Rejoinder to Paul

 I’ll begin by paraphrasing a witty apology once given by Blaise Pascal: I’m sorry that this letter is so long; I didn’t have time to make it shorter.

>>yes the article you linked was also focussed on vaccine induced herd immunity, but so were your own words in your own comment.

Let me just address this point, quickly.

I’ll just go line by line, in my original comment, keeping track of what my “focus” was intended to have been.

Sentence 1 (The rewrite is certainly Orwellian.): Focus: The Orwellian nature of the WHO’s rewrite.

Sentence 2 (But the idea that "herd immunity" is obvious, observational datum is arguably false.): Focus: “herd immunity” of any kind, including any supposed “observational” examples of natural induction.

Sentence 3 (It's a theoretical construct that was postulated in the early 20th century and subsequently co-opted by pharmaceutical-company advertisements.): Focus: “herd immunity” as it was originated postulated – which was in reference to natural induction. (The specific case was an outbreak of measles in Baltimore early in the 20^th century. I gave the citation in a follow-up message. See, again, A. Hedrich, "Monthly estimates of the child population 'susceptible' to measles, 1900–1931, Baltimore, Maryland," American Journal of [Public] Hygiene, vol. 17, pp. 613-636, 1933.)

Sentence 4 (The fact that it's taught in children's biology textbooks is as much an indictment of the education system as any other piece of propaganda used to justify the NWO.): Focus: I was objecting – in my mind – to the fact that “herd immunity” of any kind (including alleged, naturally induced varieties) is being taught as fact.

Sentence 5 (At any rate, 60 years of compulsory vaccinations (at schools) hasn't produced the elusive "herd immunity" for *any* disease.) Focus: unclear. I confessed the difficulty in my follow-up comment. I said: “…I am not personally ‘equating herd immunity with vaccine induced herd immunity’. However, I can understand how you were left with that false impression, since the article I linked to is primarily a discussion of (alleged) vaccine-induced ‘herd immunity.’” So, since this reference was vague, I’ll give you the point. Count this sentence as a reference to vaccine-induced immunity only.

Final count:

·       5 total sentences.

·       Sentences focused on vaccine-induced herd immunity = 1.

·       Sentences not focused on vaccine-induced herd immunity = 4.

·       Sentences focused on naturally induced herd immunity = 3

Therefore, considering all sentences, 1 out of 5 (i.e., 20%) were “…focussed [sic] on vaccine induced herd immunity”.

Considering sentences focused on “herd immunity” of any kind, 1 out of 4 (or 25%) were “…focussed [sic] on vaccine induced herd immunity”.

Either way you cut it, fully 75-80% of my words (by sentence count) were not focused on vaccine-induced herd immunity.

>>But so now that you do refer to both natural and vaccine induced herd immunity, let's go through those points you mention (which are however again taken from an article that addresses vaccine induced herd immunity), …

The main theme of the quoted article is irrelevant because the points I extracted are applicable to (alleged) naturally induced herd immunity.

Additionally, the link was intended to be an expedient way to communicate the points, rather than serve as an authoritative source. In my view, the points rest on the force of the objections themselves.

>>…but firstly I would like to mention that the definition of herd immunity does not state it offers 100% immunity, but that this mechanism eventually makes the virus a negligible problem, …

Part of my skepticism about “herd immunity” – of any sort, including a supposedly “naturally induced” kind – is the lack of rigor in the concept’s characterization. (Indeed, it’s not even clear to me what the definition of “herd immunity” is supposed to be.)

The hand-waving reference to “negligibility” is an example of this. Just how “negligible” does a the risk have to be?

Intuitively, the answer will depend on the virus, the health and identity of the subpopulation, the properties of transmissibility, and much else besides.

As a quick illustration of this point about the looseness of the concept of “negligibility,” consider Ebola. Ebola is, right now – herd immunity or no – a “negligible problem” for me, given my health and geographical location.

>>…but now those points then, starting with:

>>1 yes virusses do mutate, but as also this latest COVID-19 variety of coronavirusses showed, up to 60% of people are already immune to it without ever having been exposed to this particular variety, because we have different mechanisms within our immune systems, one of which are the highly specific antibodies which only develop after exposure to the ONE specific viral variety they target, but then we also have many other layers of defence in our immune systems, one of which are the much less specific T-cells, which in the case of COVID-19 have been trained to respond to ANY type of coronavirus, and although those T-cells were found in the blood of "only" 60% of people, Dr. Bhakdi is convinced they may be found in the bodies of upto 100% of people, as many are stored within our organs and therefore cant be found in our blood.

I’m inclined to have sympathy for much of what you’ve written, above. I think our God-given immune systems are quite powerful, when we support our general health correctly.

Assuming that there is any virus, if I get COVID and don’t die, then my body will produce antibodies against COVID. These antibodies – along with other “layers of defence” (like T-cells) – will tend to protect me, personally, against future encounters with COVID. And the may also assist me in future encounters with any mutated strains, call them COVID*.

To my untutored eyes, you’ve just given a competent, albeit low-level, description of how our individual immune systems function.

In other words, as far as I can see, all your references to our multi-layered defense systems – as well-taken as they may be – pertain to immunity, period. I don’t see any specific relevance to “herd immunity.”

My basic thought was:

·       If herd immunity protects a group of people from Virus x, then Virus x has to persist over time.

·       If Virus x mutates (e.g., by changing into Virus x*), then Virus x doesn’t persist over time.

·       Therefore, if Virus x mutates, then herd immunity doesn’t protect a group from Virus x.

This is true, it seems to me, even if individuals still have multi-layered immune-defense systems and, therefore, have resources enough to fight Virus x*.

But, it’s individuals fighting Virus x* with the individual immune systems. “Herd immunity” doesn’t enter into it.

>>2 yes asymptomatic individuals can shed viral material (and/or exosomes), but as even Dr. Fauci admitted himself: in the history of diseases no pandemic has EVER been driven by asymptomatic carriers.", and this is also confirmed by the 97% of false positives that the PCR test registers at the common cycle threshold of 35 and above as positive, because in that case they are carrying (and therefore MIGHT be shedding) SOME viral material, but the amount is SO little that this viral material can not even be replicated in near perfect laboratory conditions, and that ONLY happens with asymptomatic individuals, because symptomatic individuals have a much higher viral load and therefore dont require such high Ct values to make that PCR test positively.

I think I may have expressed myself inadequately.

Let me try to rephrase my point.

·       If we’re in a good position to say whether herd immunity protects a group, g, of people from Virus x, then we’re in a good position to say who is infected with Virus x and who isn’t infected with Virus x.

·       But if there are asymptomatic carriers of Virus x within g, then we’re not in a good position to say who (in g) is infected and who isn’t.

·       Therefore, if there are asymptomatic carriers of Virus x within g, then we’re in not a good position to say that herd immunity protects people in g from Virus x.

>>3 yes people travel more now than in the 1930's, so in today's global village herd immunity is a global phenomenon.

Well, for one thing, not every virus afflicts wide area of the earth.

Consider, again, Ebola.

(I’m using Ebola because it is an extreme example. It’s a large example, if you like. Sometimes, blowing things up – as when we examine things under a microscope, or through a telescope – makes them easier to see.)

Ebola is a clear example of a virus that has (at least, heretofore) been limited to a particular geographical area.

For another thing, well… let me move to your point #4.

>>4 I don't see how those 2 assumptions are essential for herd immunity to be effective.

Previously, I had quoted Children’s Health Defense to the following effect:

The wooly notion of “herd immunity” depends upon the joint assumptions “...that all members of the population are equally susceptible to infectious disease and that all persons behave identically in spreading disease.”

Now, you say that you “don’t see how those 2 assumptions are essential for herd immunity to be effective.”

To me, this underscores a difficulty I mentioned earlier; namely, the concepts we’re wrestling with are ill defined.

What’s the definition of “herd immunity”?

A quick Google “define herd immunity” yields this: “resistance to the spread of an infectious disease within a population that is based on pre-existing immunity of a high proportion of individuals as a result of previous infection or vaccination.”

Leaving off the bit about vaccination is easy.

We are left with: “resistance to the spread of an infectious disease within a population that is based on pre-existing immunity of a high proportion of individuals as a result of previous infection…”.

But, defined this way, I don’t see that “herd immunity” is anything other than a shorthand way of saying “people who survive infections get immunity; when a lot of people have survived infections, a lot of people are immune.”

I haven’t seen any good reason to think that “herd immunity” has any real or independent existence anywhere.

Maybe “herd immunity” is something like a glint.

Have you ever walked down a street and a sudden burst of light, perhaps sunlight reflected off a car bumper, strikes you in the eye?

You see a glint.

But, if we want to make a list of all the things that really exist in the “glint” case, we’ll enumerate things like the following: the sun, the sun’s rays, the car, the bumper, your eye, etc.

There’s not really a “glint,” anywhere. Plausibly, it’s not as if some extra thing – a “glint” – pops into existence a moment …and then vanishes.

Rather, it’s that when the sun, the bumper, and you are aligned in a particular way, it creates a visual sensation that we refer to as a “glint.”

Now, I’m not saying that “herd immunity” is perspectival.

But what I am saying is that it appears to me that “herd immunity” is – at best – just a way of referring to a state of affairs in which we assign a low probability to some subpopulation getting infected with some pathogen. It’s just a label.

The really existing things, in my view, would be something like these: the population, the subpopulation, the pathogen, the facts about who has so far been infected, the facts about transmission, etc.

Statisticians may then project their estimates regarding some population’s risk of infection from the relevant pathogen, given the facts of transmission.

Now… if “herd immunity” is just a label that gets stuck on a particular kind of probability estimate – namely, one that assigns a low-level risk to a subpopulation’s likelihood of infection – then, fine.

But, I don’t see that “herd immunity” is anything more than a label on certain probability estimates.

So, to your remark that you “…don't see how those 2 assumptions are essential for herd immunity to be effective”, I’d say two things.

Number one, labels aren’t the sorts of things that can be “effective.”

If “herd immunity” is a label, then it’s not “effective” or “ineffective” – though, surely, it may be applied correctly or incorrectly.

Number two, the assumptions are vital for assessing whether that label has been applied correctly.

My contention is that, because most estimates don’t responsibly take the assumptions on board, both high- and low-probability risk estimates are virtually worthless.

Frankly, I find the concept of “herd immunity” to be a mess. In my view, it is badly in need of clarification – or abandonment. But, I won’t hold my breath, since discourse currently is shot through with vague and poorly defined concepts (think: “liberal,” “socialism,” “fascism,” “climate change,” and on and on).

Anyway…

I’ll leave things, here, though.

Thanks for prompting me to give these matters another “think.”

Best,

Matthew Bell

Rejoinder to Chris

 Here are some brief reactions to your comments.

>>I’m struggling to see any connection between your stated thesis and the attached article.<<

This is probably (partially) my fault since I used the circumlocution “a certain respiratory virus” in an attempt to evade Facebook’s Draconian penchant for “filtering” or presuming to stand in judgment of references to COVID-19.

I may restate my concern (personally, I would have reservations about describing it as a “thesis”) more straightforwardly, as follows.

I am concerned that, for some people, particular COVID prophylactics (such as vaccines) may have worse effects than COVID itself has, had, or would have.

Given that the linked-to article is titled “AstraZeneca puts coronavirus vaccine trials on pause after patient had a serious side effect,” I hope that its connection to my (precisified) statement is now clear to you.

But, in case it still isn’t clear to you, let me further say: In the AstraZeneca case, the contemplated vaccine has seemingly triggered “a potentially unexplained illness” in one human-trial participant and, for all we know, this “unexplained illness” could have worse effects on the affected individual than COVID would have had.

>>(Potentially) lifelong organ damage from COVID-19 has been documented from the outset of the pandemic,[…]<<

My (admittedly untutored) survey of the relevant literature suggests the following to me.

(1.)  Although it appears to be true that there have been reports of damage to the heart, kidneys, and lungs of some COVID patients, …[1]

(2.)  …the jury is still out on the question of whether the relevant damage is “lifelong”; unless…

(3.)  …you count people who suffered organ damage as part of an acute bout of COVID and then promptly died. (In which cases, the pertinent damage would count as “lifelong” only insofar as their lives concluded prematurely – in a matter of days or weeks, for example.)

(4.)  For most people, risk factors for long-term (and not necessarily “lifelong”) complications[2] include advanced age and comorbidities such as cardiovascular disease, diabetes, obesity, and so on. One Healthline article phrases “The Bottom Line” like this: “COVID-19 can be a severe illness, especially in people over 60 years of age or those with chronic diseases like diabetes and cardiovascular issues.”[3]

(5.)  For the marginal cases in which younger people have died or experienced organ (e.g., lung) damage,[4] it’s not clear (to me) whether the damage was due to COVID or to medical interventions such as ventilation (which is also well documented to cause organ damage, such as in cases of “Ventilator-Induced Lung Injury,” or VILI.)[5]^,[6]

>>[…]whereas vaccine side-effects tend to be auto-immune responses to a novel stimulus.<<

Here, it’s my turn to express some puzzlement. You seem to be drawing a(n implicit) distinction between “organ damage” and “auto-immune responses”[7] in terms of duration.

When I Google “most common auto-immune responses,” Google returns the following Healthline article: “Autoimmune Diseases: Types, Symptoms, Causes, and More.”[8]

The article lists fourteen[9] of the “most common” auto-immune diseases.[10]

In the order presented, the 14 are: Type 1 diabetes; Rheumatoid arthritis (RA); Psoriasis/psoriatic arthritis; Multiple sclerosis (MS); Systemic lupus erythematosus (SLE); Inflammatory bowel disease (IBD); Addison’s disease; Graves’ disease; // Sjögren’s syndrome; Hashimoto’s thyroiditis; Myasthenia gravis; Autoimmune vasculitis; Pernicious anemia; Celiac disease.

We can construct follow-up searches according to the following schema, “is [whatever condition] a lifelong disease,” where we substitute each disease name, in turn, for the bracketed variable. Doing so, I got these top results – that is, Google’s 0-position result on the search page (the so-called “snippets”).

-        “is type 1 diabetes a lifelong disease”: “Type 1 diabetes is a lifelong (chronic) disease in which there is a high level of sugar (glucose) in the blood.”[11]

-        “is Rheumatois arthritis a lifelong disease”: “RA is a lifelong condition,…”[12]

-        “is Psoriatic arthritis a lifelong disease”: “Psoriatic arthritis tends to be lifelong.”[13]

-        “is Multiple sclerosis a lifelong disease”: “Multiple sclerosis …[i]s a lifelong condition …”[14]

-        “is Inflammatory bowel disease a lifelong disease”: “IBD is a lifelong (chronic) condition.”[15]

-        “is Systemic lupus erythematosus a lifelong disease”: “Lupus …is lifelong and can become severe…”[16]

-        “is Addison’s disease a lifelong disease”: “…Addison’s is a life-long condition…”[17]

-        “is Graves’ disease a lifelong disease”: “Graves disease is an ongoing (chronic) condition that needs lifelong treatment.”[18]

-        “is Sjögren’s syndrome a lifelong disease”: “Sjögren’s syndrome is generally a lifelong disease.”[19]

-        “is Hashimoto’s thyroiditis a lifelong disease”: “Most patients with Hashimoto’s thyroiditis will require lifelong treatment…”[20]

-        “is Myasthenia gravis a lifelong disease”: “Myasthenia gravis is a lifelong health condition.”[21]

-        “is Autoimmune vasculitis a lifelong disease”: “There are many types of vasculitis, and most of them are rare. Vasculitis might affect just one organ, or several. The condition can be short term (acute) or long lasting (chronic).”[22]

-        “is pernicious anemia a lifelong disease”: “People who have pernicious anemia may need lifelong treatment.”[23]

-        “is celiac disease a lifelong disease”: “Individuals with celiac disease cannot outgrow the disease since it is a lifelong autoimmune disorder like diabetes and rheumatoid arthritis.”[24]

With the possible exceptions of Autoimmune Vasculitis and Pernicious Anemia, which could be acute or chronic, the other twelve of the “most common autoimmune diseases” are manifestly lifelong conditions.

>>Are you saying that handwashing and other general precautions to avoid a cold/flu/virus infection will cause a coronavirus to react differently within an exposed body?<<

What I actually typed was: “Some people who may otherwise have recovered from a certain respiratory virus without lasting ill effects will possibly be stricken with lifelong debilities in a misguided attempt (imo) to shield themselves from it.”

The final word, “it” was intended to refer back the aforementioned circumlocution, “a certain respiratory virus.”

So, the first alteration I would make to your paraphrase would be this.

Translated into your phraseology, what I was talking about was (something like):

How “…handwashing and other general precautions to avoid a [certain respiratory] infection [a.k.a., coronavirus]” relate to how an exposed body” will “react” to coronavirus.

This emendation having been performed, I would also take exception to the causal claim embedded in your paraphrase.

No, I don’t think that “general precautions”[25] taken by an individual “will cause a coronavirus [in an of itself] to…” do anything whatever.

However, I think that something (again, translated partially into your verbiage) in the vicinity is true, namely:

Some interventions (such as vaccinations[26]), designed to avoid a COVID infection, will cause exposed bodies to react differently to COVID than those bodies would have reacted without the intervention.

And, sometimes, “react differently” will unfortunately mean than the intervention will make things worse.

>>Does HIV, herpes, etc react differently because someone has avoided it until the moment they catch it?

Just a bit of a worry… “catch it” is not a little vague.

Presumably, firstly, a person could be “exposed” to a pathogen without that pathogen taking up residence (so to speak) within a person’s body.

Secondly, a pathogen could take up residence a person’s body and begin to replicate without that person ever displaying symptoms – being asymptomatic, in other words.

Thirdly, even where the pathogen takes up residence and replicates sufficiently to produce symptoms of clinical infection, such a disease is usually said to evolve along a roughly five-stage trajectory.

-        The “incubation” stage is that period after an organism is exposed to a pathogen during which the pathogen is replicating.

-        Although the point of demarcation is hazy, at some time, this incubation period gives away to a “prodromal” stage in which some “low-level” symptoms may appear, but before “higher-level” symptoms – perhaps those most characteristic of the disease in question – appear.

-        Once replication has advanced far enough, presumably, the individual segues into the full-blown “illness” stage, which (we’ll suppose) presents in such a way as one would typically read about in a clinical, diagnostic manual.

-        If the afflicted person doesn’t die, then the immune system eventually puts the pathogen into “decline.”

-        And, once the decline has proceeded adequately, the person begins his or her period of recovery, or “convalescence.”

Given all of these niceties, it isn’t at all clear to me what “catch it” means.

Does it designate exposure only? Or exposure + incubation – whether or not the person remains asymptomatic? Or does it only apply in cases where exposure evolves all the way to some symptomatic stage – whether prodromal or full, clinical illness?

I’m sure questions like these could be multiplied.

But, leaving this concern aside, your main question was about whether a virus (you name HIV and herpes[27]) “react[s] differently” upon “catch[ing] it… because someone ha[d theretofore] avoided it”.

To echo my previous remarks, I don’t think there’s much of a reason to think that, for some random person (let’s call her Zhang Xiu Ying), her avoidance of Pathogen x causally affects Pathogen x in and of itself.

Let me give an illustration, using the phrase in vitro.

Suppose that we have a specimen of Pathogen x in vitro and that, as of 7:00pm central time 9/9/2020, Zhang Xiu Ying “avoided” any exposure to x, whereupon she unfortunately shatters the specimen’s container and exposes herself.

That Zhang Xiu Ying successfully avoided x up to the specified time plausibly had no causal effect on x (in and of itself, in this case emphasized in virtue of being in vitro) up to 7:00pm central 9/9/2020.

However, once Zhang Xiu Ying is exposed, then whether she becomes an incubation chamber for x or manifests symptoms of clinical illness will, equally plausibly, be the result of a complex interaction.

Relevant factors might include any or all the following (and probably more besides).

Factors about Pathogen x, like:

-        how x is absorbed into a body,

-        how transmissible x is,

-        how quickly x incubates,

-        how much of x there was for Zhang Xiu Ying to be exposed to,

-        how much of x generally has to be present in order to affect incubation in an organism like the kind that Zhang Xiu Ying is,

-        etc.

Factors about the exposure circumstances, e.g.:

-        how much of x “got on” or “got into” Zhang Xiu Ying,

-        the pathway or exposure route that x traversed,

-        whether there were ancillary factors that tended to amplify or defeat x’s ability to leverage the exposure into an incubation in Zhang Xiu Ying, specifically

-        etc.

Factors about Zhang Xiu Ying herself, such as:

-        how susceptible she is to a pathogen like x, and – and this is my main point of emphasis –

-        how healthy Zhang Xiu Ying is, overall, including…

-        whether she has any comorbidities (like cardiovascular disease, diabetes, obesity, etc.), and…

-        how – let me use the word… – robust her immune system is,

-        etc.

Now… “how robust her immune system is” is, I confess, difficult to specify.

But what I am most curious about is a comparative like the following.

Call this, My Fundamental Question:

How robust is Zhang Xiu Ying’s immune system (i.e., how robust is it now, as a matter of fact) compared to and contrasted with how robust it would be[28] (i.e., counterfactually) were it not for some medical intervention or prophylaxis? (Call the intervention or prophylaxis “y.”)

Let me conclude by providing one thought experiment that, in my mind, makes it plausible that a question like My Fundamental Question is worth asking.

Suppose that our intervention/prophylaxis, y, is this:

Per impossibile, we place Zhang Xiu Ying in a hermetically sealed “bubble” suit from birth.

Suppose further that at 7:00pm central 9/9/2020, Zhang Xiu Ying simultaneously ruptures x’s petri dish and tears her suit, compromising her longstanding hermetic seal (and undermining y).

Based on this far-fetched,[29] but still instructive, scenario, I think that the following statement is more plausible than its negation:

Zhang Xiu Ying’s immunity is less robust given her longstanding reliance upon y than it would have been had she lived her life allowing her immune system to interact naturally with pathogens, without y.

If this is the case, though (that the above proposition is more plausible than its negation), then it tends to show (I think) that there is some intervention, some y, such that a person’s immunity is less given y than that person’s immunity would have been without y.

But, if this is the case, then the obvious follow-up questions are: what sort of interventions are the ones that folks have in mind to protect us from COVID: things like vaccinations and, yes, handwashing? Are they immune-enhancing interventions, or are they immune-diminishing ones?

I would argue – although, not here and not now – that these sorts of intervention can probably go either way, depending on how (and how often) they are carried out and other factors. And, as a matter of fact, they are often immune diminishing.

To be continued, presumably…

Peace.

---

[1] See, e.g., here: https://www.today.com/health/coronavirus-long-term-health-covid-19-impact-lungs-heart-kidneys-t178770.

[2] The previously cited Today article reads, in part: “Some patients have been called ‘long haulers’ as they continue to have symptoms for months after being infected with the coronavirus, perhaps because of the inflammation triggered by COVID-19.” (Loc. cit.; boldfacing added for emphasis.) Or, again, this author writes: “While most people recover from pneumonia without any lasting lung damage, the pneumonia associated with COVID-19 may be severe. Even after the disease has passed, lung injury may result in breathing difficulties that might take months to improve.” According to https://www.hopkinsmedicine.org/health/conditions-and-diseases/coronavirus/what-coronavirus-does-to-the-lungs. “Months to improve” is not synonymous with “lifelong” unless the afflicted person dies in a matter of months. (And, even then, “months to improve” must mean something else, unless we treat “die” as functionally equivalent to “improve.” …which, hey, one might do, from a Christian point of view.)

[3] https://www.healthline.com/health-news/what-we-know-about-the-long-term-effects-of-covid-19#The-bottom-line.

[4] E.g., as reported here: https://www.npr.org/sections/health-shots/2020/06/12/875486356/first-known-u-s-lung-transplant-for-covid-19-patient-performed-in-chicago.

[5] See, e.g., here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896812/.

[6] For instance, the “woman in her 20s” received numerous, invasive interventions in a hospital. We read: “For two months, she was in the intensive care unit on a ventilator and another machine, known as ECMO, that pumps and oxygenates blood outside of the body.” (Ibid.; boldfacing added.)

[7] “[T]o novel [stimuli]” whatever that is supposed to mean.

[8] https://www.healthline.com/health/autoimmune-disorders.

[9] Of “more than 80,” by Healthline’s count. Op. cit.

[10] By the way, Google freely substitutes the term “diseases” for your arguably less pointed word, “responses.”

[11] https://medlineplus.gov/ency/article/000305.htm.

[12] https://www.medicalnewstoday.com/articles/323631.

[13] https://www.health.harvard.edu/a_to_z/psoriatic-arthritis-a-to-z.

[14] https://www.nhs.uk/conditions/multiple-sclerosis/.

[15] https://www.uofmhealth.org/conditions-treatments/digestive-and-liver-health/crohns-faq.

[16] https://www.uwhealth.org/health/topic/major/lupus-systemic-lupus-erythematosus/hw123404.html.

[17] https://www.addisonsdisease.org.uk/what-is-addisons-disease.

[18] https://www.urmc.rochester.edu/encyclopedia/content.aspx?contenttypeid=160&contentid=5.

[19] https://www.health.harvard.edu/a_to_z/sjogrens-syndrome-a-to-z.

[20] https://www.thyroid.org/hashimotos-thyroiditis/.

[21] https://www.cedars-sinai.org/health-library/diseases-and-conditions/m/myasthenia-gravis.html.

[22] https://www.mayoclinic.org/diseases-conditions/vasculitis/symptoms-causes/syc-20363435.

[23] https://www.nhlbi.nih.gov/health-topics/pernicious-anemia.

[24] https://www.massgeneral.org/children/celiac-disease/faq.

[25] Of course, what I had in view primarily was vaccination, not hand washing.

[26] Incidentally, tho, I think this applies to more pedestrian interventions like handwashing.  

[27] Just what do you imagine that I’ve been doing? Tho, even in the case of herpes: “Everyone who is exposed to the virus does not develop sores…”, according to: https://healthcenter.ucsc.edu/forms/student-handbook/HC-814-Herpes-Testing_FAQ.pdf. This is unfortunate wording, from the perspective of logic. Presumably, the author does not mean “for all people who are exposed to herpes, it is the case, for those people, that all of them do not develop sores”, but rather “it is not the case that: for all people who are exposed to herpes, all of them develop sores.”

[28] Or… would have been, had the intervention never been administered.

[29] Extreme thought experiments are often useful tools. And, anyway, herpes and HIV seem to be extreme examples of viruses, so I can hardly be faulted for returning extreme example for extreme example.