One Finite Planet

Covid-19 Immunity: Layers, immunity from vaccination vs infection, and the good news.

First Published:

Table of Contents

Shrek: No. Layers. Onions have layers. Ogres have layers. Onions have layers. You get it? We both have layers.

Shrek
Instead of a single immune response, the human immune system can be though of as having several layers of immune response, that all fade at different rates. Immunity is a complex set of different layers all subject to change over time at varying rates, making comparison between immunity following vaccination or infection highly time dependant.

The “layers” description can also be useful in understanding immunity. Instead of a single immune response, the human immune system can be though of as having several layers of immune response, that all fade at different rates.

In the end, immunity is complex. Sufficiently complex, that many studies comparing between immunity from vaccination vs infection, entirely miss pieces of the puzzle and present invalid conclusions.

Immunity: Layers Of Protection.

Protection, Not Prevention.

Immunity does nothing to protect a virus from entering the body. Following on the model of thinking of the parallels between an infection and a car, immunity is like the crumple zones, air bags and seat belts, that cannot prevent the accident, but they can ensure survival. The dream level of immunity provides the protection of a Formulae 1 car, such that even dangerous collisions can be walked away from without hospitalisation. Immunity can only reduce the impact of infection, but that reduction can result in a reduction in any of spread, symptoms, severe cases or and deaths. Just like having a safe car, no safety measure will prevent serious consequences in the worse circumstances, but for all circumstances, the impact can be reduced.

The Layers Model.

While the immune system is complex with several different mechanisms, a layers model provides quite a reasonable analogy, and while I have alluded to this in other Covid-19 posts, such as the recent one on the omicron variant, I thought it was time for a dedicated page. While the layers are built by T-Cells, which include over 15 different types of cells, B-Cells, which include 8 types of cells, NK-Cells as well as a range of customised antibody cells, this page focuses only one response levels that result from combinations of these layers.

Immunity Is Like Onions, Not Cake.

The Immunity is like an onion rather than a cake analogy extents further as besides having layers, they are not all sweetness and parties. The immune system has to act as an assassin on foreign invaders. There are problems:

  • Collateral damage is common, and the effects of the immune response can be debilitating, and even fatal.
  • Mistaken identity, as with peanut allergies, resulting in unnecessary activation of the immune system can even be fatal when there was not even a real threat.

People without an immune system are extremely vulnerable, and while there are now medical solutions, life without an immune system is impractical, even though some people die from their own immune responses. With Coivd-19, in some cases the immune system can cause significant damage.

The immune response comes with a of risk and while the response can present a greater risk than the perceived threat, on balance it is far better to have a fully functioning immune system.

The same applies to vaccinations. All negative effects from modern vaccines are due to the vaccine damaging the body in a way, that damage all results from the immune system having been activated. This is the reason unnecessary vaccination should be avoided, because activating a system that can get the response to a peanut so wrong, is playing with fire.

How Layers Combine For Levels of Protection.

Level 1: All Layers Active, Virus Elimination, For Weeks.

But Persistence Of Only A Few Weeks.

Consider a person who becomes infected and recovers from the virus.

Within a person, there is a ‘curve’ for an outbreak within the cells of the body, somewhat similar to the curve for an outbreak in a society of people.

At the point of exposure, there as very little virus, and at first very few infected cells. The number of infected cells grows exponentially until the immune system activates fully, at which point the reproduction rate with the body, like an internal R0, is less than 1.0 and spread is under control, with the number of infected cells continually decreasing. In new infection was to incur at this time, it would have little effect, with infected cells quickly neutralised.

If the level of immunity that can reduce the number of infected cells could remain active, than no new infection could ever take hold, or grow to anywhere near the level required for a person to be “infectious”. Unfortunately, this level of protection is quite draining, and the body quickly puts the full level of immunity into standby mode within a few weeks. In fact, a person will normally still feel unwell for the duration of time the immune system is fully active.

Level 2, Full Standby: ‘Infection Immunity’ for Two Months.

The next level of significance, is a “standby level, where the “virus detection” layers are fully active, but the “seek and destroy” layers are just on standby. This could be thought of as ‘infection’ immunity, but there is no universal agreement on ‘infected‘.

In this mode, if the virus is again detected, the “seek and destroy” can quickly be woken, but while the system is waking, the number of infected cells rapidly multiplies. It is a race between the waking up, and the virus. While at full standby level, the waking up will win most of the time, and a person will not reach the level of being infectious.

This level 2 protection provides whatever protection there is against a person becoming infectious.

Depending on the “viral load” at the time of exposure, exactly where the infection took hold, and other factors including how far into sleep systems had become, infection may still reach the level required for the person to become infectious, but with the immune system still activating considerably early, the risk of serious illness is very low. It is also possible that a variant could evade some of the protections of a level 2 response, which could result in only a level 3 type response, even within weeks of immunity being acquired or ‘refreshed’.

These full detection systems start gradually going into standby after around a month, and waning significantly from around month3 to month 6, leaving the immune response to be tackled by level 3 immune response layers.

Level 3: On Call, Slower response for >6 months.

This is infection from serious disease.

By around 3 months, only the “low level patrols”, mostly T-Cells, are still on the lookout, and although at this “level 3” there is already some defence against the virus, or in fact anything with markers of the virus such as the spike protein, it will take a few to days at this level to activate and wake waking up the full set of layers back to level 1 for maximum defence. The “seek and destroy” layers still have the full picture of what to look for, so once activated everything is activated a person will be fully equipped to fight the virus much earlier and at a lower level of infection, but the deeper the sleep of the layers of immunity, the bigger the head start the virus can get before the immune system is again fully active. If only the low level patrols are in action, then the chance of a new infection reaching the level where the person becomes infectious is much higher, and as the watch level of the patrols drops, the chance of a new infection resulting in severe infection increase. It is possible that a variant that bypas

These on call “low level patrols”, of most T-cells, result in a more flexible response, and can catch variations or infection the get past some of the specific level 2 defences, providing a wider immunity that manages to protect against more severe disease, by may provide little protect against reaching the point of being infectious.

This level activates too slowing to be as effective in preventing spread, but with this level of protection in place, an infection will grow slower and reactivate the other mechanisms faster to reduce the impact of an infection. This level of immunity could last over 6 months, and in theory with sufficient activation could last years, even though long term resilience at this level has yet to be confirmed with for SARS-Cov2.

Immunity from Infection, vs Immunity from vaccination.

Overview.

In summary, be sceptical, as immune response differences between vaccination and infection are generally overestimated.

It’s not entirely clear why these differences in vaccine- and infection-elicited antibody responses exist. In both cases, RBD-directed antibodies are acquired from the immune system’s recognition and response to viral spike proteins. The Seattle team suggests these differences may arise because the vaccine presents the viral protein in slightly different conformations.

How Immunity Generated from COVID-19 Vaccines Differs from an Infection

All immunity is “natural immunity”, developed by a persons own immune system, in response to either virus or vaccine.

The vaccine no more “fights infection” than the virus does. Both contain a spike protein that triggers the human body to develop its own immune response.

Also note an immune response, whether triggered by virus or vaccine, is far from harmless, as any peanut allergy sufferer can attest. But negative outcomes of vaccination, are so far all a result of immune response, and also result from immune response to the virus itself. There is so far no evidence outcomes from the immune response to vaccination beyond that observed from infections, and there is evidence of reduction in negative immune response, but not necessarily sufficient to offset the greater number to people that may be vaccinated rather than infected.

Relative Immunity Effectiveness: Only Accurately Measurable In Vaccine Free Environments.

Most vaccines specify at least two does some weeks apart, and have a controlled load of “spike protein”. As most people who become infected are encountering an environment where the virus is circulating, repeated exposure to the virus acting as “booster infections” could occur any number of weeks apart, or not at all. Despite the similar exposure to spike protein to develop immunity, the different load and timing of any repeat exposure could be expected to result in different levels of immunity.

Measuring the difference between the efficacy of vaccination and prior infection, would be easy under laboratory conditions, with volunteers who would remain in isolation for the duration of the study, but organising such a study over months is at the very least highly problematic. Uyghurs perhaps? Prisoners? The challenge is to avoid the possibility of “booster” infections.

‘Booster infections’, are infections which occurring the time a person has sufficiently strong immunity that the infection will be mild and most likely go unnoticed by the infected person, but as such an infection will expose the person to the virus, their immune system will be “refreshed”, lengthening the duration of immunity in a similar manner to a vaccine booster shot.

‘Booster infections’, will occur during the time between vaccination or infection and the ‘breakthrough infection’ or reinfection, unless the data is collected in an environment where the virus is not circulating. But if the virus is not circulating then there will be no ‘breakthrough infection’ or reinfections occurring, and instead subjects but if the virus is not circulating, how would the breakthrough or reinfections occur?

The solution is to conduct the study in a location with insignificant local spread of the virus, as has been the case in Western Australia prior to December 2021, by comparing vaccinated subjects with those who were detected as infected on arrival, and then test blood serum from subjects for antibodies and other immune responses.

Instead, most analysis is done by either monitoring studying a group of people such as health care workers, or simply observing data from hospital and infection records, without any data on how different the exposure levels, or viral loads experienced are experienced within the different groups.

Vaccinations, and infections, and the amount of virus in circulation are not homogenous throughout society. A study comparing those vaccinated prior to first infection with those infected prior to vaccination, can easily end up being a comparison between the experiences of two different social groups, who are in fact exposed to very different levels of the virus.

The Common Errors In Effectiveness Studies.

  • Assuming a homogenous population with those vaccinated vs infected experiencing identical viral exposure.
  • Ignoring that as most countries vaccinated the elderly first, sample groups are normally highly age skewed, so uunless filter
  • Assuming a homogenous population with those vaccinated vs infected experiencing identical viral exposure.
  • Ignoring that as most countries vaccinated the elderly first, sample groups are normally highly age skewed, so unless filtered, results can be as much about age as about vaccination vs infection.
  • Failing to ensure, subjects in each group are from the same social background and experience the same level of exposure to the virus.
  • Failing to ensure, subjects in each group are from the same social background and experience the same level of exposure to the virus.

Confirmation Bias And Comparison Studies.

Given the enormous scope for misinterpreting data in any attempt at comparison, it should not be surprising that both pro-vaccine and anti-vaccine camps can find data support that either vaccinations out-perform immunity following infection or the opposite, depending on their choice.

This article here, is a perfect example of the application of confirmation bias. It is genuinely difficult to establish the relative effectiveness of vaccination vs infection, but it is not difficult to realise that given the amount of disease and even deaths worldwide as a result infection, even if infection does provide longer immunity, that would not invalidate the use of vaccines.

Not would vaccination outperforming infection, strengthen the case vaccinations.

Vaccines are justified as long they are infective in triggering immunity, and it would better for planning if we could analysis duration of both immunity from infection and from vaccination without an agenda of of fighting either side of the ideology war. If the virus stops circulating, neither figure matters, but if it continues circulating, then once initial immunity is established, both infection and vaccination can play a role maintaining that immunity.

Data: Studies and Analysis.

Among COVID-19–like illness hospitalizations among adults aged ≥18 years whose previous infection or vaccination occurred 90–179 days earlier, the adjusted odds of laboratory-confirmed COVID-19 among unvaccinated adults with previous SARS-CoV-2 infection were 5.49-fold higher than the odds among fully vaccinated recipients of an mRNA COVID-19 vaccine who had no previous documented infection (95% confidence interval = 2.75–10.99)

CDC USA 2021 Nov 5: Laboratory-Confirmed COVID-19 Among Adults Hospitalized with COVID-19–Like Illness with Infection-Induced or mRNA Vaccine-Induced SARS-CoV-2 Immunity — Nine States, January–September 2021

The above study is peer reviewed, and with all data sources disclosed. The increase in odds of hospitalization amongst the previously infected does seem surprising, but could explained the these occurring in areas with higher rates of infection, and as a result higher viral loads. CDC or not, this data may also be only representative of unequal circumstances..

Results SARS-CoV-2-naïve vaccinees had a 13.06-fold (95% CI, 8.08 to 21.11) increased risk for breakthrough infection with the Delta variant compared to those previously infected, when the first event (infection or vaccination) occurred during January and February of 2021.

Comparing SARS-CoV-2 natural immunity to vaccine-induced immunity: reinfections versus breakthrough infections

An example of a what at first appears, although not peer-reviewed, to be a thorough study supporting an outcome contradicting the CDC, has been shown by others already to be open to significant distortion of reality, and does include every one of the errors I highlighted earlier. But then, I have yet to finds single study so far, that provides certainty of the data used, or was able to be conducted under conditions sufficiently controlled to be certain of the conclusions.

If The Virus Continues To Circulate, Could Vaccination Because Unnecessary In Future?

Consider the following:

  • People with immunity can still be infected, although these infections are mild.
  • Being infected, even if being asymptomatic, can trigger immunity.
  • Events that can trigger immunity, can refresh immunity.
  • If a strain of the virus evade immunity sufficiently well to spread within an immune community, it could circulate and continually refresh immunity levels.

If Delta does not already achieve this, perhaps Omicron will? If this does occur, then while vaccinations would remain the best way to gain immunity, and refresh immunity in areas of low case numbers, in areas where the virus is pervasive, continued vaccinations could become unnecessary. I would not advise taking the risk on this as an individual, but rather, having it as a possible future scenario.

The Threat Of Variants.

Weaker Or Stronger: Less harm is not an evolutionary advantage for covid-19.

It has been claimed that over time, viruses will mutate to be more contagious but less harmful. I searched for a reference for the claim, but instead found another source doing a fact check. Viruses evolve in whatever way helps their survival. virulent. The following are the main points:

  • Harming the host is not the goal of the virus, but a side effect of the virus thriving.
  • Viruses do not need to harm the host, but
  • Killing the host, or causing too much harm to the host, can be a disadvantage for a virus.
  • The only goal of the virus is better spread, and more spread can mean more harm.

If the virus kills the host, or incapacitates the host prior to spread, then spread will be reduced. With covid-19, almost everyone can still be active during a significant part of their infectious period, which gives covid-19 no evolutionary benefit from becomes less harmful. A strain that killed everyone infected before they could cough or sneeze over others would not spread, but a very successful strain could kill 5% of people, provided almost everyone can still move about during part of the infectious period.

Viruses mutate often, and as a random mutation is most likely to most likely to result in a less effective virus, most mutations die out. Only the small percentage of mutations that result in a more threatening and better spreading virus survive.

Delta was more virulent than previous strains, as it had improved ability to infect cells, improving transmissibility, but also resulting in more infected cells in each infected person.

A Virus Bypassing Level 2 Immunity Becomes Almost Inevitable.

The spread of coivid-19 has been waxing and waning as overall effective immunity rises and falls. Anytime a graph of infections has a downward slope, herd immunity has been achieved, and almost every country now has a graph with multiple ‘waves’.

Around the world, on average immunity levels have been rising, as increasing numbers of people have been infected and/or vaccinated. This creates a significant percentage of the population where viral spread is limited by level 2 immunity. For the virus to become more effective in this environment, increased success means either

  • Spreading even more effectively amongst those with no immunity.
  • Evading current level 2 immunity in the increasing pool of people with immunity against spread.

As all that is takes to to evade existing level 2 immunity, is for a variant to look different enough in the spike protein.

The Good News: Overall Immunity Is Rising.

Evidence Of Immunity In Unvaccinated Populations: Omicron In Africa.

This is written just days after the omicron variant was declared a variant of concern on 26th October 2021. I have just updated that page (Dec 5), as omicron is looking far more concerning.

Officially:

  • It is not yet clear whether Omicron is more transmissible.
  • It is not yet clear whether infection with Omicron causes more severe disease compared to infection with other variants.
  • Preliminary evidence suggest there may be increased risk of reinfection with Omicron.

The very strong implication is Omicron became the dominant strain in areas of South Africa due to being able to break through level 2 immunity. There is also evidence at this time that most infections are mild, which suggests Omicron breaks through level 2 immunity, but not through level 3 immunity.

If breaking through level 2 immunity makes such a difference, then even in a country such as South Africa, with low rates of vaccination, there is now a high level of immunity. It will take time to be verified, but if this is the case, there will be a surge in infections, but a far smaller surge in serious illness and deaths. If trends so far continue, there will need to be a lower ration of serious illness, as the rise is rapid.

The good news is that globally cases may continue unabated, but with immunity from vaccinations and high prevalence of immunity even in communities with lower levels of vaccination, there rates of serious illness and death may start to decline as humanity is acquiring overall a level of immunity that can at least reduced the impact of the virus.

However, given the latest case numbers of Omicron, we may really need that good news.

Beta To Delta To Omicron: A Journey Of Increasing Immunity.

The chart to the right is already out of date for Omicron, and this is in early December 2021, but the use of the chart is to show how during each wave in South Africa, the variants changed. Note that at least until now, each wave was due to a strain which showed some increase in virulence. Despite this, the ratios peak deaths to peak cases feel from 31 per thousand during Beta to 21 per thousand during Delta. This is a reduction of 33% in a country where vaccination rates at the time of the Delta outbreak were insignificant (still less than 25% 6 months later), and that reduction was despite the new staring being more virulent. If this trend is accelerating, as evident in countries with more recent, outbreaks then the prediction of the disease becoming more ‘tolerable’ may eventuate, even in the unvaccinated, not because of less virulent strains, but due to rising immunity throughout humanity.

Topics: