Herd Immunity, R(o), and a Virus We Barely Know

Sars-Cov-2 and Covid-19 Without Politics

Sometimes, in late 2019, a new virus, which we now call Sars-Cov-2, launched an attack from somewhere in China—or at least this is how we understand. It attacked silently at first. By silence I mean that no one really understood that this was a new virus; many facilities everywhere thought they were dealing with the flu. After all, this was flu season.

I am not going to touch up on politics and will stick strictly to the virus and the disease it is causing, which is called Covid-19. As I am sure by now you know that it is a corona virus, I am not going to spend too much time on explaining what the virus looks like. It is pretty actually, with spikes.

Looks are deceiving though because it is not a pretty virus though it seems extremely efficient and effective.


Most literature initially discussed the length of time the virus is alive, or what may kill the virus. I feel it is important to clarify: viruses are not alive. The definition of “being alive” involves certain fundamental biological functions, namely respiration (exchanging electrolytes and gases with the external environment as part of feeding), and viruses have no such functions. Probably the most successful strategy for the “survival” of the virus is to not be alive. So when we talk about keeping a virus alive, we really mean “retain its integrity and virility” such that it can cause disease in a new host. A virus cannot have a symbiotic relationship with humans in a classical sense—like bacteria can serve in our gut as fermenting entity, providing us with much-needed short chain fatty acids.

Since viruses are not alive, they only need a host for propagation and provide no nutrients in return. With this said and done, there can be some benefits to viruses, and so symbiosis exists. The human genome contains an amazingly large percent viral genome (8%). This suggests that these viruses are, in some ways, part of us for some reason.

Contagion & Virility

Now that we know that viruses are not alive, we need to understand what contagion and virility means. Contagion is possible by what is referred to as viral shedding. Shedding happens when a virus presses its RNA (or DNA) into a host cell and baby viruses are created by the cell. The moment of the baby viruses release is referred to as shedding. A cell can shed a ton of baby viruses, each of which is capable then to attack another cell and force new shedding.

Before this shedding, a virus may be in a person’s blood for some time and is not detectable by any means. This is part of the incubation period, when the person is already infected but there are no symptoms, and often the virus is not detectable because simply there aren’t enough of them to be detected. Since shedding occurs, this stage is a contagion stage, because viruses can be in just about any body fluid without our knowledge.

Virility is the speed with which the virus is generated and can then be passed to another host. For example, a disease, such as HIV, has low virility because it is pretty much contained in one person and requires direct contact of body fluids with another. As a one-to-one transmission, while the virus may be fatal, the transmission requires a direct contact between participants in some way.

Sars-Cov-2 is a different virus. It transfers easily in the air, by contact, and also it remains “alive” for a long time on certain surfaces, and even in the air. So Sars-Cov-2 has a high virility. As a result, it also has a very high transfer rate. This transfer rate is referred to as R, where R(o) is the general (it should really be original) transfer rate and R(t) is a specific transfer rate at a particular time–I wish there was such as R(g,o) and R(g,t), where g stands for the geographical location. R(t) is seldom, if ever, mentioned, even though it is more important, since in some places—such as Northern Italy, for example–the initial transmission rate of Covid-19 was significantly higher than in other countries, say Iceland, at the same early stage of the disease. So there is no “generic” R(o) only geographically relevant R(o), which also changes with time, so R(g,t). For some odd reason though, the world is only using a general R(o). It is also important to note that R ==> 0 meaning the goal is to eliminate the virus, in which case we have zero infections, so R(o)=0

R(o) and Herd Immunity

At the discovery of the virus—before we knew what we were dealing with—the R(o) of the virus was very high. If R(o) = 1, an in my earlier example of HIV, it is a one to one transmission, so one person transfers the virus to one other person. With Sars-Cov-2, the R(o) in Italy, at the height of the worst transmission time, was over 3 and that represents an exponential increase where the exponent is 3.

1 person transmits to 3, and then each of that 3 transmits to 3, so that’s 9, and each of the 9 transmits to 3 and so that’s 27, so R(o)=3 is x^3 exponential curve of increase. Of course, once a magic number of people are infected, if there are no more people to infect, even the most virulent disease will tend to R(o)=0, since, in time, everyone already had the virus and they are either dead or immune. This is the “herd immunity” of ideal reach.

In a nation where over 10% of the population already has the disease, if R(o) remains 3, herd immunity can be reached amazingly fast—within days, depending on the population size. But this comes with huge risks because of hospital overuse and thus lack of resources to treat the sick. So we need to reduce R(o) to be close to 1 and then to 0 by any means possible. So in comes the flattening of the curve.

Flattening of the Curve and Social Distancing

Most people misunderstand what flattening of the curve means. Think of a balloon that has a certain amount of air you just blew into and closed the balloon at the base so air cannot escape. Now place your hand on the top of the balloon and press gently. You will see the “flattening of the curve” of the balloon but the air will not be squeezed out of it. Now assume that the air in the balloon are all the sick people. So flattening the curve doesn’t mean fewer sick people. It refers to the same number of people being sick but catching the disease at a slower rate. So rather than all people catching the disease in one month, by flattening the curve, the disease-catching time may be lengthened to several months.

To flatten the curve, many measures may be made: closing cities so transmission rate is zero because people are stuck at home, or by social distancing such that they must stay away distant enough to not catch the disease, and also by wearing protective gear that prevents transmission. So far all of these three have been used successfully to flatten the curve—meaning to give more time for the infection to spread and to allow hospital space for each person who needs treatment. Whether the treatment they get in hospitals is a good one, is going to be discussed in another blog later.

My Current Position

Here I wanted you to understand the meaning of R(o), herd immunity, and flattening the curve, since these are often discussed and very often misused and misunderstood. I also wanted to remove politics about the discussion, which is often a confusing factor.

In a future document (hopefully soon) I will detail the virus and the disease itself. It is complex and requires lots of work on my part, but I am working on a lot of other things that have priority, so keep your eyes on my blog!! It shall come! 😊

Comments are welcome as always, and are moderated for appropriateness




About Angela A Stanton, Ph.D.

Angela A Stanton, PhD, is a Neuroeconomist focusing on chronic pain--migraine in particular--physiology, electrolyte homeostasis, nutrition, and genetics. She lives in Southern California. Her current research is focused on migraine cause, prevention, and treatment without the use of medicine. As a forever migraineur from childhood, her discovery was helped by experimenting on herself. She found the cause of migraine to be at the ionic level, associated with disruption of the electrolyte homeostasis, resulting from genetic variations of all voltage dependent channels, gates, and pumps (chanelopathy) that modulate electrolyte mineral density and voltage in the brain. In addition, insulin and glucose transporters, and several other variants, such as MTHFR variants of B vitamin methylation process and many others are different in the case of a migraineur from the general population. Migraineurs are glucose sensitive (carbohydrate intolerant) and should avoid eating carbs as much as possible. She is working on her hypothesis that migraine is a metabolic disease. As a result of the success of the first edition of her book and her helping over 5000 migraineurs successfully prevent their migraines world wide, all ages and both genders, and all types of migraines, she published the 2nd (extended) edition of her migraine book "Fighting The Migraine Epidemic: Complete Guide: How To Treat & Prevent Migraines Without Medications". The 2nd edition is the “holy grail” of migraine cause, development, and prevention, incorporating all there is to know. It includes a long section for medical and research professionals. The book is full of academic citations (over 800) to authenticate the statements she makes to make it easy to follow up by those interested and to spark further research interest. It is a "Complete Guide", published on September 29, 2017. Dr. Stanton received her BSc at UCLA in Mathematics, MBA at UCR, MS in Management Science and Engineering at Stanford University, PhD in Economics with dissertation in neuroscience (culminating in Neuroeconomics) at Claremont Graduate University, fMRI certification at Harvard University Medical School at the Martinos Center for Neuroimaging for experimenting with neurotransmitters on human volunteers, certification in LCHF/ketogenic diet from NN (Nutrition Network), certification in physiology (UPEN via Coursea), Nutrition (Harvard Shool of Public Health) and functional medicine studies. Dr. Stanton is an avid sports fan, currently power weight lifting and kickboxing. For relaxation (yeah.. about a half minute each day), she paints and photographs and loves to spend time with her family of husband of 45 years, 2 sons and their wives, and 2 granddaughters. Follow her on Twitter at: @MigraineBook, LinkedIn at https://www.linkedin.com/in/angelaastantonphd/ and facebook at https://www.facebook.com/DrAngelaAStanton/
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6 Responses to Herd Immunity, R(o), and a Virus We Barely Know

  1. DrDKC says:

    Liked your approach towards the understanding the viruses. I would also ask you to go through my articles in –

    Most of the article s are based on similar topics and hence I feel you will like them.

    Liked by 1 person

  2. Paul Butler says:

    Great job as usual Angela

    Liked by 1 person

  3. Paula says:

    Hi Angela, great info. Two comments (1) my husband told me that CDC just put out new information that surface contamination is not as serious an issue as previously thought https://www.usatoday.com/story/news/health/2020/05/21/coronavirus-news-what-cdc-saying-covid-19-surfaces/5235317002/

    And (2) I heard that one reason for Northern Italy having such a horrible time with the virus is that China makes a lot of leather goods there that they can then claim are “made in Italy” (which technically they are), but there is a very high Chinese population in N. Italy as a consequence, and hence much travel to & from China. This made infection a real problem from the get-go in that corner of the world

    Liked by 1 person

    • Hi Paula,

      I agree with the CDC. I am much more of a believer in the aerosolized spread than surfaces. 🙂 In terms of Italy and China: there are many possibilities there and I know different people have different opinions on the matter. I don’t know how Chinese leather could have much to do with it, if surfaces aren’t transfer-subjects so easily. Leather goods are surfaces. There is much travel between China and everywhere but from what I have so far heard, the Italian Sars-Cov-2 is a different strain. Not sure this is true since every literature I read has a different opinion.

      In addition, California, which is the most Chinese-trade-rich state in the US, we are just now starting to increase in infection and death rates! Yet all travel had already been banned for several months now and California is not yet “open” much either. They are thinking about closing back up again because of the increasing in death rates in Los Angeles rather than decreasing.

      In Orange County, where I live, the death-rates nearly doubled in 2 days just now! So we are not near to being over with this, yet travel is nowhere… not sure Chinese trade has much to do with it.

      My personal take is this: Lombardi and Northern Italy, in general, is the most expensive region in Italy (perhaps in Europe other than Monaco) where the oldest people live(d). in addition, as we know, with “good life” comes bad eating. This will be in my next blog about the connection of metabolic health and Covid-19.

      The connection is much more complex than “obese people die from Covid-19” because many non-obese also died. It is also not just heart disease or T2D. It is also not just old age, since we saw many middle age and now even children and many young adults–at least in the US. There is a definite variability in the “selective process” by the virus that seems geographically selective. I will discuss that in the future blog article.



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