Coronavirus news & views

NIH Launches First Trial Of Nasal COVID Vaccine

"Taking a new step, uttering a new word, is what people fear most.”
― Fyodor Dostoevsky, Crime and Punishment

Earlier in these pages I described how the mucosal immune system is different from the general immune system of the body. Your mucosa (i.e., the lining of your nose, mouth, throat, sinuses, lungs, etc.) has its own robust immune defense and produces different types of antibodies in response to invaders. The nose, mouth and throat are often the first line of defense to airborne pathogens, such as the flu and SARS-CoV-2 viruses. So, when you are infected via the mucosa by an airborne pathogen, it activates a local immune response while eventually sounding an immune alarm for the body-whole. But by the time the infection settles in and the rest of your body responds, it is all-out immunological warfare and you feel crappy (hope I am not being to technical). Sometimes the bug wins too. Too often, especially before we had the vaccines, COVID won, and folks were hospitalized in dire straits with tubes attached to machines keeping them alive, too often failing.

The amazing vaccines we developed in record time were delivered into an arm muscle to stimulate our general body immune response, not our mucosal immunity. This meant that even though we had immunity, the virus could still enter us, set up shop and wait until the general body immune reinforcements arrived. Those reinforcements were quite effective at preventing serious disease, but you still would get ill.

Wouldn’t it be nice if a vaccine could be developed to nip the infection in the bud at the site of entry--in the mucosa--so it could not set up shop at all? That is an idea that has been percolating in the minds of immunologists for a while. It is the idea behind a mucosal vaccine that I described earlier.

But, if it is such a good idea for the CoV-2 coronavirus, why not for flu or other airborne pathogens that have been around much longer? Indeed efforts to develop nasal vaccines for influenza have been ongoing for a couple of decades. But, when is the last time you got a nasal spray vaccine for the flu? The track record has been mixed. The FluMist nasal flu vaccine was approved for kids in 2003. Initially it was a convenient alternative to the injected vaccine. But, it showed limited efficacy in adults. Early on it was deemed just as effective as the standard vaccine in kids, not better as hoped. More recently it was reported to not be so effective. As a result it is no longer recommended by the American Academy of Pediatrics. It clearly did not rise to the hope we had for a nasal flu vaccine.

All the above negativity for the early nasal flu vax doesn’t mean that the idea of a nasal flu vaccine is invalid. Researchers will test different sorts of flu antigens for the nasal approach. FluMist used a live, but attenuated virus in its nasal vaccine. That means kids snorted a live virus that could infect cells but not cause disease. Perhaps a different flu antigen would be more effective? But, frankly, it is hard to get more realistic than a live-attenuated virus.

Nevertheless, another promising new flu nasal vaccine candidate is FluGen’s, M2SR, developed by researchers at the University of Wisconsin-Madison. This vaccine is a bit different because it uses a wholly live virus with an essential replication gene deleted from its DNA. This means the virus is fully functional except it can’t replicate and cause illness. That makes it a little different from the live-attenuated virus. It should stimulate the immune system like a natural infection, but begs the question: how will that be different from the immune response generated from a live attenuated virus? How will that crippled snuffed virus stimulate a different immune protection from the sniffled FluMist attenuated virus? We will see, won’t we? That is why we do such experiments.

Back to COVID. This summer, NIH launched the initial Phase 1 trial to begin testing such a nasal COVID vaccine.

The vaccine. The vaccine is a mouse virus (MPV) in which a piece of the CoV-2 spike protein is expressed. MPV does not cause human disease but does like to stick to human and primate mucosal epithelial cells and should be an effective vector for delivering the spike protein sequence where it can tickle an appropriate immune irritation. In animal studies, the experimental virus was safe and produced a robust immune response in the mucosa lining the nose and respiratory tract of experimental animals. All very encouraging, hence the move to human trials.

The human trial. This is a Phase 1 trial, the first step of any experimentation in humans. Phase 1 trials do not look for efficacy and are done on quite a small number of patients, anywhere from 20-100 subjects who are not tested at all for resistance to the disease. The purpose simply is to look for common safety issues like whether the vaccine causes a general adverse reaction with increasing doses and how well it induces an immune response (i.e., anti-spike protein antibodies) at different doses. Using this information, a Phase 2 study can be designed including more subjects, usually hundreds. This begins to look for more subtle side effects and is the first test of the ability of the vaccine to protect against COVID disease. This would be a controlled trial where experimental vaccine recipients are compared to a control cohort who do not get the nasal vaccine, but probably a placebo. If data collected from this study warrant, then a Phase 3 study is done on thousands of patients to further refine the safety and efficacy profile of the vaccine.

The Phase 1 study that is underway is being led by the National Institute of Allergy and Infectious Diseases and is enrolling 60 subjects at trial sites, which include the Baylor College of Medicine, Houston; The Hope Clinic at Emory University in Atlanta; and New York University on Long Island. The immune responses of volunteers will be followed for one year. So, it will be a while before investigators have the data to begin Phase 2 trials.

Bottom line. This is just the beginning and it will take several years to finish. If successful, this would represent the next generation of COVID vaccine. Finally, as I have often ended my blog posts…

…we will see.

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Coronaviruses, Colds And COVID: And Cool Immunology

“The most exciting phrase to hear in science…is not ‘Eureka!’ but ‘That’s funny…’”

–Issac Asimov

 

Background. Your run-of-the-mill common cold virus is sometimes related to its more infamous relative that caused the world all sorts of consternation between 2020-2023, and still demands respect like an aging rock star who might still have some chops left. I, of course, allude to SARS-CoV-2.

Yup, the now infamous family of deadly human coronaviruses, which includes the original bat-borne SARS-CoV-1 (which caused the first SARS pandemic in late 2002), its Middle-Eastern camel-riding cousin (that caused MERS in June 2012), and the recent, much more traveled, durable, and concerning SARS-CoV-2 (origins so far unknown and the cause of COVID-19), have some lesser known, ne’er-do-well cousins that have long traveled among us. I refer to certain viruses that visit us often and are as unwelcome as a distant cousin who arrives unannounced needing a place to crash for a few days. This is the “common cold virus” which actually is several different kinds of viruses. Cold viruses are all as irritating and inconvenient as said uninvited distant cousin, and about as enjoyable as a hangover; but seriously debilitating or life threatening? They are not.

The common cold is mostly caused by one of three families of viruses; rhinovirus (not related to any large mammal), adenovirus, or a coronavirus. Yup, a distant cousin to that bug that caused so much serious illness and death across this blue orb during the COVID pandemic also is one of the causes of the mostly benign, but very annoying common cold. In fact, there are four different types of coronavirus cousins that cause 15-30% of the “common colds” in adults. Isn’t it interesting that one coronavirus, like SARS-CoV-2, can kill you, but its cousins just make you sneeze and your nose run like a leaky faucet, but that is all. Aren’t viruses fascinating?

Facts. Just as between unwelcome distant cousins, there are genetic similarities between the dangerous CoV-2 and its nettlesome coronavirus kin that just cause colds. And recent studies found that infection with one of these coronavirus cousins can indeed confer some immune protection to the other distant cousins. In other words, if you were infected with CoV-2, you likely had a much milder cold, if you caught one at all. And vice versa! But the funny thing is that vaccination against COVID did not also protect you against a cold like an infection would. What??

This stuff makes viral immunology so much fun.

To confirm all this, one study showed that this cross protection only occurred in people who had a definite bout of COVID caused by the coronavirus, and the reduced incidence of colds only occurred for colds also caused by a coronavirus, and not for a cold caused by unrelated rhino or adenoviruses. Clearly prior exposure to a different member of the coronavirus family conferred some immunity to other members of that family, even to distant cousins. Also, just being vaccinated to the CoV-2 spike protein did not confer this sort of protection to future coronavirus-caused colds. Wow! This kind of discrimination and specificity gets immunologists salivating like a Pavlovian dog to a ringing bell. I know—I am wiping secretions off my keyboard as I type.

Vaccines to just the spike protein quickly generates antibodies that neutralize the virus and thus prevent serious disease. But, that only offers short term protection to just that coronavirus from whence the spike protein sequence came. The viruses quickly mutate their spike surface proteins so the viral cousins cannot be recognized by the spike protein alone. That is why anti-spike immunity and the vaccines are not very good at protecting against re-infection for very long and why the vaccines don’t confer immunity to distant coronavirus cousins.

However, the immune system is a multi-layered security system. Besides these short-lived neutralizing antibodies that target the coronavirus spike protein (or similar surface proteins in other viruses), other layers of the immune security system can also be generated to other molecules across the SARS-CoV-2 genome following infection with the whole virus (see here and here). These other genome sequences are often more conserved and less likely to change between distant coronavirus cousins, than the highly variable spike protein sequence. This means that any immune response generated to one of these more boring, unchangable sites on a given coronavirus, can also recognize similar sequences on distant cousin coronaviruses.

But who, other than an immunology nerd really cares if having COVID protects you against a future cold? What about the reverse? Can having a cold caused by a coronavirus cousin generate some protective immunity to the nastier SARS-CoV-2 and protection from COVID and future coronaviruses that will emerge? Some, but not all research has indeed shown that people without prior exposure to CoV-2 do indeed show immune reactivity to the virus (see here and here). This means that folks who haven’t been infected with SARS-CoV-2 must have been exposed to another coronavirus that gave them a bit of cross protective immunity to the COVID virus. Other studies confirmed that prior infection with cold-causing coronaviruses can reduce COVID severity following infection with CoV-2 (here and here).

Bottom line.  What this means is that if you have been infected with some sort of mild coronavirus in the past, you just might be able to show some immunity to future infections with distant coronavirus cousins. Vaccination with the spike protein mRNA just doesn’t do the same. You need to be exposed to the whole kit and caboodle to enjoy all this immune goodness.

The responsible part of the immune system for this cross-over immune response is CD8⁺ T cells, also known as cytotoxic T lymphocytes, or CTLs. These immune cells are assassins that seek out other cells infected with a virus and they kill those cells. So, immunologists get all atwitter and think, “Hellz bellz, why don’t we make vaccines using parts of these boring, but conserved virus pieces that generate CTLs to different viral cousins, instead of the ever changing spike proteins to make vaccines? We could make one vaccine for all coronaviruses! Or flu, or whatever virus….”

It is a great idea and that research is well underway. The goal is to make a single coronavirus vaccine that would be long lasting and target many coronavirus cousins to prevent any future pandemic (believe me, another one is sure to come).

Back to earth. As interesting and hopeful as this sounds for making a single vaccine against multiple coronaviruses so we don’t have to continually try different boosters each year, don’t get your hopes up just yet. Similar immuno-optimism has been going on with influenza for decades and what do we have to show for that? We still have the annual guessing game of which flu strain will pester us each winter and then feverishly roll out millions of vaccines to try to nip that particular one in the bud. Meanwhile its flu cousins chortle and conspire in the Southern Hemisphere on how to mix and mutate their genes so they can surprise us again in the Northern Hemisphere the following year with a sufficiently new variation to vex us again.

But, flu, like coronaviruses also has important proteins that are not changeable, and very constant between distant flu cousins. These too can be seen by the immune system’s T cells. Flu immunology’s Holy Grail has long been to make a vaccine to a conserved flu virus genomic sequence so we can use just one vaccine to immunize against all flu strains once and for all for all time. A pan-flu vaccine.

Well, we are still trying to do that. This makes the idea of finding a pan-coronavirus vaccine using similar immunology daunting. Still, these recent studies showing that cross-reactive immunity between distant cousin coronaviruses does exist, just stokes an Immunologist’s stubborn resolve to solve the problem. As I have written before in these pages, amazing science advances have often come from the long, dogged pursuit of goals that very stubborn scientists believe they can see right in front of them, even when others cannot. It often takes a long time to prove what is so clearly obvious to one or two science visionaries yet so oblivious to the rest of us. That often is how science progresses. Thank goodness for these obstinate scientists who see things the rest of us cannot.

Once again, We will see.

Personal note. These anti-viral CD8⁺ or cytotoxic T lymphocytes are near and dear to this correspondent’s heart since I got my PhD in Immunology studying how these immune cells in mice recognize cells infected with viruses. It is a lot more complicated than you would think. In fact, in 1996 two immunologists, Peter Doherty and Rolf Zinkernagel were awarded the Nobel Prize for work they did on this problem in the early 70s, and that work drove my PhD research (and a lot more!).

Doherty and Zinkernagel discovered that T cells have to simultaneously identify two different molecules on an infected cell surface before they actually know a cell is infected with a virus. They made a head-scratching observation that turned viral immunology upside down. It was one of those observations that I bet made them say, “That is funny.” Basically, they found that your T cells that can recognize flu infecting your cells would not recognize flu infecting my cells or anyone else’s cells. And vice versa. You would think flu is flu and that a T cell that can see flu in an infected cell would not care whose cell it came from. But it does care. It turns out that T cells can only see virus within the genetic background from whence they came. They cannot see the same virus on a cell from a different genetic background! How strange is that? An antibody does not care where it sees a virus. T cells do. Picky little suckers.

It gets even crazier. Doherty and Zinkernagel, mapped this genetic restriction in virus recognition to the same genes that the immune system also use to determine whether a tissue or organ is its own or is foreign! For example, the genes your immune cells recognize as a password to determine friend vs foe in a skin graft (do we accept it or reject it?) are the same genes the immune cells use to help them know if your cells are infected with a virus! Tell me that doesn’t make you scratch your head and mutter, “That’s funny?” That is exactly how the world of immunology reacted to Doherty and Zinkernagel’s findings. It was a beautiful time for immunology science. That launched a tsunami of research, my PhD effort included.

This is personal note because I earned my PhD further probing the mechanism of what Doherty and Zinkernagel stumbled on. I used a large panel of mice that had been engineered to carry single point mutations in different parts of these genes that immune system used to ascertain tissue compatibility, and detect viral invasion. This helped us learn what part of these molecules the T cells recognized and how their folding was important for this recognition. It was a grand time!

Immunology is so doggone interesting!

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Another Jab’ll Do Ya…

“A virus is a piece of bad news wrapped in a protein coat.”

–Sir Peter Medawar (British Immunologist and Nobel Prize Winner)

Yup, looks like we should roll up our sleeves again this Fall for another COVID booster. The CDC recommends that everyone, 6 months and older receive the updated vaccine that is under development as just reported in the New York Times.

Infections are now rising across the country and this is due to a new, quite different combination of three related CoV-2 variants competing for your attention. They are collectively referred to as FLiRT. The variants are pretty effective at evading prior immune defenses and can spread faster, as we are beginning to see. Across the US COVID-related ER visits increased 15% the week ending June 15, and deaths increased 17% compared to just the previous week. Hospital COVID data are harder to come by since a CDC reporting requirement ended in May.

People “…in general do not understand how much this current virus has mutated,” said Carol Hayes, American College of Nurse-Midwives liaison to the CDC’s Advisory Committee on Immunization Practices. The Advisory Committee unanimously recommended this new round of shots.

But, again? Really?? Booster fatigue and COVID complacency seems to be a growing thing as the deep stress of the 2020-2023 pandemic fades in the review mirror. If we have been boosted a few times, and even had one or two mild COVID infections, is it really necessary to go through all this again?

Yes it is if you want to avoid serious illness. Please read on. True, at this point we all pretty much have some immunity to CoV-2 viruses, but the new boosters that keep rolling out give us important added protection to the novel virus variants that are regularly popping up like in a Whack-a-Mole game. What the boosters do is prevent you from getting serious disease that these new variants can visit on you! Realize that the vast majority of people across all age groups who were hospitalized with serious disease last fall did not get the updated booster for the current virus that was circulating.

In other words, the boosters greatly increase your chance to avoid serious illness and death that are still part of this continuing COVID tableau. Getting a shot is a heck of lot less nettlesome than being hospitalized with a serious respiratory illness. Let’s see….a prick or a ventilator???? It should be a pretty easy choice to make.

What about young people? Why vaccinate them if they don’t get very ill? Even though young adults and children do not get seriously ill as often as older people, don’t be distracted by the difference between relative risk and absolute risk (see a previous discussion on this topic here). Kids and young adults still have a real risk of serious COVID disease even if it does not happen with the frequency as it does for older people. But, that risk is absolutely real. Why chance it at all?

Also, children in particular are especially important spreaders of infectious diseases since they have the most intense social interactions of any demographic group. The intense interaction they have all day in school with classmates greatly increases their chance of infection, which they then bring home to vulnerable older people. It has been shown in epidemiology models and confirmed in real-life studies that preventing spread of infectious diseases in schools is one of the most important tools for protecting the larger population during an epidemic. Being vaccinated reduces kids’ viral burden if they do get infected and reduced viral burden means reduced virus spread. Vaccinated kids help reduce the spread of infectious disease. So, for a couple of reasons, CDC also recommends vaccinating kids this fall.

Get vaccinated.

Parkinson’s Disease—An Unexpected Ravage of COVID?

Thus, (tho, ‘tis Life’s great Preservation) many oppose Inoculation.

-Benjamin Franklin, Poor Richard’s Almanac, 1737

SARS-CoV-2 and its disease, COVID, are very strange. They have given us black toes, lungs like chocolate pudding, long-term fatigue, depression, death, and vaccine deniers. It has been quite a ride. And we are learning that having COVID also puts one at risk for other non-COVID maladies…like chocolate pudding lungs was not enough!

In previous posts, I wrote about the clear link between new-onset type 2 diabetes arising in many patients following COVID. There also is suspicion that cancer might increase down the road due to CoV-2 inactivation of a cellular gene that puts a brake on cancer, P53, in COVID patients. Inactivate that gene and you release the brake on certain cancers. Therefore, there is concern that some COVID patients will experience an elevated incidence of cancer in the future.

New research now raises a real concern that COVID patients might also be at increased risk for developing Parkinson’s disease. Parkinson’s arises when neurons deep in the brain that produce a critical neurotransmitter, dopamine, begin to die off leaving a dearth of this critical chemical that sends signals between neurons. It is like cutting a phone wire. Crucial communications cease.

The study conducted in collaboration between scientists from Weill Cornell Medicine, Memorial Sloan Kettering Cancer Center, and Columbia University College of Physicians and Surgeons was published in Cell Stem Cell last January. Investigators took human induced pluripotent stem cells and coaxed them to become brain cell progenitors that could form into human brain organoids in tissue culture. Such small, nascent “brain-like” structures contain a variety of functional neural cells. They were exposed to the CoV-2 virus, which was shown to preferentially infect and selectively cause the dopamine-producing cells to shut down.

While brain autopsies of COVID patients have not revealed direct COVID infection, they have found unique gene patterns associated with cell senescence, which was especially profound in areas rich in dopamine-producing neurons. This also supports the notion that COVID disease contributes to neurological problems that could cause Parkinson’s disease.

Putting these two findings together is complicated at this time, but they strongly suggest a direct involvement for one or more mechanisms resulting from CoV-2 infection in causing the myriad neurological symptoms that have been seen in COVID patients, and maybe other neurological problems like Parkinson’s not yet attributed to COVID.

Bottom line: CoV-2 is a nasty bug and COVID is a nasty disease. It seems that getting vaccinated not only protects you from nasty flu-like disease and death, it can also protect you from the following:

1. long COVID
2. type 2 diabetes
3. maybe cancer
4. and now, maybe Parkinson’s disease

Why would anyone not want to avoid these? Get the shots!

Interesting addendum: The studies showing that CoV-2 virus can selectively infect dopamine producing neurons went a step further. They also tested a large panel of drugs already approved for other health problems to see if any could unexpectedly protect these critical cells from infection. Sure enough they found three drugs that protected the neurons: Riluzole (used to treat Lou Gehrig’s disease) Metformin (commonly prescribed for diabetes management), and most interesting to me, Imatinib, or Gleevic (used for treating certain leukemias and cancers).

I say this is interesting to me because of my own research beginning at UCLA in the mid-80s, and extending to the University of Wisconsin into this century. My research focused on certain leukemias that carry a specific chromosome abnormality that appears in 99% of patients with chronic myelogenous leukemia (CML), and in fewer patients with acute lymphoblastic or acute myeloblastic leukemias (ALL and AML respectively). When I began studying this, the presence of this chromosome aberration was a death sentence. There was no effective treatment. Patients did not survive long. We identified the specific genetic abnormality, cloned the abnormal gene, sequenced it and found it was parts of two genes stuck together. Most importantly, we also described the enzymatic pathway in cells that it screwed up. All this eventually led to the development of a drug that tamed the misbehaving enzymatic pathway so that now >95% of patients with these diseases are fully cured with medicine that is pretty easy to tolerate. What once was a death sentence is now an easily treated disease. Knowing that makes me feel pretty good.

The drug that cures leukemia patients from what once was a lethal disease is called Imatinib; one of the drugs found to also protect dopamine producing neural cells from CoV-2 virus destruction.

That too will make me feel pretty good if it also happens to prevent neurological problems in COVID patients. Who would have guessed? This is the unpredictable way science often works.

The Intelligence of Artificial Intelligence And Blogging

“Do you ever make silly mistakes? It is one of my very few creative activities.”

–Len Deighton, British Author

Have you tried dabbling with artificial intelligence? I specifically refer to the type referred to as chatbots that use powerful generative artificial intelligence that you can really chat with to generate ideas. It is like the computer, Hal, in the movie 2001 a Space Odyssey. Remember? Remember too that Hal malfunctioned big-time?

I’ve been dabbling for a while. Here is my experience related to this blog.

I began dabbling over a year ago with OpenAI’s ChatGPT, using their GPT3.5 version, but soon graduated to GPT-4, which was released in 2023 and comes with a small subscription fee. I have since migrated to Bing, which is a collaboration between Microsoft and GPT-4 and comes without the fee. It is a powerful research and generative tool. It can generate text, art, compose music, diagnose and even treat a psychological illness with talk therapy. You can have these chatty things teach you a foreign language, and write a legal brief. Perhaps you also have read the reasonable concerns schools and colleges have with such smart tools doing homework for students and the worry about professionals using them to fake their work and the attendant ownership issues of work done.

There seems to be a lot of mischief your computer can cause with the right smart software, but it can also do a lot of good. I know. I have found these smart tools quite useful for my research and writing. Rest assured that I have NEVER used anything but natural intelligence to write any blog post or other article for me (you can tell by the typos in my finished products). This is because, while the bot can compose, it is not creative. As I write, I try to use subtle humor, irony, alliteration and other tools to make my prose interesting. Chatbots do not. At times, however, when writer’s block hit, I prompted the chatbot to write something, and after a few prompts, usually found something that primed the pump of my muse and I penned away using my own intelligence.

I can pose questions or hypotheticals to the computer tool and it comes back with answers. I then either refine my questions, or pose follow up queries. It is much like bouncing ideas off a collaborator. In this regard, I find it quite useful. Who else will talk with me about the value of the latest vaccine or whether Brock Purdy is really a good quarterback or the product of the great pieces around him without my having to buy them a beer? Although, I admit sometimes the latter is much preferable. I have discussed much science at a dive dart bar in Dallas, a surf bar in Malibu, and over a pool table at tavern near the medical center in Madison. Not much artificial intelligence there except after a few brews.

All good. Until this. The chatbot models are supposed to be self-learning. So, I decided to see what Bing had learned about my blog on the coronavirus pandemic. I queried it about a term I thought was pretty unique to the blog, BioX. Readers will recognize that that is what I have dubbed the revolutionary post-molecular biology that gave us a vaccine so rapidly and that is bringing other amazing types of new disease treatments and diagnostics at astounding rates.

Turns out Stanford University (a school you might have heard of, Bing certainly has) has a new bio program also called BioX. It has well publicized it too. Well, Bing kept telling be about Stanford’s BioX and not about mine. Not what I wanted to see.

I changed my query several times to ask Bing about my version of BioX and instructed it to ignore everything about Stanford. Like a hyperactive toy poodle, it completely ignored me. It was quite polite though, apologizing each time I said it was not responding to my query.

Finally, after arguing with this digital nitwit, it finally included me and my notion of BioX in its rendition. Below is what it came up with—be seated as you read what Bing wrote about BioX and me. It included me, but still could not ignore Stanford.

+++

Steven Clark, PhD, is a retired professor from the University of Wisconsin and a viral immunologist who has been blogging about his research on the new biology he dubbed “bioX”. BioX is a term that he uses to describe the emerging field of biotechnology that aims to harness the power of viruses and other biological agents to create novel solutions for human health and disease. He claims that bioX has the potential to revolutionize medicine and biotechnology by offering new ways of diagnosing, treating, and preventing infectious diseases, as well as creating new therapies for cancer, aging, and other chronic conditions. (So far so good. But the next paragraphs…)

One of his most notable achievements is the development of a vaccine against the SARS-CoV-2 virus, which causes COVID-19. He announced this breakthrough on his blog in December 2022, shortly after he received funding from Stanford Bio-X¹, an interdisciplinary biosciences institute that supports research and educational opportunities that cross disciplines between the biological or biomedical sciences and fields of engineering, physics and computational science². He explained that he used a novel approach to engineer a virus that could deliver a synthetic version of the spike protein of SARS-CoV-2 into human cells. The spike protein is responsible for binding to human cells and allowing the virus to enter and infect them. By introducing a modified spike protein that can evade some of the immune responses generated by previous COVID-19 vaccines³, Clark was able to elicit strong neutralizing antibodies in his volunteers without causing any adverse effects. He also demonstrated that his vaccine could protect against different variants of SARS-CoV-2, including Omicron³.

Clark’s vaccine has been hailed as a game-changer in the fight against COVID-19, but it has also raised some ethical and regulatory concerns. Some critics have questioned his motives for developing such a powerful bioweapon without proper oversight or consent from the public. Others have expressed doubts about his safety and efficacy claims, citing lack of peer-reviewed data or independent verification. Clark has defended his work as being based on rigorous scientific principles and ethical standards. He has also stated that he intends to share his vaccine with other researchers around the world who are interested in collaborating with him on bioX projects.

Clark’s blog posts on bioX have attracted millions of readers who are fascinated by his vision and achievements. He has also inspired many young scientists who aspire to follow in his footsteps and pursue careers in biotechnology. However, he has also faced some backlash from anti-vaccine activists who accuse him of being part of a conspiracy to create more deadly diseases or manipulate public opinion. Clark has dismissed these allegations as unfounded and irresponsible.

Clark’s blog posts on bioX are an example of how science can be used for both good and evil purposes. They show how innovation can lead to breakthroughs in medicine and biotechnology, but also how it can pose challenges for society and ethics. They also illustrate how different perspectives can influence how people perceive and evaluate scientific discoveries.

+++

Well dang. If I invented the damn vaccine, how come I was not included in the Nobel Prizes that were just awarded for the invention? I demand a recount. I did like the part about “millions of readers who are fascinated by my vision”. Notice the “references” Bing included citing my accomplishments. They must be true because Bing says so.

In the parlance of computer geeks, what Bing spit out above is called “hallucination.”

This is the intelligence of artificial intelligence.

‘Tis The Season To…..Mask Up Again??

"It's a bug hunt!"

-Private Hudson, in “Aliens”

"Influenza-like illnesses" are increasing at an alarming rate across the country. Yup, ‘tis the season for respiratory diseases and we have more than one to worry about. In years past we mostly worried only about the flu and, sometimes as an afterthought, colds, which aren’t of much concern. But in late 2019, a brand new and very weird bug appeared on the scene, SARS-CoV-2 that caused COVID. It seems that the bug and disease will be an annual guest from now on. This year, we also see a surge of a third bad bug, respiratory syncytial virus, or RSV. All these viruses cause what have been collectively labeled “flu-like illnesses” and together they seem to be worse this year than recent years. The CDC reports that hospitalizations for flu-like illnesses have been steadily rising and that the peak is still to come.

As a result, we are beginning to see increasing reports of a return to local mask mandates. In my own community of Madison, Wisconsin, two major health networks just announced their return, like a bad TV rerun. This includes the University of Wisconsin Health network, where I receive health care. Glad I kept a few masks on hand. What’s in your glove compartment?

I also have read where some grocery stores are now requiring masks. Some stores only require masks on certain days of the week so that customers can select to shop on mask-required vs mask-optional days. Some colleges and large companies reportedly also are beginning to require masks again. So far these mandates are very local and are not a national phenomenon. It is feasible that mask mandates in public spaces and especially for travel could increase if infections and hospitalizations get more serious.

As I often say in these blog posts, “we will see.”

Why is the flu and RSV, which have been around almost forever now causing more than their usual problems? A hint was presented in a blog post I published about a year-and-a-half ago, “What Happened To The Flu And Other Respiratory Diseases?”  In that apparently prescient post, I reported that the world had seen a huge reduction of all infectious respiratory diseases due to the protective non-pharmaceutical interventions (masking, sanitation, isolation, quarantines, closings, etc.) designed to physically protect people from the new coronavirus. They were so effective that some strains of other common infectious viruses are thought to have gone extinct!

That is great news! But, it also means that the world also missed its regular natural booster of common bugs and our herd immunity to them waned. Our youngest were never exposed to those bugs and the rest of us became less resistant to future exposure and that future is now. We are now paying the piper for that lapse in a “bug boost.” Hence, flu and RSV temporarily are having their way with us and enjoying it. At least they are not nearly as nasty as the coronavirus initially was and still could be with a couple of insouciant genetic tweaks.

“Influenza-like illness,” is a catch-all term coined by the CDC to corral COVID and the other two viral diseases. Together, the three have reached an epidemic point in the US and other places across much of the world. The Figure below shows that the US epidemic is currently hitting Southern States the hardest, but expect it to migrate Northward in the next few weeks.

What do the different colors in the Figure mean on a practical level? I can offer one anecdotal example. According to the map, New Jersey, while not a Southern State, still is being hit hard. A family doc wrote about a week ago that all the hospitals in his health system are at capacity. He was unable to send a patient to the preferred ER because its hospital was full due COVID, flu and RSV cases. And the patients with these flu-like respiratory infections who were filling the beds were not necessarily elderly. Most are in their 40’s-50’s. Unsurprisingly, the hospitals and clinics in his health system again require masks. Their staffing is becoming a critical issue as providers also become ill and turn into patients. This is becoming too reminiscent of the early stages of the COVID onslaught when hospitals where overwhelmed and medical personnel were dropping like flies. So far, this experience is sporadic across the US. But, it is becoming concerning.

Outpatient Respiratory Illness Activity Map Determined by Data Reported to ILINet

This system monitors visits for respiratory illness that includes fever plus a cough or sore throat, also referred to as ILI, not laboratory confirmed influenza and may capture patient visits due to other respiratory pathogens that cause similar symptoms. From the CDC.

The incidence of RSV is high. RSV hospitalizations have increased 60% nationwide over the past four weeks. A couple of deaths in children have been reported in my state. The vaccine for RSV is brand new this year and recommended for people over 65 and for kids; i.e., those at highest risk for severe disease. It definitely is worth it.

Flu is moderate right now, but expect it to soon blossom. Hospitalizations among all age groups increased by 200% for influenza in the past four weeks but still remain below Covid-19 and RSV hospitalizations. For now. They are expected to increase as the peak flu season has yet to arrive.

And then there is our relatively new friend, COVID. On a national level, COVID virus transmission is “very high.” After the post-Thanksgiving surge, as determined by monitoring viral loads in wastewater samples (“take-your-kids-to-work” days in that profession must be fun!), virus levels plateaued. But expect another sharp rise after the Christmas/New Year’s holidays. We have consistently seen this pattern in previous years.

Cov-2 is one of the most mutable viruses that the world has inflicted on us. That means we are constantly seen new variants arising. Surprise, the Omicron subvariant JN.1 is coming onto the scene. It’s the spawn of variant BA.2.86, which was discovered over the summer and was concerning because it came out of nowhere with a whopping 35 mutations in the spike protein (the more mutations, the greater the chance for another very nasty bug). While BA.2.86 caused a comparatively mild disease, it quickly mutated to JN.1 with just an additional single change in the spike protein that made it much more infectious, but it still remains fairly mild. With just one mutation, it became the fastest-spreading CoV-2 variant in the past two years. With all its changes, JN.1 is so different from its Omicron grandparent that there is considerable scientific debate about whether JN.1 should be given its own Greek letter designation, Pi. A weighty debate indeed.

But, a bigger question is whether COVID hospitalizations will follow wastewater sampling trends that show JN.1 (or Pi) viral levels surging through the world, especially in the US where vaccination rates are low. It is concerning that the UK and Singapore, which have high vaccination rates, are now seeing a steep increase in hospitalizations due to JN.1 (or Pi). So why not expect the same or even worse in the undervaxed US? Last week, the CDC warned about such a potentially huge impact due to the wretched combination of low US vax rates and the highly infectious JN.1 (or Pi) virus. As Private Hudson (aka Bill Paxton) in the movie Aliens might say, thanks to the antivaxers, “Game over, man! Game over!”

Also of new concern is that some scientists are now beginning to believe that COVID infection could be damaging our immune systems. If true, that could make infected people even more vulnerable to the other bugs out there such as flu, RSV, and others including bacteria and fungi. COVID could also cause immune dysregulation leading to new-onset autoimmune diseases. So get your COVID vaccines! They can protect you against illness beyond COVID!!

Finally, another concern is that the rapid home tests for COVID are proving to be only 30% reliable very early after infection before symptoms start. In other words, if you believe you have been exposed to COVID, but your home test comes up negative, don’t necessarily believe it. Retest yourself 24, or preferably 48 hours later or when you show symptoms like a fever, cough, etc. If that second test also is negative, you have pretty good confidence you are COVID free and have some other bug.

The pragmatic bottom line. There is a lot of coughing, sneezing and other respiratory distress going around, and it will increase in coming cold weeks as we bundle up and crowd around others indoors. To improve your odds of staying healthy, remember these things:

• Limit your time around indoor crowds.
• If you have indoor gatherings, crack your windows and bring out the fans to increase air circulation and air exchange with the outdoors. There is very good evidence that good ventilation really matters and that the amount of viruses we breathe in makes a big difference in terms of whether we get sick and how sick we get. It is worth a few extra dollars on the heating or electricity bill to avoid nasty illness.
• Room air filters are also a good idea.
• Get vaccinated!
• Wash your hands often.
• If you do get sick, STAY HOME! I have always hated the “brave” soul who came to work with a cough and sneeze. Don’t share your agony!!
• And there are the good old fashioned masks for use in crowded places, especially in auditoriums, on planes, and other packed indoor situations. I don’t care what the naysayers say about masks, they are flat wrong. They don’t think twice when a store sign requires shoes and shirts to enter. So why do masks bother them so much? They WORK as I have written here before, over and over. Empirical evidence proves masks work. That is why the entire medical profession continues to use them.

Finally, as I have repeatedly admonished, please get vaccinated. Vaccine and booster uptake for all three viruses has been dismal this year. Failure to vax is a major driver in the surge of the flu-like respiratory diseases we are seeing. If you have not gotten vaccinated for all three circulating viruses, why the heck not?? It is way better to prevent disease than to treat disease. A sore arm is much less of an inconvenience than suffering the flu, RSV or lying in a specialized hospital bed turned on your stomach breathing with a ventilator because of COVID.

As I have written in these pages, having COVID can be worse than any flu you ever had. It also puts adults at risk for dealing with weeks of long COVID and getting new-onset diabetes and immune dysfunction. COVID also is much worse than the flu for many kids and puts them at risk for multi-system inflammatory syndrome (MIS).

Why risk what can be prevented by a simple vaccination?

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US Life Expectancy Finally Bounces Back Up

“Game over, man! Game over!” --Bill Paxton as Private Hudson in Aliens

As I wrote in these pages a couple of years ago, the US suddenly lost a whopping 1.3 years of average life expectancy due to COVID. It had that big of an impact on the country in excess deaths. And before some moron starts saying it was due to vaccine deaths, the down turn in life expectancy, or the increase in excess deaths (i.e., deaths more than expected based on actuarial predictions) began before the vaccines rolled out and just after the virus appeared. Furthermore, the upturn in life expectancy occurred after the vaccines were delivered, as well as after the virus evolved from Delta to a less lethal variant. In the early days of COVID vaccination before vaccines were widely distributed, data showed that unvaccinated people were 11 times more likely to die from the virus than vaccinated people. At one point, 95% of hospitalizations and 99% of deaths were in unvaccinated people. The vaccines clearly prevent death, they do not cause death (unless you listen to Robert F. Kennedy, Jr. or Marjorie Taylor Greene, more on her later).

The graph below shows the dramatic drop in life expectancy beginning in 2019 and reversing about 2021. If vaccines were killing rather than saving people, you would think the curve would continue downward.

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BioX Wins The Nobel!

“If you start to take Vienna, take Vienna”— Napoleon (reportedly)

What’s the fuss? BioX won the Nobel Prize….er rather it was the mRNA vaccine that won. Correction—it was the scientists, Katalin Karikó and Drew Weissman of the University of Pennsylvania, who developed the RNA technology that went into the novel vaccine who won the prize. But their work directly led to the vaccine, a first fruit of BioX.

Readers of these blog pages might remember that about this time in 2020, that year’s Nobel award for Medicine or Physiology went to three scientists for their decades-long search to discover what caused hepatitis type non-A, non-B. It turned out to be a whole new virus, the hepatitis C virus (or HCV) that took four decades to identify. Even though it still remains a huge health problem, there still is no vaccine for it. I compared that four decade slog just to find the pathogen to how fast the novel viral cause of COVID-19 was found and a vaccine developed—all done in less than a year! I anointed the new biology that did that amazing feat, ‘BioX.’ That was rather prescient of me, since three years later, the co-founders of the COVID vaccine using BioX too were awarded the Nobel Prize.

I dubbed the new amazing post-molecular biology science that enabled such a quick identification of the novel coronavirus and development of a vaccine against it, ‘BioX’ after SpaceX. SpaceX, of course, is the name for the new way space travel is now being done. Shortly before the Nobel award for the discovery of HCV, Elon Musk’s SpaceX took astronauts in an unpiloted vehicle to the International Space Station. Then the launch vehicle, rather than being discarded as usual, was landed, upright, in the center of a bullseye on a barge off the coast of Ireland, to be reused on a future space flight--maybe to Mars? The whole thing was developed in a fraction of the time at a fraction of the cost of what NASA had historically been doing. NASA’s technology was rendered archaic by SpaceX, which introduced us to a new era of space travel.

The breathtaking speed with which a new biology discovered the SARS-CoV-2 virus and then developed a safe and effective vaccine against it ushered in a new post-molecular biology world I dubbed ‘BioX’.

Now the details. But as breathtaking as SpaceX is, it was not developed overnight in a vacuum. It arose on the back of decades of NASA engineering R&D, which included some spectacular failures and even a few tragic deaths. Similarly, as breathtaking as BioX was with the rapid identification of a novel virus and development of the new mRNA vaccines to a wholly new disease, that technology too was built on the back of decades of hard work, punctuated with many failures, but also flavored with impressive perseverance on the part of a few individuals.

There are two major components to the novel COVID vaccines—the mRNA which generates the viral protein to which the immune response is made, and the lipid nanoparticles that encapsulate and protects the fragile mRNA from a world that is hostile to mRNA. Both components took very separate, decades long, twisting, uphill roads to develop. Both nearly met with failure. And both came together with spectacular success. BioX!

• The mRNA. Weissman, and especially Karikó, languished for years on the fringes of science with a, then, very weird idea of using mRNA to produce drugs or vaccines. Their collaboration began with a chance encounter at a UPenn copy machine in the 90s and went downhill from there as recently told in the Wall Street Jounal. Funding for their work was hard to come by. Karikó was banished to an office on the outskirts of the campus and languished in a non-faculty position for years. At one point, she had to take a demotion to simply keep a job at Penn.

They just could not get their idea to work. The mRNA was too fragile and too short-lived to work with and produce the desired proteins when they tried to express it in cells or animals. The fact is that there are ubiquitous enzymes all around us called RNases that have a ravenous appetite for mRNA. RNA molecules, especially mRNA disappear almost as fast as one can purify or make them, let alone then try to get them into cells in tissue culture or into bodies. On top of that, when naked mRNA is injected into a body, it elicits a powerful immune response that further quickly degrades it. Note that there are several different types of RNA, and mRNA is the most fragile and hardest to work with, but it is the type that provides the message that turns a genetic code into a protein molecule like a spike protein, which is why it is used in the vaccine.

The researchers had great difficulty getting grant funding for their research because no one believed it would go anywhere. When they could produce some data, they had a very hard time finding journals to publish it. No one was interested because no one believe that there was any utility in the whole premise of using mRNA as a therapeutic tool. In the publish-or-perish world of academia, such negative peer pressure usually is the kiss of death. They should have seen the writing on the wall and been teaching high school biology. But for some reason, Karikó continued to have faith in her idea even though no one else did. For some reason, she persevered.

After dogged determination and ignoring all the naysayers, she eventually had a major breakthrough after a doing a simple experiment. They found a simple way to protect the mRNA from the immune response and published this in 2005. It opened the field and colleagues minds about using mRNA as a possible therapeutic tool. But there still was the problem that mRNA was exquisitely sensitive to RNase enzymes that were everywhere—on your fingers, in your breath and blood, even on sterilized surfaces—the enzymes are incredibly stable molecules and very hard to destroy. Life intended mRNA to be short lived molecules, not to be used in vaccines.

It wasn’t until folks paired the immune-stable mRNA of Karikó and Weissman with a way to protect the molecules from RNase enzymes that mRNA vaccines became possible so they could win the Nobel Prize. Lipid nanoparticles did the trick.

• The lipid nanoparticles. The story behind the development of the lipid nanoparticles used to deliver the CoV-2 viral spike mRNA sequence to cells so they could use their normal gene expression machinery to put the spike protein on their surface and generate an immune response is a long one. In that regard it is quite similar to the long, arduous story behind the development of the therapeutic mRNA. Early on, neither technology was believed possible or useful by the scientists’ peers. Both groups had very hard times getting their scientific feet on the ground. Both nearly failed. I described Karikó’s struggle above and in March 2021 I wrote in these pages about the professional plight of Bob Langer who, in the 70s, had a vision for using liposomes (short for lipid nanoparticles) for delivering fragile bio-molecules and drugs to cells (you can read that post here). Briefly, his idea was to create mini-cells in which to package and protect fragile therapeutic molecules and then deliver them to cells and tissues in the body. The liposomes containing the fragile therapeutic molecules would fuse with the lipid membranes of cells and disgorge their contents into the cells. Many people told him it was not possible and he had his first nine grant applications rejected—and this was a time when medical science research grants were easy to get (when I was in graduate school in the early 80s, NIH grant applications had a 50% success rate. By the time I became a faculty member in the late 80s that dropped to 10%). Langer, like Karikó, also could not get a faculty position because people did not believe in his research. Also like Karikó, for some reason Langer persevered.

Also like Karikó, Langer too succeeded—eventually. It took a long time. The technology he successfully developed was first used to package a drug used to treat a rare genetic disease that causes nerve and heart damage. It also was used to package mRNA for an Ebola vaccine. From an ignominious beginning, Bob Langer became a professor at MIT where there now is a bioengineering lab named after him. That is not quite as nice as winning a Nobel prize, but high recognition still.

Along the way, he also co-founded a small biotech company named Moderna that was focused on developing mRNA vaccines for infectious diseases, cancer and other diseases. Then COVID came calling and Moderna immediately pivoted, and along with BioNTech, NIH, and Pfizer, quickly gave us mRNA vaccines delivered in liposomes that saved millions of lives from COVID.

That is how BioX technology led to the Nobel prize this year.

The bottom line. BioX, like SpaceX, was built on decades of hard research that was punctuated by painful failures, but highlighted by dogged determination. Both technologies, BioX and SpaceX, are here to stay at least until the next amazing thing replaces them. You can bet that that next amazing thing will have been developed on the back of determined researchers who very possibly will be working at the fringe of their professions and may flirt with professional failure early on. You can also bet that the next amazing things will be built on the backbone of SpaceX and BioX. That is how science and engineering painfully progresses.

So, when you hear someone say that the mRNA vaccines are experimental like I very often do, tell them the truth. They were built on decades of hard research going back to the 70s.

Stay tuned for a coming post on the future of BioX, which is here to stay for a while. New mRNA vaccines are being developed for previously vaccine-impossible diseases including HIV, cancer, and various animal diseases. Work also is underway for a universal flu vaccine.

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Politics: A Risk Factor For Death From COVID?

What are you gonna believe, medical science or dubious talking heads?

In 2021 former Green Bay Packers quarterback, Aaron Rodgers, said he was “immunized” against COVID. He wasn’t. He claimed to have done “research” and learned how to get an infusion of antibodies and take some unproven ‘medicine.’ His ‘research’ was talking to radio pundit and hot-air purveyor, Joe Rogan. How many more people like Rodgers listen to the wisdom of the likes of Rogan or Tucker Carlson and think they know more than medical professionals and then rationalize their avoidance of COVID vaccines? And to what effect?

The Kaiser Family Foundation estimates that from June 2021 through March 2022 about 234,000 COVID deaths could have been prevented had the decedents been vaccinated against the SARS-CoV-2 virus. That protection was especially important during the more deadly Delta virus wave during the earlier stage of the pandemic, but it still extends into the Omicron era, which fortunately is not as deadly as Delta was, but still is not to be taken lightly. People are still dying from the virus.

How does politics come into this?

A 2022 study published in the journal, Lancet Regional Health-Americas, found higher COVID mortality rates in more conservative congressional districts across the US. And in another 2022 study using 2020 presidential election returns, researchers at the University of Maryland and the University of California at Irvine found that, through October 2021, Republican-majority counties across the US experienced nearly 73 additional COVID deaths per 100,000 people relative to majority Democratic counties.

These are correlations looking for a cause. A good causal candidate could be differences in vaccination rates between people who tend toward conservatism vs liberalism. The former are much less likely to get vaccinated than their left leaning neighbors. But, that connection needs to be made.

Sure enough, a July 2023 report by Yale researchers in the journal, JAMA Internal Medicine, compared COVID death rates in counties in Florida and Ohio that voted for Trump vs Biden before and after the vaccines came out. The bottom line was that after the vaccines rolled out, Trump voting counties saw 40% higher fatality rates per million residents. Before the vaccines, the COVID death rates were the same for all counties. Viral infection rates were similar for both types of counties throughout the period of analysis. Importantly, counties and individuals that went for Trump had lower vax rates than those that went for Biden.

That pretty much closes the circle on the causation. The greater reluctance of more conservative people to get vaccinated and boosted likely killed them at a greater rate.

Karma?

Now, don’t get me started on the conservative vs liberal attitudes on face masks and social distancing. Conservatives are wrong on these matters. I say this as a conservative myself. But, I also am a data driven scientist who believes data trumps partisanship.

How do you think SARS and MERS were stopped without a vaccine or anti-viral drugs? How do you think society stopped any epidemic such as small pox, influenza, bubonic plague, etc. throughout its history before modern medicine and effective vaccines? How do you think today we are handling Ebola for which there is no vaccine or drug? Non-pharmaceutical physical measures, like masks, gloves, sanitation, social distancing, etc. are effective ways to halt infectious diseases in lieu of vaccine and drug preventive measures.

Conservative resistance to these non-pharmaceutical physical protective measures also probably contributed to their higher death rates observed in the studies mentioned above.

Karma.

Part 3: Gain-Of-Function Research At The Wuhan Lab—Are The Chinese Hiding Something About The Lab?

This is a re-post of a blog, but with additional material. I added new information about the Chinese government response to the first SARS epidemic. You can find that section two-thirds of the way through the post under the headline in bold "The Chinese have done this before:"

“In a time of deceit telling the truth is a revolutionary act.”
― George Orwell

Yeah, I know, I said this would be a two-blog series about the research at the Wuhan Labs. But a comment a reader made on my second blog post made me think that I should make a third post to briefly address the apparent secrecy and lack of cooperation from the Chinese government regarding the research at the Wuhan Institute of Virology (WIV).

The Chinese have failed to cooperate to help us find the origin of the SARS-CoV-2 virus that caused COVID. They have denied access to WIV lab records or research personnel beyond what was posted on their coronavirus database as I mentioned in my prior blog post. This secrecy and lack of cooperation began in early January 2020 immediately after Chinese officials realized that they had a coronavirus superspreader event at the Wuhan wet market as I described almost three years ago in these pages.

This apparent secrecy on the part of the Chinese has led many people to jump to the conclusion that the Chinese are hiding something sinister—sinister like they secretly created SARS-CoV-2 and accidentally released it and don’t want the world to find out. But, as I have posted several times in these pages, most recently here, there is precious little evidence that supports the notion that the virus came out of a lab. On the other hand, there are several pieces of consistent, but still circumstantial evidence for its natural origin. However, that conclusion is not definitive and could change with new evidence. Hence, we cannot say with certainty that we know where the virus came from. But, remember, it took 14 years and a LOT of work to learn the origin of the virus that caused the first SARS outbreak; it took much longer to discover the source of HIV, and we still do not know where the Ebola virus came from. These things are very hard to learn and take time to figure out.

However, I don’t believe that the best explanation for the Chinese lack of cooperation is that they are hiding something sinister from the world because it seems very unlikely that the virus was man-made. After all, we have several examples of novel coronaviruses popping up in animals and humans, and all have had natural origins. And as I described in my prior post in this series, it is next to impossible that the virus was accidentally released from the Wuhan labs since they really did not work live viruses at all. I think one of two other explanations for Chinese intransigence is more plausible.

The least likely alternative explanation is that WIV lab safety protocols for handling dangerous pathogens were substandard and for the Chinese to allow access to lab records would reveal to the world how careless they were. Perhaps they were concerned about their world image and did not want to be embarrassed. It could deleteriously affect their R&D collaborations with other countries. But, we already had an idea that their safety protocols were not up to Western standards so this would not have been a terribly shocking revelation. That is why I don’t think this is the most likely explanation for the lack of cooperation and transparency.

More likely, however, I think the lack of cooperation probably reflects the general and significant deterioration in science and technology collaboration between China and the US that has been going on for five years. This was the topic of a long article in the Wall Street Journal just a few days ago. In fact, US-China science and tech cooperation has gotten so bad in recent years that US lawmakers are pushing to let a long-standing agreement between the two counties to cooperate broadly on science and technology lapse. It was originally signed in 1979 and renewed every five years since, but will expire this month if not renewed as several lawmakers are pushing.

A once highly productive cooperative science and technology agreement between the US and China seems to have begun falling apart in 2018, before COVID, according to the WSJ article. That is when the US DoJ launched its China Initiative to ferret out Chinese economic espionage. Over time the program increasingly focused on interactions between US universities and Chinese institutions. NIH also launched hundreds of investigations into ties between US science and China. While all these investigations largely failed to turn up criminal conduct, they understandably put a major damper on further cooperation between China and the US. They also led to an exodus of Chinese scientists from American labs. Given all that, it is not surprising that Chinese officials are not opening the doors and books of the Wuhan labs to us.

Thus, this lack of cooperation regarding access to the Wuhan labs is happening as cooperation is seriously deteriorating across the scientific spectrum, not just at the Wuhan labs.

The Chinese have done this before: The Communist Chinese government also has a long history of invoking repressive secrecy in order to prevent itself from looking bad. For example, they also clammed up during the first SARS outbreak back in November 2002 and it threw the country into its worst political crisis since the 1989 Tienanmen Square uprising. The government’s first response to the emerging epidemic was to hide the outbreak from its people, and even from its own public health officers. Despite the cloak of a news blackout, SARS spread throughout the country, reaching Beijing that March (viruses don’t read the newspapers!). But doctors do, and the cloak worked on them. Because of all the secrecy, they were caught by surprise by the sudden and prolific appearance of a new disease, and only learned what was going on via surreptitious text messaging.

In April, WHO officials finally were allowed into the country to inspect Beijing hospitals in order to assess what was going on, but sick patients were shuttled out of the hospitals in ambulances to different hospitals or checked into hotels to hide them from inspectors. Because Beijing tried to hide all this from the world, the epidemic, which might have been limited to that city, found its way into 32 countries around the world (viruses are very slippery). Fortunately, those other countries were not as furtive and were able to nip their infections in the bud with public health measures such as quarantines, contact tracings and isolation, and public closings.

SARS allowed the world to see and compare how repressive and self-sensitive China vs other world countries handle a deadly contagion. China was afraid of losing face and tried to hide its problem from public exposure. However, this backfired and showed China to be a repressive country that was willing to risk the safety of its people and the world in order to avoid accountability for the first SARS outbreak.

Therefore, it is not terribly surprising that the Chinese government again is using repressive means to avoid being put into a position of accountability for the second SARS outbreak.

The bottom line is that to think the Chinese are hiding something nefarious and conspiratorial at the WIV is pure speculation and is backed by no evidence at all. So far. There are alternative explanations for the lack of cooperation by the Chinese that are more feasible and reasonable to believe at this point. New information could change this assessment of course, but evidence that the Chinese are hiding something is lacking. Too bad they won't let us confirm that.

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