We’re missing one fundamental piece of information. It’s the Omicron question. This article will look at what we know so far to zero in on that big question.
Good analysis in the later portion of the article. However, you omitted the more recent preliminary finding that suggests WHY the mortality rate is lower in Omicron.
> Omicron SARS-CoV-2 can infect faster and better than Delta in human bronchus but with less severe infection in lung <
I take issue with the proposition that nothing is "actionable." I subscribe to the PHYSICAL BARRIER solution as 99.9% protection from unsanitary humans who simply cannot help but spit on each other.
It really is that simple -- "build a wall" and stop every variant & strain from immigrating to the body-nation. However, I am an engineer with clean room experience, and I am quite aware of the movement of particles which I cannot see. Most people can't even keep fecal particles off their toothbrush.
For example, at NIH Clinical Center; Bethesda, MD, Ebola "magically" spread to a completely separate wing. Yet a Frontline documentary plainly showed staff entering and exiting the "contaminated zone" without even cleaning the soles of their shoes or the wheels on carts. In my opinion, the pandemic is ultimately the result of human ignorance, arrogance, and unwillingness to track the spread of human filth. Only the "vaccine" of both intellectual and emotional education can cure that. See e.g., https://ycei.org/
I wear a P100 respirator, and goggles. Respirator body cost $23 on Amazon (3M 6500 series), and the filters cost $8-12 on ebay (3M 7093 or 2291). The filters last about 6-8 months, since I am not in a "dusty" environment. I.e., use them until the airflow is unacceptably reduced or "clogged." Also, the respirator is designed to be worn every work day, all day, and is an order of magnitude more comfortable than disposable masks. Don't even get me started about "surgical" style masks, which a recent study found to be equivalent to N30, due to significant leakage.
Note: filtration media degrades as moisture causes the material to clump together. Thus, a bidirectional N95 mask has a much shorter life span than a unidirectional respirator filter.
I also routinely disinfect hands with hydrogen peroxide or benzalkonium chloride, particularly when transitioning between isolated and exposed locations. Yes, I even pour H2O2 on the ground and clean the soles of my shoes. Even wiping down the surfaces of a grocery cart, I clean parts of the handle that are NEVER cleaned by anybody, and remove black "gunk."
Another masterful presentation of information using clear visuals. Thanks for writing this piece. The ICU and ventilation data from S. Africa are encouraging, with the caveat that many of those infected thus far are young and therefore unlikely to experience severe symptoms. I do want to comment on your description of the virus' evolution, as in "If 90% of people are not immune yet and 10% are, as a virus you want to optimize for those not immune yet. But if it’s the opposite, and now 90% of people are immune, you’ll switch your efforts and evolve to increase your transmission rate among immune people." Just to be clear, evolution is not teleological; the virus doesn't have a master plan for how to infect the greatest number of people. Evolution occurs through random processes of mutation and natural selection. Changes in the nucleotide sequence of DNA or RNA occur randomly during replication; as a rough rule of thumb, a mistake in one or more nucleotides occurs about 1 out of every 100,000,000 times the DNA/RNA is copied, each of which can lead to a mutation. Most changes are neutral or deleterious to the virus, but some mutations are beneficial (for the virus) by increasing its ability to enter host cells, spread between cells, evade host antibodies, transmit between hosts, and so on. If a new virus variant has one or more beneficial mutations, it may spread rapidly through a host population and out compete other variants that lack its advantages. This is what seems to be occurring with omicron. This is a purely random process. The virus isn't trying to reach a goal point, its only "purpose" is to replicate itself in the cells of a host. We face the challenge of responding to new mutations as they arise, with no early warning system as to the nature of those mutations. Fortunately, we have good defenses in vaccination (with booster), masking, and distancing when necessary.
Wow! The Stanford Infectious disease group would love to claim you as one of theirs. I'll have to read this several more times to grasp it but am smart eno to follow your advice. I'm sending it to all my bright friends who may explain it to me. Wonderful figures as usual for you.
The average age of the South Africa Society is about 28 years. This figure is quite lower than for most Western Countries. It is well known that immune responses are age-dependent and drop in the elderly people. Therefore it looks probable independent of the inherent pathogenicity caused by the omicron variant that mild illnesses occur less frequent under different demographic circumstances. In my country (Switzerland) for example the average age of the population is 42 years and the underlying immunity against SARS-CoV-2 is considerably lower than in SA due to more immunnaive people (about 31% isn't vaccinated). Even in the case of an attenuated pathogenicity I assume due to the high virulence driven by immun escape and/or RBD adaptation that severe clinical courses will occur frequently. This is by the way the reason why a free-running pandemic does not work and containment is crucial in order to limit the number of victims.
It's the potential for many types of Long COVID that bothers me the most. So on top of the recognisable symptoms that have been much written about, the pervasive vascular damage may be setting up ongoing waves of delayed fatalities.
Como siempre, el artículo aporta una visión clara, especial y con datos actualizados de un tema que se les está de nuevo escapando a los asesores epidemiólogos y a los dirigentes
The graph used for weekly admissions is outdated. Hospitalizations always get a massive backlog jump on Tuesdays in SA. Weekly admissions are 116 per million last week not 55.
It also contains information on all hopitalizations for both Delta and Omicron and even gives information on when hospitalized people were testet positive by PCR
This is what a South African study found. Uninfected people (called “naive”) were less likely to be infected by Omicron than with Delta, but those with a previous infection were more likely to be infected. No doubt, there is immune evasion to a higher degree concerning people with an established immunity due to undergone infections and/or vaccination. But on the other hand experimental data tells us, that there is probably a higher receptor binding affinity suggesting also contribute to higher transmissibility.
C.S. Lupala, et.al. Mutations on RBD of SARSCoV-2 Omicron variant result in stronger binding to human ACE2 receptor, Biochemical and Biophysical Research Communications (2022), https://doi.org/10.1016/j.bbrc.2021.12.079. Omotuyi, I. O, et.al. SARS-CoV-2 Omicron Spike Glycoprotein Receptor Binding Domain Exhibits Super-Binder Ability with ACE2 but not Convalescent Monoclonal Antibody. https://doi.org/10.1101/2021.12.09.471885.
But higher receptor binding affinity could also mean, that binding is too tight to host cells of immunnaive people thereby explaining, that cell entry could be hindered. The receptor of the host cell must not only bind to the virus RBD but also release the virus in order to achieve cell entry. One can imagine that the binding affinity may be different in the presence or absence of host antibodies against the altered spike glycoprotein of the omicron variant.
A simpler explication for this paradox of relatively underscored infections in immunnaive people is an overestimation of their proportion.
Simply put, if the vast majority of the population had been infected or vaccinated before the omicron wave occurred, the relative proportion of primary infections drops.
Good analysis in the later portion of the article. However, you omitted the more recent preliminary finding that suggests WHY the mortality rate is lower in Omicron.
> Omicron SARS-CoV-2 can infect faster and better than Delta in human bronchus but with less severe infection in lung <
https://www.med.hku.hk/en/news/press/20211215-omicron-sars-cov-2-infection
I take issue with the proposition that nothing is "actionable." I subscribe to the PHYSICAL BARRIER solution as 99.9% protection from unsanitary humans who simply cannot help but spit on each other.
https://doi.org/10.1371/journal.pcbi.1009629
It really is that simple -- "build a wall" and stop every variant & strain from immigrating to the body-nation. However, I am an engineer with clean room experience, and I am quite aware of the movement of particles which I cannot see. Most people can't even keep fecal particles off their toothbrush.
For example, at NIH Clinical Center; Bethesda, MD, Ebola "magically" spread to a completely separate wing. Yet a Frontline documentary plainly showed staff entering and exiting the "contaminated zone" without even cleaning the soles of their shoes or the wheels on carts. In my opinion, the pandemic is ultimately the result of human ignorance, arrogance, and unwillingness to track the spread of human filth. Only the "vaccine" of both intellectual and emotional education can cure that. See e.g., https://ycei.org/
I wear a P100 respirator, and goggles. Respirator body cost $23 on Amazon (3M 6500 series), and the filters cost $8-12 on ebay (3M 7093 or 2291). The filters last about 6-8 months, since I am not in a "dusty" environment. I.e., use them until the airflow is unacceptably reduced or "clogged." Also, the respirator is designed to be worn every work day, all day, and is an order of magnitude more comfortable than disposable masks. Don't even get me started about "surgical" style masks, which a recent study found to be equivalent to N30, due to significant leakage.
Note: filtration media degrades as moisture causes the material to clump together. Thus, a bidirectional N95 mask has a much shorter life span than a unidirectional respirator filter.
I also routinely disinfect hands with hydrogen peroxide or benzalkonium chloride, particularly when transitioning between isolated and exposed locations. Yes, I even pour H2O2 on the ground and clean the soles of my shoes. Even wiping down the surfaces of a grocery cart, I clean parts of the handle that are NEVER cleaned by anybody, and remove black "gunk."
Another masterful presentation of information using clear visuals. Thanks for writing this piece. The ICU and ventilation data from S. Africa are encouraging, with the caveat that many of those infected thus far are young and therefore unlikely to experience severe symptoms. I do want to comment on your description of the virus' evolution, as in "If 90% of people are not immune yet and 10% are, as a virus you want to optimize for those not immune yet. But if it’s the opposite, and now 90% of people are immune, you’ll switch your efforts and evolve to increase your transmission rate among immune people." Just to be clear, evolution is not teleological; the virus doesn't have a master plan for how to infect the greatest number of people. Evolution occurs through random processes of mutation and natural selection. Changes in the nucleotide sequence of DNA or RNA occur randomly during replication; as a rough rule of thumb, a mistake in one or more nucleotides occurs about 1 out of every 100,000,000 times the DNA/RNA is copied, each of which can lead to a mutation. Most changes are neutral or deleterious to the virus, but some mutations are beneficial (for the virus) by increasing its ability to enter host cells, spread between cells, evade host antibodies, transmit between hosts, and so on. If a new virus variant has one or more beneficial mutations, it may spread rapidly through a host population and out compete other variants that lack its advantages. This is what seems to be occurring with omicron. This is a purely random process. The virus isn't trying to reach a goal point, its only "purpose" is to replicate itself in the cells of a host. We face the challenge of responding to new mutations as they arise, with no early warning system as to the nature of those mutations. Fortunately, we have good defenses in vaccination (with booster), masking, and distancing when necessary.
Wow! The Stanford Infectious disease group would love to claim you as one of theirs. I'll have to read this several more times to grasp it but am smart eno to follow your advice. I'm sending it to all my bright friends who may explain it to me. Wonderful figures as usual for you.
I am sure you have seen this already, but here is some very early and uncertain data about Omicron severity from South Africa: https://twitter.com/miamalan/status/1470684351151157252
This graph has been made using the data from the Danish authorities. I estimates hospitalization rate to be 1,4% in Denmark. It It was made by Lars Risbo https://www.facebook.com/photo/?fbid=10228501646353299&set=a.1869990556621
The average age of the South Africa Society is about 28 years. This figure is quite lower than for most Western Countries. It is well known that immune responses are age-dependent and drop in the elderly people. Therefore it looks probable independent of the inherent pathogenicity caused by the omicron variant that mild illnesses occur less frequent under different demographic circumstances. In my country (Switzerland) for example the average age of the population is 42 years and the underlying immunity against SARS-CoV-2 is considerably lower than in SA due to more immunnaive people (about 31% isn't vaccinated). Even in the case of an attenuated pathogenicity I assume due to the high virulence driven by immun escape and/or RBD adaptation that severe clinical courses will occur frequently. This is by the way the reason why a free-running pandemic does not work and containment is crucial in order to limit the number of victims.
Enjoyed the article very much. Got the level exactly right I think. Much of this is non obvious to the layman.
https://twitter.com/AndrewEwing11/status/1469781019993821184?s=20
It's the potential for many types of Long COVID that bothers me the most. So on top of the recognisable symptoms that have been much written about, the pervasive vascular damage may be setting up ongoing waves of delayed fatalities.
Como siempre, el artículo aporta una visión clara, especial y con datos actualizados de un tema que se les está de nuevo escapando a los asesores epidemiólogos y a los dirigentes
The graph used for weekly admissions is outdated. Hospitalizations always get a massive backlog jump on Tuesdays in SA. Weekly admissions are 116 per million last week not 55.
Quite the jump.
The best source for information i the world is from Denmark. Denmark has the largest sequencing capacity and the largest test capacity compared to population size in the world. The authorities make a daily report on Omicron. You can get it here: https://files.ssi.dk/covid19/omikron/statusrapport/rapport-omikronvarianten-13122021-i30w
It also contains information on all hopitalizations for both Delta and Omicron and even gives information on when hospitalized people were testet positive by PCR
Any more updates on Omicron?
E.g., vaccine escape rate, infection fatality rate, infection prevalence rate, when the peak will be, etc?
This is what a South African study found. Uninfected people (called “naive”) were less likely to be infected by Omicron than with Delta, but those with a previous infection were more likely to be infected. No doubt, there is immune evasion to a higher degree concerning people with an established immunity due to undergone infections and/or vaccination. But on the other hand experimental data tells us, that there is probably a higher receptor binding affinity suggesting also contribute to higher transmissibility.
C.S. Lupala, et.al. Mutations on RBD of SARSCoV-2 Omicron variant result in stronger binding to human ACE2 receptor, Biochemical and Biophysical Research Communications (2022), https://doi.org/10.1016/j.bbrc.2021.12.079. Omotuyi, I. O, et.al. SARS-CoV-2 Omicron Spike Glycoprotein Receptor Binding Domain Exhibits Super-Binder Ability with ACE2 but not Convalescent Monoclonal Antibody. https://doi.org/10.1101/2021.12.09.471885.
But higher receptor binding affinity could also mean, that binding is too tight to host cells of immunnaive people thereby explaining, that cell entry could be hindered. The receptor of the host cell must not only bind to the virus RBD but also release the virus in order to achieve cell entry. One can imagine that the binding affinity may be different in the presence or absence of host antibodies against the altered spike glycoprotein of the omicron variant.
A simpler explication for this paradox of relatively underscored infections in immunnaive people is an overestimation of their proportion.
Simply put, if the vast majority of the population had been infected or vaccinated before the omicron wave occurred, the relative proportion of primary infections drops.
Thank you for the very detailed article. Any updates since Dec 13th (now that we have 14 more days of data)?
Why such doomsday conclusion after presenting data that is to the contrary?
2-dose MRNA + Booster offers 80% omicron protection.
So, why: "If you haven’t had COVID before, you’re going to get it."