Tag Archives: Transmissability

COVID Cases Decline Despite New Variants

19 Friday Feb 2021

Posted by in Coronavirus, Pandemic

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For weeks, even months, we’ve been hearing about dangerous new mutations of the coronavirus, and they’ve been identified in cases in the U.S. There’s a UK strain, a South African strain, a Brazilian strain, and still others, which differ in seemingly minor ways. Nevertheless, these variants are said to be more infectious. It’s also been reported that the South African and Brazilian strains might resist antibodies from prior infections from earlier strains.

Kyle Lamb has provided the following charts to put things in perspective:

Just to round things out, here is the trend in cases worldwide:

There is a great deal of concern about the new variants. A search for “COVID-19 variants” turns up plenty of scary articles. However, there is some evidence that the new variants are not as dangerous as alarmists contend. The resistance to specific antibodies does not necessarily imply resistance to protection by T-cells. As Youyang Gu points out, even if a new strain becomes “dominant”, that does not imply that cases will reverse their decline. This study indicates that the Pfizer vaccine is protective against both the UK and South African strains, and there is evidence that other vaccines offer adequate protection as well (and see here).

The charts demonstrate that the new strains haven’t arrested or reversed the declines in infections witnessed worldwide since early January. That doesn’t mean the mutations haven’t made a difference: perhaps the declines would have been faster in their absence. And we don’t know what the future will hold as the virus in various forms becomes endemic. Still, it’s reassuring to see that the increased transmissibility of the new strains hasn’t overcome factors that have contributed to the recent declines, which in all likelihood are related to increasing immunity in the population with a minor assist from vaccinations (thus far). As Lamb wryly notes about the recent declines in transmission: “Just saying”.

Spate of Research Shows COVID Lockdowns Fail

27 Sunday Dec 2020

Posted by in Lockdowns, Public Health

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For clarity, start with this charming interpretive one-act on public health policy in 2020. You might find it a little sardonic, but that’s the point. It was one of the more entertaining tweets of the day, from @boriquagato.

A growing body of research shows that stringent non-pharmaceutical interventions (NPIs) — “lockdowns” is an often-used shorthand — are not effective in stemming the transmission and spread of COVID-19. A compendium of articles and preprints on the topic was just published by the American Institute for Economic Research (AEIR): “Lockdowns Do Not Control the Coronavirus: The Evidence”. The list was compiled originally by Ivor Cummins, and he has added a few more articles and other relevant materials to the list. The links span research on lockdowns across the globe. It covers transmission, mortality, and other health outcomes, as well as the economic effects of lockdowns. AIER states the following:

“Perhaps this is a shocking revelation, given that universal social and economic controls are becoming the new orthodoxy. In a saner world, the burden of proof really should belong to the lockdowners, since it is they who overthrew 100 years of public-health wisdom and replaced it with an untested, top-down imposition on freedom and human rights. They never accepted that burden. They took it as axiomatic that a virus could be intimidated and frightened by credentials, edicts, speeches, and masked gendarmes.

The pro-lockdown evidence is shockingly thin, and based largely on comparing real-world outcomes against dire computer-generated forecasts derived from empirically untested models, and then merely positing that stringencies and “nonpharmaceutical interventions” account for the difference between the fictionalized vs. the real outcome. The anti-lockdown studies, on the other hand, are evidence-based, robust, and thorough, grappling with the data we have (with all its flaws) and looking at the results in light of controls on the population.”

We are constantly told that public intervention constitutes “leadership”, as if our well being depends upon behavioral control by the state. Unfortunately, it’s all too typical of research on phenomena deemed ripe for intervention that computer models are employed to “prove” the case. A common practice is to calibrate such models so that the outputs mimic certain historical outcomes. Unfortunately, a wide range of model specifications can be compatible with an historical record. This practice is also a far cry from empirically testing well-defined hypotheses against alternatives. And it is a practice that usually does poorly when the model is tested outside the period to which it is calibrated. Yet that is the kind of evidence that proponents of intervention are fond of using to support their policy prescriptions.

In this case, it’s even worse, with some of the alleged positive effects of NPI’s wholly made-up, with no empirical support whatsoever! So-called public health experts have misled themselves, and the public, with this kind of fake evidence, when they aren’t too busy talking out of both sides of their mouths.

COVID Immunity, Herd By Herd

01 Tuesday Sep 2020

Posted by in Coronavirus, Herd Immunity

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Too many public health authorities remain in denial, but epidemiologists are increasingly convinced that heterogeneity implies a coronavirus herd immunity threshold (HIT) that is greatly reduced from traditional models and estimates. HIT is the share of the population that must be infected before the contagion begins to recede (and the transmission ratio R falls below one). Traditional models, based on three classes of individuals (Susceptibles, Infectives, and Recovered – SIR), predict a HIT of 60% or more. However, models that incorporate variation in susceptibility, transmissibility, and occupational or social behavior reduce the HIT substantially. Many of these more nuanced models show that the HIT could be in a range of just 15% to 25%. If that is the case, many regions are already there!

For background, I refer you to the first post I wrote about heterogeneity in late March, more detailed thoughts from early May, examples and more information on the literature later in May. I’ve referenced it repeatedly in other posts since then. And now, more than five months later, even the slow kids at the New York Times have noticed. The gist of it: if not everyone is equally susceptible, for example, a smaller share of the population needs to be “immunized via infection” to taper the spread of the virus.

Some supporting evidence appears in the charts below, courtesy of Kyle Lamb on Twitter. The first chart shows a seven-day average of C19 cases per million of population for ten states that reached an estimated 10% antibodies. These antibodies confer at least short-term immunity against C19. Most of these states saw cases/m climb at least through the day when the 10% level was reached, though Rhode Island appears to have been an exception.

The second chart shows the seven-day average of cases/m in the same states starting seven days after the 10% immunity level was reached. I’d prefer to see the days in the interim as well, but the changes in trend are still noteworthy. All of these states except Louisiana had a downturn in the seven-day average of new cases within a few weeks of breaching the 10% infection level (Louisiana had distinct and non-coincident outbreaks in different parts of the state). These striking similarities suggest that things turned as the infection level reached 15% or more, consistent with many of the epidemiological models incorporating heterogeneity.

Next, take a look at the states in which C19 surged most severely this summer. The new cases are not moving averages, so the charts are not quite comparable to those above. However, the peaks seem to occur prior to the breach of the 15% infection level.

Speculation about early herd immunity has been going on for several months with respect to various countries and even more “micro” settings such as cruise ships and military vessels, where populations are completely isolated. Early on, this “early” herd immunity was discussed under the aegis of “immunological dark matter”, but we know now that T-cell immunity has played an important role. In any case, anti-body expression (or seroprevalence) at around 20% has been linked to reversals in C19 cases and deaths in several countries. As Yinon Weiss notes, New York City and Stockholm were both C19 hotspots in the spring, both have seen deaths decline to low levels, and they have little in common in terms of public health policy. London as well. The one thing they share are similar levels of seroprevalence.

An important qualification is that herd immunity is not relevant at high levels of aggregation. That is, herd immunity won’t be achieved simultaneously in all regions. The New York City metro area might have reached its HIT in April, but Florida (or perhaps only Miami) might have reached a HIT in July. Many areas of the Midwest probably still aren’t there.

In the absence of a new mutation of C19, the final proof of herd immunity in many of the former hotspots will be in the fall and winter. We should expect at least a few cases in those areas, but if there are more intense contagions, they should be confined to areas that have not yet seen a level of seroprevalence near 15%.

Some Cheery COVID Research Tidbits

16 Thursday Jul 2020

Posted by in Pandemic, Public Health, Uncategorized

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Here’s a short list of new or newish research developments, some related to the quest to find COVID treatments. Most of it is good news; some of it is very exciting!

Long-lasting T-cell immunity: this paper in Nature shows that prior exposure to coronaviruses like severe acute respiratory syndrome (SARS) and even the common cold prompt an immune reaction via so-called T-cells that have long memories and are reactive to certain proteins in COVID-19 (SARS-CoV-2). The T-cells were detected in both C19-infected and uninfected patients. This comes after discouraging reports that anti-body responses to C19 are short-lived, but T-cells are a different form of acquired immunity. Derek Lowe says the following:

“This makes one think, as many have been wondering, that T-cell driven immunity is perhaps the way to reconcile the apparent paradox between (1) antibody responses that seem to be dropping week by week in convalescent patients but (2) few (if any) reliable reports of actual re-infection. That would be good news indeed.”

The herd immunity threshold (HIT) is much lower than you think: I’ve written about the effect of heterogeneity on the HIT before, here and here. This new paper, by three Oxford zoologists, shows that the existence of a cohort having some form of prior immunity, innate or acquired, reduces the number of infections required to achieve the HIT. For example, if initial transmissibility (R0) is 2.5 and 40% of the population has prior immunity (both reasonable assumptions for many areas), the HIT is as low as 20%, according to the authors’ calculations. That’s when the contagion begins to recede, though the final infected share of the population would be higher. This might explain why new cases and deaths have already plunged in places like Italy, Sweden, and New York, and why protests in NYC did not lead to a new wave of infections, while those in the south appear to have done so.

Seasonal effects: viral loads might be decreasing. From the abstract:

“Severity of COVID-19 in Europe decreased significantly between March and May and the seasonality of COVID-19 is the most likely explanation. Mucosal barrier and mucociliary clearance can significantly decrease viral load and disease progression, and their inactivation by low relative humidity of indoor air might significantly contribute to severity of the disease.”

The BCG vaccine appears to be protective: this is the bacillus Calmette-Guérin tuberculosis vaccine administered in some countries, This finding is not based on clinical trials, so more work is needed.

Is there no margin in plasma? No subsidy? This is the only “bad news” item on my list. It’s widely agreed that blood plasma from recovered C19 patients can be incorporated into an immune globulin drug to inoculate people against the virus. It’s proven safe, but for various reasons no one seems interested. Not the government. Not private companies. Did Trump happen to mention it or something?

C19 doesn’t spread in schools: this German study demonstrates that there is little risk in reopening schools. One of the researchers says:

“Children act more as a brake on infection. Not every infection that reaches them is passed on…. This means that the degree of immunization in the group of study participants is well below 1 per cent and much lower then we expected. This suggests schools have not developed into hotspots.”

Also worth emphasis is that remote learning leaves much to be desired, as acknowledged by the National Academies of Science, Engineering and Medicine, which has recommended that schools reopen for younger children and those with special needs.

Can angiotensin drugs (ACE Inhibitors/ARBs) reduce mortality? This meta-analysis of nine studies finds that these drugs reduce C19 mortality among patients with hypertension. The drugs were also associated with a reduction in severity but not with statistical significance. These results run contrary to initial suspicions, because ACEI/ARB drugs actually “up-regulate” ACE-2 receptors, to which C19 binds. Researchers say the drugs might be working through some other protective channel. This is not a treatment per se, but this should be reassuring if you already take one of these medications.

Tricor appears to clear lung tissue of C19: this research focused on C19’s preference for an environment rich in cholesterol and other fatty acids:

“What they found is that the novel coronavirus prevents the routine burning of carbohydrates, which results in large amounts of fat accumulating inside lung cells – a condition the virus needs to reproduce.”

Tricor reduces those fats, and the researchers claim it is capable of clearing lung tissue of C19 in a matter of days. This was not a clinical trial, however, so more work is needed. Tricor is an FDA approved drug, so it is safe and could be administered “off label” immediately. Tricor is a fibrate; the news with respect to statins and C19 severity is pretty good too! These are not treatments per se, but this should be reassuring if you already take one of these medications.

Hydroxychloroquine works: despite months of carping from media and leftist know-it-all’s dismissing the mere possibility of HCQ as a potential C19 treatment, evidence is accumulating that it is effective in treating early-stage infections after all. The large study conducted by the Henry Ford Health System found that treatment with HCQ early after hospitalization, and with careful monitoring of heart function, cut the death rate in half relative to a control group. Here’s another: an Indian study found that four-plus maintenance doses of HCQ acted as a prophylactic against C19 infection among health care workers, reducing the odds of infection by more than half. An additional piece of evidence is provided by this analysis of a 14-day Swiss ban on the use of HCQ in late May and early June. The ban was associated with a huge leap in the C19 deaths after a lag of less than two weeks. Resumption of HCQ treatment brought C19 deaths down sharply after a similar lag.

Meanwhile, a study in Lancet purporting to show that HCQ was ineffective and posed significant risks to heart health was retracted based on the poor quality of the data.

Remdesivir also cuts death rate: by 62% in a smaller controlled study by the drug maker Gilead Sciences.

Pet ownership might confer some immunity: this one is a little off-beat, and perhaps the research is under-developed, but it is interesting nonetheless!

I owe Instapundit and Marginal Revolution hat tips for several of these items.