 deaths were reported.[15] Italian physician Carlo Urbani was the first to identify SARS as probably a new and dangerously contagious viral disease.[16][17]
Early in the epidemic, the Chinese government discouraged its press from reporting on SARS, delayed reporting to WHO, and initially did not provide information to Chinese outside Guangdong province, where the disease is believed to have originated.[18] Also, a WHO team that travelled to Beijing was not allowed to visit Guangdong province for several weeks.[19] This resulted in international criticism, which seems to have led to a change in government policy in early April.[20][21]
January 2003
The first super-spreader, Zhou Zuofen, a fishmonger, checked in to the Sun Yat-sen Memorial Hospital in Guangzhou on 31 January, where he infected 30 nurses and doctors. The virus soon spread to nearby hospitals.[22]
February 2003
Hong Kong
Ninth floor layout of the Hotel Metropole in Hong Kong, showing where a super-spreading event of the severe acute respiratory syndrome (SARS) occurred
In February 2003, Hong Kong's SARS index patient was Liu Jianlun, who had come to attend a family wedding gathering; Liu was on the staff at Sun Yat-Sen Memorial Hospital in Guangzhou and had treated SARS patients.[23]
On 21 February, Liu and his wife checked into room 911 on the ninth floor of the Metropole Hotel. Despite feeling ill he visited with his family and they traveled around Hong Kong. By the morning of 22 February, he knew he was very sick and walked to nearby Kwong Wah Hospital to seek treatment. He warned staff that he was very sick and to put him in isolation. He never recovered and died in the intensive care unit on 4 March.[citation needed]
Liu is believed to have been a SARS super-spreader: 23 other Metropole guests developed SARS, including seven from the ninth floor. Liu's brother-in-law, who sought treatment in late February, was hospitalized in Kwong Wah Hospital on 1 March and died on 19 March. It is estimated that around 80% of the Hong Kong cases were due to Liu.[24]
source:
https://en.wikipedia.org/wiki/Timeline_of_the_SARS_outbreak
• do not believe in everything you read
____________________________________
• "GGR," or the law of gradual granularity refinement. [ ]
Written by Bill Buxton
JND significance ~ 1 / familiarity.
JND (just noticeable difference)
"What is the smallest level of differentiation that you can perceive as being significant?"
The tilde character (~) means "varies with."
Hence, the law says that the granularity at which we distinguish meaningful differences gets finer the more our familiarity with a subject grows. Conversely, it also says the less familiar we are with something, the coarser the granularity will be before we can distinguish differences as being significant.
Predictable and Avoidable
Let me tie all of this back to our two scenarios. Each is the result of differences in JND (the granularity of recognizing differences of significance) at play between the two parties involved.
In the first, you had the insight and saw something significant in it because you were immersed in the problem space. The granularity of your analysis was really refined. But the subtlety required to appreciate the essence of the idea fell below the threshold of your audience's ability to see any difference between it and what they had seen before.
In the second, the roles were reversed. Yes, you had all of the data. But what you didn't have was the ability to see the significance buried within. The granularity of your analysis was too coarse compared to that of your competitor. Most likely, despite your hard work, you simply weren't sufficiently familiar with the problem space to fully appreciate the significance of its subtleties.
The reason that I've taken the seemingly pretentious step of declaring the GGR as a law is to help emphasize there are no villains or stupid people in any of this. The behaviors in both scenarios are human nature. But that means they are predictable and avoidable――so there are some lessons that can be drawn from all of this.
source:
gradual granularity refinement
https://www.billbuxton.com/BW%20Assets/02a.%20A%20Familiar%20Problem%20Published.pdf
• do not believe in everything you read
____________________________________
It takes time to gain experience and familiarity that lead to the fineness of granularity wherein the sweet spots lie. And, no, we haven't found a solution to time travel. But the history of technology is full of discoveries of how to move [slower], finer, smoother. That is the heart of your quest to find ways to [slow down] the rate and quality of gaining experience that get you to the fine level. What all of this says is that to be successful, we need to innovate around the whole package, not just one part.”; ([ you need to work on each part, the interaction between the parts, the whole package, and avoid doing all things at the same time ])
── Bill Buxton, February 06, 2008
Innovation & Design :
A Familiar Problem,
gradual granularity refinement
http://www.bloomberg.com/bw/stories/2008-02-06/a-familiar-problembusinessweek-business-news-stock-market-and-financial-advice
https://www.billbuxton.com/BW%20Assets/02a.%20A%20Familiar%20Problem%20Published.pdf
https://www.billbuxton.com/
https://en.wikipedia.org/wiki/Bill_Buxton
• do not believe in everything you read
____________________________________
Patricia S. Churchland and Terrence J. Sejnowski, The computational brain [ ]
pp.113-114
Following training, the accuracy of the classification of new echoes was very good--as good or better than trained humans and other classification methods. In a network with three hidden units, it was possible to analyze the features discovered by the training procedure (figure 3.35). The most important features of the input signals were the frequency bandwidth, the onset time, and the rate of decay of the signal. These general features, which could have been discovered by data analysis techniques, accounted for about 50% of the successfully classified echoes. The remainder of the echoes were more difficult to classify because they did not follow the general trend. To classify these exceptional cases, the hidden units developed weights that recognized clusters of echoes that shared the same spectral features. The most closely the input resembles the prototype, the more near will be the activation vector to the prototypical activation vector. The two-pronged strategy adopted by the hidden units exploited large-scale regularities and finer scale distinctions in different ways.
p.113
Training of the net correctly to categorize proceeds in the following way. We give the net examples of mine echoes and rock echoes, one by one. For each case, the actual values of the output units is measured against what the values ought to have been, given the input. This difference is a measure of error, which can then be used to compute small changes in the weights of the units in the system. This is a gradient-descent procedure, and slowly the weights of the network are adjusted so that when fed a mine echo, either a familiar old example or a brand new case, it gives a value of <1,0>, or close to that, and when fed a rock echo, it responds with something close to <0,1>. (For a more detailed but still basic account, see P. M. Churchland 1989.)
p.464
gradient descent Procedure for reducing error while training a neural network based on taking the derivative of the error with respect to each parameter, then changing the parameters such that the net moves down the error gradient to an error minimum.
(Churchland, Patricia Smith., The computational brain / Patricia S. Churchland and Terrence J. Sejnowski., 1. brain--computer simulation., 2. neural networks (computer science)., 3. neural circuitry., 4. neurosciences--methods., 1992, 1993, )
____________________________________
SARS-CoV-2 virus (human infection)
(dog infection)
(cat infection)
rate of mutation
____________________________________
molecular biology
constant rate of mutation
mammals
genetic dating
genetic dating using constant rate of mutation in mammals
mitochondrial mutation rate variation
molecular clocks
____________________________________
Abstract
Knowledge of the rate of point mutation is of fundamental importance, because mutations are a vital source of genetic novelty and a significant cause of human diseases. Currently, mutation rate is thought to vary many fold among genes within a genome and among lineages in mammals. We have conducted a computational analysis of 5,669 genes (17,208 sequences) from species representing major groups of placental mammals to characterize the extent of mutation rate differences among genes in a genome and among diverse mammalian lineages. We find that mutation rate is approximately constant per year and largely similar among genes. Similarity of mutation rates among lineages with vastly different generation lengths and physiological attributes points to a much greater contribution of replication-independent mutational processes to the overall mutation rate. Our results suggest that the average mammalian genome mutation rate is 2.2 × 10−9 per base pair per year, which provides further opportunities for estimating species and population divergence times by using molecular clocks.
source:
https://www.pnas.org/content/99/2/803
____________________________________
Also, genetics have revealed other surprises, the total genome size of species does not translate “simple” life from “complex” life as expected. “Molecules to Man” evolution puts bacteria on the bottom and mankind at the top, but it is flowering plants (and not humans) which have the largest genomes.
source:
https://www.evolutionisamyth.com/dating-methods/mutational-molecular-clocks-are-calibrated-by-assumptions/
https://www.evolutionisamyth.com/wp-content/uploads/2019/09/genome-distribution-deceptive-vs-factual-1024x448.png
____________________________________
https://upload.wikimedia.org/wikipedia/commons/thumb/8/80/Genome_Sizes.png/220px-Genome_Sizes.png
source:
https://en.wikipedia.org/wiki/Genome_size
____________________________________
genome size, chromosomes, genes, base pairs
____________________________________
https://gerardofurtado.com/gs/genes.html
____________________________________
____________________________________
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