Tag Archives: Antigenic Drift

Fall Coronavirus Season

16 Friday Oct 2020

Posted by in Coronavirus, Pandemic, Uncategorized

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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.

COVID Seasonality and Latitudes

23 Sunday Aug 2020

Posted by in Pandemic

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The coronavirus (C19), or SARS-CoV-2, has a strong seasonal component that appears to closely match that of earlier SARS viruses as well as seasonal influenza. This includes the two distinct caseloads we’ve experienced in the U.S. 1) in the late winter/early spring; and 2) the smaller bump we witnessed this summer in some southern states and tropics. 

COVID Seasonal Patterns and Latitude

The Ethical Skeptic on Twitter recently featured the chart below. It shows the new case count of C19 in the U.S. in the upper panel, and the 2003 SARS virus in the lower panel. Both viruses had an initial phase at higher latitudes and a summer rebound at lower latitudes.

 

 

 

 

 

 

 

 

 

 

I particularly like the following visualizations from Justin Hart demonstrating the pandemic’s pattern at different latitudes (shown in the leftmost column). The first table shows total cases by week of 2020. The second shows deaths per 100,000 of population by week. Again, notice that lower latitudes have had a crest in the contagion this summer, while higher latitudes suffered the worst of their contagion in the spring. Based on deaths in the second table, the infections at lower latitudes have been less severe.

Viral Patterns in the South

Many expected the pandemic to abate this summer, including me, as it is well known that viruses don’t thrive in higher temperatures and humidity levels, and in more direct sunlight. So it is a puzzle that southern latitudes experienced a surge in the virus during the warmest months of the year. True, the cases were less severe on average, and sunlight and humidity likely played a role in that, along with the marked reduction in the age distribution of cases. However, the SARS pandemic of 2003 followed the same pattern, and the summer surge of C19 at southern latitudes was quite typical of viruses historically.

A classic study of the seasonality of viruses was published in 1981 by Robert Edgar Hope-Simpson. The next chart summarized his findings on influenza, seasonality, and latitude based on four groups of latitudes. Northern and southern latitudes above 30° are shown in the top and bottom panels, respectively. Both show wintertime contagions with few infections during the summer months. Tropical regions are different, however. The second and third panels of the chart show flu infections at latitudes less than 30°. Influenza seems to lurk at relatively low levels through most of the year in the tropics, but the respective patterns above and below the equator look almost like very muted versions of activity further to the north and south. However, some researchers describe the tropical pattern as bimodal, meaning that there are two peaks over the course of a year.   

So the “puzzle” of the summer surge at low latitudes appears to be more of an empirical regularity. But what gives rise to this pattern in the tropics, given that direct sunlight, temperature, and humidity subdue viral activity?

There are several possible explanations. One is that the summer rainy season in the tropics leads to less sunlight as well as changes in behavior: more time spent indoors and even less exposure to sunlight. In fact, today, in tropical areas where air conditioning is more widespread, it doesn’t have to be rainy to bring people indoors, just hot. Unfortunately, air conditioning dries the air and creates a more hospitable environment for viruses. Moreover, low latitudes are populated by a larger share of dark-skinned peoples, who generally are more deficient in vitamin D. That might magnify the virulence associated with the flight indoors brought on by hot and or rainy weather.   

Mutations and Seasonal Patterns

What makes the seasonal patterns noted above so reliable in the face of successful immune responses by recovered individuals? And shouldn’t herd immunity end these seasonal repetitions? The problem is the flu is highly prone to viral mutation, having segments of genes that are highly interchangeable (prompting so-called “antigenic drift“). That’s why flu vaccines are usually different each year: they are customized to prompt an immune response to the latest strains of the virus. Still, the power of these new viral strains are sufficient to propagate the kinds of annual flu cycles documented by Hope-Simpson.

With C19, we know there have been up to 100 mutations, mostly quite minor. Two major strains have been dominant. The first was more common in Southeast Asia near the beginning of the pandemic. It was less virulent and deadly than the strain that hit much of Europe and the U.S. Of course, in July the media misrepresented this strain as “new”, when in fact it had become the most dominant strain back in March and April.

What Lies Ahead

By now, it’s possible that the herd immunity threshold has been surpassed in many areas, which means that a surge this coming fall or winter would be limited to a smaller subset of still-susceptible individuals. The key question is whether C19 will be prone to mutations that pose new danger. If so, it’s possible that the fall and winter will bring an upsurge in cases in northern latitudes both among those still susceptible to existing strains, and to the larger population without immune defenses against new strains.

Fortunately, less dangerous variants are more more likely to be in the interest of the virus’ survival. And thus far, despite the number of minor mutations, it appears that C19 is relatively stable as viruses go. This article quotes Dr. Heidi J. Zapata, an infectious disease specialist and immunologist at Yale, who says that C19:

“… has shown to be a bit slow when it comes to accumulating mutations … Coronaviruses are interesting in that they carry a protein that ‘proofreads’ [their] genetic code, thus making mutations less likely compared to viruses that do not carry these proofreading proteins.”

The flu, however, does not have such a proofreading enzyme, so there is little to check its prodigious tendency to mutate. Ironically, C19’s greater reliability in producing faithful copies of itself should help ensure more durable immunity among those already having acquired defenses against C19.

This means that C19 might not have a strong seasonal resurgence in the fall and winter. Exceptions could include: 1) the remaining susceptible population, should they be exposed to a sufficient viral load; 2) regions that have not yet reached the herd immunity threshold; and 3) the advent of a dangerous new mutation, though existing T-cell immunity may effectively cross-react to defend against such a mutation in many individuals.