Tag Archives: Immunity

Herd Immunity To Public Health Bullshitters and To COVID

16 Monday Aug 2021

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My last post had a simple message about the meaning of immunity: you won’t get very sick or die from an infection to which you are immune, including COVID-19. Like any other airborne virus, that does NOT mean you won’t get it lodged in your eyeballs, sinuses, throat, or lungs. If you do, you are likely to test positive, though your immunity means the “case” is likely to be inconsequential.

As noted in that last post, we’ve seen increasing COVID case counts with the so-called Delta variant, which is more highly transmissible than earlier variants. (This has been abetted by an uncontrolled southern border as well.) However, as we’d expect with a higher level of immunity in the population, the average severity of these cases is low relative to last year’s COVID waves. But then I saw this article in ScienceAlert quoting Sir Andrew Pollard, a scientist affiliated AstraZeneca and the University of Oxford. He says with Delta, herd immunity “is not a possibility” — everyone will get it.

Maybe everyone will, but that doesn’t mean everyone will get sick. His statement raises an obvious question about the meaning of herd immunity. If our working definition of the term is that the virus simply disappears, then Pollard is correct: we know that COVID is endemic. But the only virus that we’ve ever completely eradicated is polio. Would Pollard say we’ve failed to achieve herd immunity against all other viruses? I doubt it. Endemicity and herd immunity are not mutually exclusive. The key to herd immunity is whether a virus does or does not remain a threat to the health of the population generally.

Active COVID infections will be relatively short-lived in individuals with “immunity”. Moreover, viral loads tend to be lower in immune individuals who happen to get infected. Therefore, the “infected immune” have less time and less virus with which to infect others. That creates resistance to further contagion and contributes to what we know as herd immunity. While immune individuals can “catch” the virus, they won’t get sick. Likewise, a large proportion of the herd can be immune and still catch the virus without getting sick. That is herd immunity.

One open and controversial question is whether uninfected individuals will require frequent revaccination to maintain their immunity. A further qualification has to do with asymptomatic breakthrough infections. Those individuals won’t see any reason to quarantine, and they may unwittingly transmit the virus.

I also acknowledge that the concept of herd immunity is often discussed strictly in terms of transmission, or rather its failure. The more contagious a new virus, like the Delta variant, the more difficult it is to achieve herd immunity. Models predicting low herd immunity thresholds due to heterogeneity in the population are predicated on a given level of transmissibility. Those thresholds would be correspondingly higher given greater transmissibility.

A prominent scientist quoted in this article is Paul Hunter of the University of East Anglia. After backing-up Pollard’s dubious take on herd immunity, Hunter drops this bit of real wisdom:

“We need to move away from reporting infections to actually reporting the number of people who are ill. Otherwise we are going to be frightening ourselves with very high numbers that don’t translate into disease burden.”

Here, here! Ultimately, immunity has to do with the ability of our immune systems to fight infections. Vaccinations, acquired immunity from infections, and pre-existing immunity all reduce the severity of later infections. They are associated with reductions in transmission, but those immune responses are more basic to herd immunity than transmissability alone. Herd immunity does not mean that severe cases will never occur. In fact, more muted seasonal waves will come and go, inflicting illness on a limited number of vulnerables, but most people can live their lives normally while viral reproduction is contained. Herd immunity!

Sadly, we’re getting accustomed to hearing misstatements and bad information from public health officials on everything from mask mandates, lockdowns, and school closings to hospital capacity and vaccine hesitancy. Dr. Pollard’s latest musing is not unique in that respect. It’s almost as if these “experts” have become victims of their own flawed risk assessments insofar as their waning appeal to “the herd” is concerned. Professor Hunter’s follow-up is refreshing, however. Public health agencies should quit reporting case counts and instead report only patients who present serious symptoms, COVID ER visits, or hospitalizations.

Effective Immunity Means IF YOU CATCH IT, You Won’t Get Sick

12 Thursday Aug 2021

Posted by in Coronavirus, Uncategorized, Vaccinations

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Listen very carefully: immunity does NOT mean you won’t get COVID, though an infection is less likely. Immunity simply means your immune system will be capable of dealing with an infection successfully. This is true whether the immunity is a product of vaccination or a prior infection. Immunity means you are unlikely to have worse than mild symptoms, and you are very unlikely to be hospitalized. (My disclaimer: I am opposed to vaccine mandates, but vaccination is a good idea if you’ve never been infected.)

I emphasize this because the recent growth in case numbers has prompted all sorts of nonsensical reactions. People say, “See? The vaccines don’t work!” That is a brazenly stupid response to the facts. Even more dimwitted are claims that the vaccines are killing everyone! Yes, there are usually side effects, and the jabs carry a risk of serious complications, but it is minuscule.

Vaccine Efficacy

Right out of the gate, we must recognize that our PCR testing protocol is far too sensitive to viral remnants, so the current surge in cases is probably exaggerated by false positives, as was true last year. Second, if a large share of the population is vaccinated, then vaccinated individuals will almost certainly account for a large share of infected individuals even if they have a lower likelihood of being infected. It’s simple math, as this explanation of base rate bias shows. In fact, according to the article at the link:

“… vaccination confers an eightfold reduction in the risk of getting infected in the first place; a 25-fold reduction in risk of getting hospitalized; and a 25-fold reduction in the risk for death.”

The upshot is that if you are vaccinated, or if you have acquired immunity from previous exposure, or if you have pre-existing immunity from contact with an earlier COVID strain, you can still “catch” the virus AND you can still spread it. Both are less likely, and you don’t have as much to worry about for your own health as those having no immunity.

As for overall vaccine efficacy in preventing death, here are numbers from the UK, courtesy of Phil Kerpen:

The vertical axis is a log scale, so each successive gridline is a fatality rate 100x as large as the one below it. Obviously, as the chart title asserts, the “vaccines have made COVID-19 far less lethal.” Also, at the bottom, see the information on fatality among children under age 18: it is almost zero! This reveals the absurdity of claims that children must be masked for schools to reopen! In any case, masks offer little protection to anyone against a virus that spreads via fine aerosols. Nevertheless, many school officials are pushing unnecessary but politically expedient masking policies

Delta

Ah, but we have the so-called Delta variant, which is now dominant and said to be far more transmissible than earlier variants. Yet the Delta variant is not as dangerous as earlier strains, as this UK report demonstrates. Delta had a case fatality rate among unvaccinated individuals that was at least 40% less than the so-called Alpha variant. This is a typical pattern of virus mutation: the virus becomes less dangerous because it wants to survive, and it can only survive in the long run by NOT killing its hosts! The decline in lethality is roughly demonstrated by Kelly Brown with data on in-hospital fatality rates from Toronto, Canada:

The case numbers in the U.S. have been climbing over the past few weeks, but as epidemiologist Larry Brilliant of WHO said recently, Delta spreads so fast it essentially “runs out of candidates.” In other words, the current surge is likely to end quickly. This article in Issues & Insights shows the more benign nature of recent infections. I think a few of their charts contain biases, but the one below on all-cause mortality by age group is convincing:

The next chart from Our World In Data shows the infection fatality rate continuing its decline in the U.S. The great majority of recent infections have been of the Delta variant, which also was much less virulent in the UK than earlier variants.

Furthermore, it turns out that the vaccines are roughly as effective against Delta and other new variants as against earlier strains. And the newest “scary” variants, Kappa and Lambda, do not appear to be making strong inroads in the U.S. 

Fading Efficacy?

There have been questions about whether the effectiveness of the vaccines is waning, which is behind much of the hand-wringing about booster shots. For example, Israeli health officials are insisting that the effectiveness of vaccines is “fading”, though I’ll be surprised if there isn’t some sort of confounding influence on the data they’ve cited, such as age and co-morbidities. 

Here is a new Mayo Clinic study of so-called “breakthrough” cases in the vaccinated population in Minnesota. It essentially shows that the rate of case diagnosis among the vaccinated rose between February and July of this year (first table below, courtesy of Phil Kerpen). However, the vaccines appear only marginally less effective against hospitalization than in March (second table below).

The bulk of the vaccinated population in the U.S. received their jabs three to six months ago, and according to this report, evidence of antibodies remains strong after seven months. In addition, T-cell immunity may continue for years, as it does for those having acquired immunity from an earlier infection. 

Breakthroughs

It’s common to hear misleading reports of high numbers of “breakthrough” cases. Not only will these cases be less menacing, but the reports often exaggerate their prevalence by taking the numbers out of context. Relative to the size of the vaccinated population, breakthrough cases are about where we’d expect based on the original estimates of vaccine efficacy. This report on Massachusetts breakthrough hospitalizations and deaths confirms that the most vulnerable among the vaxed population are the same as those most vulnerable in the unvaxed population: elderly individuals with comorbidities. But even that subset is at lower risk post-vaccination. It just so happens that the elderly are more likely to have been vaccinated in the first place, which implies that the vaccinated should be over-represented in the case population.

Conclusion

The COVID-19 vaccines do what they are supposed to do: reduce the dangers associated with infection. The vaccines remain very effective in reducing the severity of infection. However, they cannot and were not engineered to prevent infection. They also pose risks, but individuals should be able to rationally assess the tradeoffs without coercion. Poor messaging from public health authorities and the crazy distortions promoted in some circles does nothing to promote public health. Furthermore, there is every reason to believe that the current case surge in Delta infections will be short-lived and have less deadly consequences than earlier variants.

Bottom-Line Booster Shots

17 Saturday Apr 2021

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The barrage of precautionary COVID missives continues, and with a familiar “follow-the-money” twist. The CEOs of both Pfizer and Moderna say that booster shots are likely to be needed a year after initial administration of their COVID vaccines, and almost certainly every year thereafter. Of course, this message is for those who felt compelled to be vaccinated in the first place, whether out of concern for their own health, high-minded community spirit, fear of social ostracism, or fear of possible vaccine passport requirements. It’s probably also intended for those who acquired immunity through infection.

There are reasons to believe, however, that such a booster is unnecessary. This case was made a few days ago in a series of tweets by Dr. Monica Ghandi, an infectious disease expert and Professor of Medicine at UCSF. Ghandi says immunity from an infection or a vaccine can be expected to last much longer than a year, despite the diminished presence of antibodies. That’s because the immune system relies on other mechanisms to signal and produce new antibodies against specific pathogens when called upon.

So-called B cells actually produce antibodies. Another cell-type known as T cells act to signal or instruct B cells to do so, but so-called “killer” T cells destroy cells in the body that have already been infected. Dr. Ghandi’s point is that both B and T cells tend to have very long memories and are capable of conferring immunity for many years.

While our experience with COVID-19 is short, long-lasting immunity has been proven against measles for up to 34 years, and for other SARS-type viruses for at least 17 years. Dr. Ghandi links to research showing that survivors of the 1918 flu pandemic were found to have active B cells against the virus 90 years later! The COVID vaccines cause the body to produce both B and T cells, and the T cells are protective against COVID variants.

A last point made by Dr. Ghandi is intended to dispel doubts some might harbor due to the relatively ineffectual nature of annual flu vaccines. The flu mutates much more aggressively than COVID, so the design of each year’s flu vaccine involves a limited and uncertain choice among recent strains. COVID mutates, but in a more stable way, so that vaccines and adaptive immunity tend to retain their effectiveness.

While I’m sure the pharmaceutical companies believe in the benefits of their vaccines, there are undoubtedly other motives behind the push for boosters. There is money to be made, and much of that money will be paid by governments eager to jump on the precautionary bandwagon, and who are likely to be very insensitive to price. In fact, the vaccine producers might well have encouraged those pushing vaccine passports to include annual booster requirements. This would be another unwelcome imposition. The very discussion of boosters gives government officials more running room for other draconian but ultimately ineffective mandates on behavior. And the booster recommendation gives additional cover to public health “experts” who refuse to acknowledge real tradeoffs between the stringency of non-pharmaceutical interventions, economic well being, and other dimensions of public health.

Fall Coronavirus Season

16 Friday Oct 2020

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We’ve known for some times that COVID-19 (C19) follows seasonal patterns typical of the flu, though without the flu’s frequent antigenic drift. Now that we’re moving well into autumn, we’ve seen a surge in new C19 case counts in Europe and in a number of U.S. states, especially along the northern tier of the country.

The new case surge began in early to mid-September, depending on the state, and it’s been coincident with another surge in tests. From late July through early October, we had a near doubling in the number of tests per positive in the U.S. An increase in tests also accompanied the previous surge during the summer, which claimed far fewer lives than the initial wave in the early spring. In the summer, infections were much more prevalent among younger people than in the spring. Vitamin D levels were almost certainly higher during the summer months, our ability to treat the virus had also improved, and immunities imparted by prior infections left fewer susceptible individuals in the population. We have many of those advantages now, but D levels will fade as the fall progresses.

As for the new surge in cases, another qualification is that false positives are still a major testing problem; they inflate both case counts and C19-attributed deaths. In the absence of any improvement in test specificity, of which there is no evidence, the exaggeration caused by false positives grows larger as testing increases and positivity rates fall. So take all the numbers with that as a caveat.

How deadly will the virus be this fall? So far in Europe, the trends look very promising. Kyle Lamb provided the following charts from WHO on Twitter yesterday. (We should all be grateful that Twitter hasn’t censored Kyle yet, because he’s been a force in exposing alarmism in the mainstream media and among the public health establishment.) Take a look at these charts, and note particularly the lag between the first wave of infections and deaths, as well as the low counts of deaths now:

If the lag between diagnosis and death is similar now to the spring, Europe should have seen a strong upward trend in deaths by now, yet it’s hardly discernible in most of those countries. The fatality rates are low as well:

As Lamb notes, the IFRs in the last column look about like the flu, though again, the reporting of deaths and their causes are often subject to lags.

What about the U.S.? Nationwide, C19 cases and attributed death reports declined after July. See the chart below. More recently, reported deaths have stabilized at under 700 per day. Note again the relatively short lags between turns in cases and deaths in both the spring and summer waves.

Clearly, there has been no acceleration in C19 deaths corresponding to the recent trend in new cases. Northeastern states that had elevated death rates in the spring saw no resurgence in the summer; southern states that experienced a surge in the summer have now enjoyed taperings of both cases and deaths. But with each season, the virus seems to roll to regions that have been relatively unscathed to that point. Now, cases are surging in the upper Midwest and upper mountain states, though some of these states are lightly populated and their data are thin.

A few state charts are shown below, but trends in deaths are very difficult to tease out in some cases. First, here are new cases and reported deaths in Michigan, Wisconsin, and Minnesota. There is a clear uptrend in cases in these states along with a very slight rise in deaths, but reported deaths are very low.

Next are Idaho, Montana, North Dakota, and South Dakota. A slight uptrend in cases began as early as August. Idaho and Montana have had few deaths, so they are not plotted in the second chart. The Dakotas have had days with higher reported deaths, and while the data are thin and volatile, the visual impression is definitely of an uptrend in deaths.

The following states are somewhat more central in latitude: Colorado, Illinois, and Ohio. There is a slight upward trend in new cases, but not deaths. Illinois is experiencing its own second wave in cases.

Out of curiosity, I also plotted Massachusetts, Pennsylvania, and New Jersey, all of which suffered in the first wave during the spring. They are now experiencing uptrends in cases, especially Massachusetts, but deaths have been restrained thus far.

The upshot is that states having little previous exposure to the virus are seeing an uptrend in deaths this fall. The same does not seem to be happening in states with significant prior exposure, at least not yet.

There are major questions about the reasons for the lingering death counts in the U.S.. But consider the following: first, the infection fatality rate (IFR) keeps falling, despite the stubborn level of daily reported deaths. Second, deaths reported have increasingly been pulled forward from deaths that actually occurred in the more distant past. This sort of “laundering” lends the appearance of greater persistence in deaths than is real. Third, again, false positives exaggerate not just cases, but also C19 deaths. Hospitals test everyone admitted, and patients who test positive for C19 are reimbursed at higher rates under the CARES Act; Medicare reimburses at a higher rates for C19 patients as well.

We’re definitely seeing a seasonal upswing in C19 infections in the US., now going on five weeks. In Europe, the surge in cases began slightly earlier. However, in both Europe and the U.S., these new cases have not yet been associated with a meaningful surge in deaths. The exceptions in the U.S. are the low-density upper mountain states, which have had little prior exposure to the virus. The lag between cases and deaths in the spring and summer was just two to three weeks, and while it’s too early to draw conclusions, the absence of a surge in deaths thus far bodes well for the IFR going forward. If we’re so fortunate, we can thank a combination of factors: a younger set of infecteds, earlier detection, better treatment and therapeutics, lower viral loads, and a subset of individuals who have already gained immunity.

Cases Climb, Most Patients Faring Better

30 Tuesday Jun 2020

Posted by in Pandemic, Public Health

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There’s been much speculation about whether recent increases in confirmed cases of COVID-19 (first chart above) will lead to a dramatic increase in fatalities (second chart). More generally, there is curiosity or perhaps hope as to whether the virus is not as dangerous to these new patients as it was early in the pandemic. I have discussed this point in several posts, most recently here. Based on the national data (above), we’re at the point at which an upturn in deaths might be expected. Based on the experience of many individual states, however, deaths should have trended upward by now, but they haven’t done so. Cases are generally less severe and are resolving more quickly.

Of course, more testing produces more cases (though there has been a mild uptick in test positivity over the past two weeks), but that doesn’t really explain the entire increase in cases over the past few weeks. In particular, why are so many new cases in the south? After all, there is evidence that the virus doesn’t survive well in warm, humid climates with more direct sunlight.

As I have mentioned several times, heavy use of air-conditioning in the south may have contributed to the increase. Nate Silver speculates that this is the case. The weather warmed up in late May and especially June, and many southerners retreated indoors where the air is cool, dry, and the virus thrives. Managers of public buildings should avoid blasting the AC, and you might do well to heed the same advice if you live with others in a busy household. In fact, nearly all transmission is likely occurring indoors, as has been the case throughout the pandemic. At the same time, however, with the early reopening of many southern states, younger people flocked to gyms, bars and other venues, largely abandoning any pretense of social distancing. So it’s possible that these effects have combined to produce the spike in new cases.

Some contend that the protests following George Floyd’s murder precipitated the jump in confirmed cases. Perhaps they played a role, but I’m somewhat skeptical. Yes, these could have become so-called super-spreader events; there are certain cities in which the jump in cases lagged the protests by a few weeks, such as Austin, Houston, and Miami, and where some cases were confirmed to be among those who protested. But if the protests contributed much to the jump, why hasn’t New York City seen a corresponding increase? Not only that, but the protests were outside, and the protests dissuaded many others from going out at all!

The trend in coronavirus fatalities remains more favorable, despite the increase in daily confirmed cases. One exception is New Jersey, which decided to reclassify 1,800 deaths as “probable” COVID deaths about six days ago. You can see the spike caused by that decision in the second chart above. Reclassifications like that arouse my suspicion, especially when federal hospital reimbursements are tied to COVID cases, and in view of this description from Bloomberg (my emphasis):

“… those whose negative test results were considered unreliable; who were linked to known outbreaks and showed symptoms; or whose death certificates strongly suggested a coronavirus link.”

Deaths necessarily lag new cases by anywhere from a few days to several weeks, depending on the stage at the time of diagnosis and delays in test results. The lag between diagnosis and death seems to center on about 12 – 14 days. Thus far, there doesn’t appear to be an upward shift in the trend of fatal cases, but the big updraft in cases nationally only started about two weeks ago. More on that below.

Importantly, a larger share of new cases is now among a younger age cohort, for whom the virus is much less threatening. The most vulnerable people are probably taking more precautions than early in the pandemic, and shocking as might seem, there is probably some buildup in immunity in the surviving nursing home population at this point. We are also better at treatment, and there is generally plenty of hospital capacity. And to the extent that the surge in new cases is concentrated in the south, fewer patients are likely to have Vitamin D deficiencies, which is increasingly mentioned as a contributor to the severity of coronavirus infections.

I decided to make some casual comparisons of new cases versus COVID deaths on a state-by-state basis, but I got a little carried away. Using the COVID Time Series web site, I started by checking some of the southern states with recent large increases in case counts. I ended up looking at 15 states in the south and west, and I added Missouri and Minnesota as well. I passed over a few others because their trends were basically flat. The 17 states all had upward trends in new cases over the past one to two months, or they had an increase in new cases more recently. However, only four of those states experienced any discernible increase in daily deaths over the corresponding time frames. These are Arizona, Arkansas, Tennessee, and Texas, and their increases are so modest they might be statistical noise.

Again, deaths tend to lag new cases by a couple of weeks, so the timing of the increase in case counts matters. Five of the states were trending upward beginning in May or even earlier, and 13 of the states saw an acceleration or a shift to an upward trend in new cases after Memorial Day, in late May or June. Of those 13, the changes in trend occurred between one and five weeks ago. Six states, including Texas, had a shift within the past two weeks. It’s probably too early to draw conclusions for those six states, but in general there is little to suggest that fatal cases will soar like they did early in the pandemic. Case fatality rates are likely to remain at much lower levels.

We’ll know much more within a week or two. It’s very encouraging that the upward trend in new cases hasn’t resulted in more deaths thus far, especially at the state level, as many states have had case counts drift upward for over a month. If it’s going to occur, it should be well underway within a week or so. Much also depends on whether new cases continue to climb in July, in which case we’ll be waiting in trepidation for whether more deaths transpire.

On the Meaning of Herd Immunity

09 Saturday May 2020

Posted by in Pandemic, Public Health, Risk

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Immunity doesn’t mean you won’t catch the virus. It means you aren’t terribly susceptible to its effects if you do catch it. There is great variation in the population with respect to susceptibility. This simple point may help to sweep away confusion over the meaning of “herd immunity” and what share of the population must be infected to achieve it.

Philippe Lemoine discusses this point in his call for an “honest debate about herd immunity“. He reproduces the following chart, which appeared in this NY Times piece by Carl T. Bergstrom and Natalie Dean:

Herd immunity, as defined by Bergstrom and Dean, occurs when there are sufficiently few susceptible individuals remaining in the population to whom the actively-infected can pass the virus. The number of susceptible individuals shrinks over time as more individuals are infected. The chart indicates that new infections will continue after herd immunity is achieved, but the contagion recedes because fewer additional infections are possible.

We tend to think of the immune population as those having already been exposed to the virus, and who have recovered. Those individuals have antibodies specifically targeted at the antigens produced by the virus. But many others have a natural immunity. That is, their immune systems have a natural ability to adapt to the virus.

Heterogeneity

At any point in a pandemic, the uninfected population covers a spectrum of individuals ranging from the highly susceptible to the hardly and non-susceptible. Immunity, in that sense, is a matter of degree. The point is that the number of susceptible individuals doesn’t start at 100%, as most discussions of herd immunity imply, but something much smaller. If a relatively high share of the population has low susceptibility, the virus won’t have to infect such a large share of the population to achieve effective herd immunity.

The apparent differences in susceptibility across segments of the population may be the key to early herd immunity. We’ve known for a while that the elderly and those with pre-existing conditions are highly vulnerable. Otherwise, youth and good health are associated with low vulnerability.

Lemoine references a paper written by several epidemiologists showing that “variation in susceptibility” to Covid-19 “lowers the herd immunity threshold”:

“Although estimates vary, it is currently believed that herd immunity to SARS-CoV-2 requires 60-70% of the population to be immune. Here we show that variation in susceptibility or exposure to infection can reduce these estimates. Achieving accurate estimates of heterogeneity for SARS-CoV-2 is therefore of paramount importance in controlling the COVID-19 pandemic.”

The chart below is from that paper. It shows a measure of this variation on the horizontal axis. The colored, vertical lines show estimates of historical variation in susceptibility to historical viral episodes. The dashed line shows the required exposure for herd immunity as a function of this measure of heterogeneity.

Their models show that under reasonable assumptions about heterogeneity, the reduction in the herd immunity threshold (in terms of the percent infected) may be dramatic, to perhaps less than 20%.

Then there are these tweets from Marc Lipsitch, who links to this study:

“As an illustration we show that if R0=2.5 in an age-structured community with mixing rates fitted to social activity studies, and also categorizing individuals into three categories: low active, average active and high active, and where preventive measures affect all mixing rates proportionally, then the disease-induced herd immunity level is hD=43% rather than hC=1−1/2.5=60%.”

Even the celebrated Dr. Bergstrom now admits, somewhat grudgingly, that hereogeniety reduces the herd immunity threshold, though he doesn’t think the difference is large enough to change the policy conversation. Lipsitch also is cautious about the implications.

Augmented Heterogeneity

Theoretically, social distancing reduces the herd immunity threshold. That’s because infected but “distanced” people are less likely to come into close contact with the susceptible. However, that holds only so long as distancing lasts. John Cochrane discusses this at length here. Social distancing compounds the mitigating effect of heterogeneity, reducing the infected share of the population required for herd immunity.

Another compounding effect on heterogeneity arises from the variability of initial viral load on infection (IVL), basically the amount of the virus transmitted to a new host. Zvi Mowshowitz discusses its potential importance and what it might imply about distancing, lockdowns, and the course of the pandemic. In any particular case, a weak IVL can turn into a severe infection and vice versa. In large numbers, however, IVL is likely to bear a positive relationship to severity. Mowshowitz explains that a low IVL can give one’s immune system a head start on the virus. Nursing home infections, taking place in enclosed, relatively cold and dry environments, are likely to involve heavy IVLs. In fact, so-called household infections tend to involve heavier IVLs than infections contracted outside of households. And, of course, you are very unlikely to catch Covid outdoors at all.

Further Discussion

How close are we to herd immunity? Perhaps much closer than we thought, but maybe not close enough to let down our guard. Almost 80% of the population is less than 60 years of age. However, according to this analysis, about 45% of the adult population (excluding nursing home residents) have any of six conditions indicating elevated risk of susceptibility to Covid-19 relative to young individuals with no co-morbidities. The absolute level of risk might not be “high” in many of those cases, but it is elevated. Again, children have extremely low susceptibility based on what we’ve seen so far.

This is supported by the transmission dynamics discussed in this Twitter thread by Dr. Muge Cevik. She concludes:

“In summary: While the infectious inoculum required for infection is unknown, these studies indicate that close & prolonged contact is required for #COVID19 transmission. The risk is highest in enclosed environments; household, long-term care facilities and public transport. …

Although limited, these studies so far indicate that susceptibility to infection increases with age (highest >60y) and growing evidence suggests children are less susceptible, are infrequently responsible for household transmission, are not the main drivers of this epidemic.”

Targeted isolation of the highly susceptible in nursing homes, as well as various forms of public “distancing aid” to the independent elderly or those with co-morbidities, is likely to achieve large reductions in the effective herd immunity ratio at low cost relative to general lockdowns.

The existence of so-called super-spreaders is another source of heterogeneity, and one that lends itself to targeting with limitations or cancellations of public events and large gatherings. What’s amazing about this is how the super-spreader phenomenon can lead to the combustion of large “hot spots” in infections even when the average reproduction rate of the virus is low (R0 < 1). This is nicely illustrated by Christopher Moore of the Santa Fe Institute. Super-spreading also implies, however, that while herd immunity signals a reduction in new infections and declines in the actively infected population, “hot spots” may continue to flare up in a seemingly random fashion. The consequences will depend on how susceptible individuals are protected, or on how they choose to mitigate risks themselves.

Conclusion

I’ve heard too many casual references to herd immunity requiring something like 70% of the population to be infected. It’s not that high. Many individuals already have a sort of natural immunity. Recognition of this heterogeneity has driven a shift in the emphasis of policy discussions to the idea of targeted lockdowns, rather than the kind of indiscriminate “dumb” lockdowns we’ve seen. The economic consequences of shifting from broad to targeted lockdowns would be massive. And why not? The health care system has loads of excess capacity, and Covid infection fatality risk (IFR) is turning out to be much lower than the early, naive estimates we were told to expect, which were based on confirmed case fatality rates (CFRs).