As is often pointed out, the SARS-CoV2 virus is new, and therefore we have limited data on its characteristics, as well as the disease it causes, COVID-19. This complicates our modeling of what is likely to happen, and recommendations about best practices. But scientists around the world are busy studying this pandemic as it is occurring, and therefore our models and recommendations are evolving.

Already we know quite a bit. For example, one review of NYC patients found:

Among the 393 patients, the median age was 62.2 years, 60.6% were male, and 35.8% had obesity. The most common presenting symptoms were cough (79.4%), fever (77.1%), dyspnea (56.5%), myalgias (23.8%), diarrhea (23.7%), and nausea and vomiting (19.1%). Most of the patients (90.0%) had lymphopenia, 27% had thrombocytopenia, and many had elevated liver-function values and inflammatory markers. Between March 3 and April 10, respiratory failure leading to invasive mechanical ventilation developed in 130 patients (33.1%); to date, only 43 of these patients (33.1%) have been extubated. In total, 40 of the patients (10.2%) have died, and 260 (66.2%) have been discharged from the hospital; outcome data are incomplete for the remaining 93 patients (23.7%).

One question, which is especially important as the northern hemisphere approaches summer, is if SARS-CoV2 is less virulent in warmer temperatures. Coronaviruses in general tend to spread less in warmer months, so there is some reason to hope this will be the case. However, a new review of COVID-19 data pokes a hole in this hope. The authors looked at many countries around the world and correlated the number of new cases with various factors, including temperature and humidity.

To estimate epidemic growth, researchers compared the number of cases on March 27 with cases on March 20, 2020, and determined the influence of latitude, temperature, humidity, school closures, restrictions of mass gatherings and social distancing measured during the exposure period of March 7 to 13.

They found no correlation between the number of cases and temperature, and only a weak association of reduced spread with increased humidity. This is, perhaps, the most comprehensive study to date. There have been numerous previous studies, mostly regional, that do show a negative correlation with virus spread and temperature. The authors suggest this is due partly to lack of rigor in those studies. Also, an expert review of this data (prior to the most recent study) urged caution. They note that the studies showed inconsistent results, and it is difficult to generalize the data to what is likely to happen in the world with COVID-19.

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In journalism “burying the lede” means that the truly newsworthy part of a story is not mentioned until deep in the story, rather than up front where it belongs. I tried to find if there is a term that means the opposite – to take something that is not really part of the story and present it as if it the lede.  I could not find it. Perhaps it doesn’t exist (if anyone knows of such a term, let me know). So I made up my own – spoofing the lede.

This is very common is science journalism. It entails taking a study, finding, or discovery and not reporting the actual findings of the study up front, but rather reporting one possible implication of the study. This might be purely speculative, even fanciful. For example, take any study that discovers anything about viruses, and the headline might read, “Scientists find possible cure for the common cold.” The study may have nothing at all to do with the common cold.

This comes from journalists (and often those in the press office whose job it is to “sell” the research of their institution) asking the question – what does this mean? What are the implications of this finding that average people can relate to? That is fine, as far as it goes, but there are often two main problems with implementation. The first is when the possible implication is a real stretch. The connection is super thin, even strained. No, that metamaterial will not lead to a “Harry Potter-like invisibility cloak.”

The second is when that thin possible implication of the research is presented as if it is the actual results of the study. That is the false lede that should be buried – put that toward the end of the article, and put it into proper perspective. This kind of research (for example) helps us understand viral replication, and any such knowledge might lead to potential treatments for viral illness, like the common cold. However, it takes decades for such basic research to lead to direct applications, which cannot be predicted.

I do think this is nothing less than a massive systematic failure of popular science communications – focusing on the sexy speculative implication of research, and burying the actual research.

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A promotional video on YouTube for a new documentary, Plandemic, is making the rounds and promoting quite a response. The video features Dr. Judy Mikovits, and is basically an interview with her. Unfortunately this is a slick piece of utter nonsense and conspiracy mongering. Mikovits has zero credibility in any of her claims, but they are combined with music and clips of videos to create the impression that there is some reality behind her outrageous claims. Let me focus on a few claims to show how low her and the filmmaker’s credibility are.

In her introduction the narrator states that she authors a study in Science that “sent shockwaves through the scientific community” because it showed that fetal and animal tissue in vaccines was causing an epidemic of chronic illness. This is straight up lie, but that is the narrative of this video – that she is a courageous fighter going against the establishment, which is killing people for profit and trying to destroy her for calling them out.

Here is the original Science paper. It alleges to have found the XMRV virus in patients with chronic fatigue syndrome. This did make a splash when it was published because it purported to find a possible cause of an otherwise mysterious illness. It has nothing to do with vaccines at all (although you could argue, falsely that the virus came from vaccines, but that is not what the research was on). But then, here is a retraction of the paper by Science. Was it retracted as part of some global conspiracy against Mikovits? No – it was retracted because:

“Multiple laboratories, including those of the original authors, have failed to reliably detect xenotropic murine leukemia virus-related virus (XMRV) or other murine leukemia virus (MLV)-related viruses in chronic fatigue syndrome (CFS) patients,” says the retraction notice. “In addition, there is evidence of poor quality control in a number of specific experiments in the Report.”

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When I was in college I had just finished a course on social psychology (certainly one of the most memorable courses I took in college), and while back home I was visiting with my then girlfriend. When I arrived they were in the middle of dealing with a door-to-door textbook salesperson. That’s right – the product was a mathematics textbook that combined the K-12 curriculum into one giant tome. My girlfriend’s parents asked my advice, so I sat down to listen to the spiel.

The salesman was sitting in their living room, sitting on one side while the family members were all opposite. He had a velcro cast on one of his legs (the kind that can be removed and put back on) and was sporting crutches. His tactic was largely highlighting some feature of the book, then asking someone specifically if they thought that feature would be helpful. “Do you think it would be helpful to all this information in one location?” The answer, of course, was always yes. He mentioned that a neighbor down the street had just purchased the book for their high school student.

It was a fascinating experience for me, because I had just learned about all of the techniques the salesman was using. He was garnering sympathy with the cast. Using peer pressure by mentioning their neighbors. Getting them to agree that the product was useful, so they would feel inconsistent if they then decided not to buy. He positioned the family all on one side so they could not make eye contact with each other during his presentation.

After the pitch, while the book salesman was still waiting in the living room, I told the parents not to buy the book. I explained all the manipulative techniques he was using. Further, they simply did not need the book, and it was expensive. They understood, but bought the book anyway. They felt he had invested so much time in the sales visit they could not say no. His emotional manipulations worked – even when they knew they were being manipulated. It would have been simply too socially awkward to send him away with no sale.

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We appear to be at the beginning of the end of the first wave of COVID-19 (at least in the US – other countries are at different places). We are at the point where states are starting to relax the physical distancing requirements, and there is discussion about how to transition to the next phase. That next phase might include disease tracking, targeted isolation, and “immunity passports.” But planning this next phase is complicated by the fact that we still do not fully understand this virus. We don’t know if there will be a second wave (or more), if it is seasonal, and if you can catch it twice. How we handle this next phase will likely determine if there is a second wave.

But what comes after that? When can we transition to the final phase – return to normal, even if it is a new normal? These next transitions will depend largely on the natural immunity that results from infection, and how long it will take to create a vaccine and how effective that vaccine is. Here is what we know and don’t know so far.

The big question for the next phase is – how much immunity results from natural infection? This is a more complicated question than it may first seem. But the short answer is, we don’t know.

The adaptive part of the immune system will remember infections, B-cells that create specific antibodies targeting the infecting organism will develop throughout an infection, and some of those B-cells are memory B-cells – they will hang around for a long time, ready to produce specific antibodies the next time the same organism is encountered. But there are important variables to how effective this adaptive immune strategy is. the virus or infecting organism itself is the main variable. What parts of itself does it expose to the immune system? Perhaps the critical functional proteins are hidden deep within folds that antibodies cannot get to. Another variable is how quickly does it mutate? If the parts that antibodies can target change quickly, then immunity does not last. Some organisms also evolve specific strategies to evade or compromise the immune system.

Another variable is the severity of the infection itself. The more severe and long lasting the infection, the greater the stimulation to the immune system and the greater the adaptive response.

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This is a very cool study, with the massive caveat that it is extremely preliminary – but scientists have concluded an in vitro study of nanodevices that can reduce one of the pathological changes thought to be a significant cause of Alzheimer’s disease. This has to be put into context, but let me first describe what they did.

Alzheimer’s disease (AD) is a neurodegenerative disorder that affects the brain diffusely. Little by little brain cells die, the brain atrophies, and cognitive ability slowly declines causing dementia. The disease affects about 10% of people over 65, producing a huge burden on individuals, families, and society. As our population ages, it is becoming even more prevalent. There is extensive research on how Alzheimer’s disease progresses, looking for clues that might lead to an effective treatment. However, it has proven a tough nut to crack. We have many clues, but nothing that has lead to a treatment that can prevent, stall, or reverse the neurodegeneration. It is, in short, a complex disease.

One piece of this complex puzzle is the β-amyloid peptide (Aβ), which is a breakdown product of an amyloid protein precursor. The simple version is that this peptide is normally cleared from brain cells as a waste product, but in some individuals it is not sufficiently cleared and there is enough hanging around to form conglomerations or clumps of the protein. These clumps form plaques, which are a major pathological sign of AD. However, the picture is more complex than that. The amount of plaques in the brain don’t necessarily correlate with the severity of the dementia in AD, so it is clearly not the whole picture. More recent studies have found:

Substantial evidence now indicates that the solubility of Aβ, and the quantity of Aβ in different pools, may be more closely related to disease state. The composition of these pools of Aβ reflects different populations of amyloid deposits, and has definite correlates with the clinical status of the patient.

There are also pathological processes in AD that are not related to amyloid plaques, so again we are only dealing with part of the picture here. Still, researchers have been looking for ways to prevent plaque formation as a possible way to slow, stop, or even reverse AD. So far nothing has led to an approved treatment. (Current treatments for AD are only symptomatic.)

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