Category: Modern Science

A Very Promising Possibility for COVID-19 Treatment

A person using an inhaler, which is the way the drug in the study is delivered (click for credit)

There are several drug treatments that are currently being investigated for COVID-19. However, of all the studies I have seen so far, this one looks the most promising. In the study, UK-based Synairgen chose 101 hospital patients and randomly assigned them to get a placebo or a chemical called “interferon beta,” a protein that has antiviral properties and is naturally produced by the human body. Both the placebo and the protein were administered through inhalers so that they ended up in the lungs. Over the roughly two-month study, patients getting the protein were 79% less likely to develop severe symptoms that required a ventilator. Also, while three of the patients who received the placebo died, none of those who received the protein died.

The study seems well designed. For example, patient ages were very similar. The placebo group’s average age was 56.5 years, while the protein group’s average age was 57.8 years. The difference is very small, but note that it favors the placebo group. In other words, since the patients getting the placebo were younger, they were automatically a bit less at risk than the protein group. In addition, the average amount of time the patients exhibited COVID-19 symptoms before getting the treatment was very similar, 9.8 days for the placebo group and 9.6 days for the protein group.

I do, however, see two potential problems. First, the number of patients in the study is small. As a result, they made a lot of other interesting observations, but they couldn’t determine whether those observations were the result of the protein or random chance. For example, the patients who received the protein were roughly twice as likely to recover within the two-month period than the ones who did not receive the protein. However, because the number of patients is so small, mathematics tells us it is possible that this result is caused by chance and not by a difference between the placebo and the protein.

The other problem, of course, is that this study was performed and reported by the pharmaceutical company that wants to produce and sell the drug. Initially, of course, this makes sense. Studies cost money, so the company that wants to make and sell the drug should spend the money to do the studies. However, before the drug can be approved for general use, there will need to be a larger study with independent analysis. I eagerly await that kind of study.

Can a COVID-19 Virus Communicate with Other COVID-19 Viruses?

I am writing this post because a reader asked me a question that I thought was very interesting and relates to a broader concept in biology. Before I answer her question, however, I want to make an important point about the virus that causes COVID-19 and how we should react to it. A few weeks ago, I gave the commencement address to a group of homeschoolers. Before I started my official remarks, I said this:

I am not going to say much about this virus, but I will say this: As a scientist, let me assure you that no one really knows what we should be doing. There are a lot of experts saying a lot of different things, and you should listen to all of them. Then, you should decide what works best for you and your family, and you should start doing it. But once you decide what you and your family should be doing, please please please show grace to those who choose to do something different. Since the experts can’t agree on a proper course of action, there is no reason to expect your neighbor to agree with your course of action.

I think that is the best way to approach this pandemic. The experts still can’t agree on exactly what to do because we just don’t know enough about this virus to make definitive choices. As a result of this ignorance, we must all muddle through this as best we can and realize that none of us has all the correct answers.

Now let me share my reader’s question:

Recently I came across a discussion online about quorum sensing in viruses. The initial topic had been the difference between groups meeting indoors verses outdoors, as many churches are now doing. I had never heard of quorum sensing before, so I did a little research, but I wondered if you would consider addressing this sometime. It sounds pretty fascinating to think viruses and such can actually monitor their environment.

Continue reading “Can a COVID-19 Virus Communicate with Other COVID-19 Viruses?”

Another Peer-Reviewed Paper Favoring Intelligent Design

A figure from the paper being discussed, showing how a protein complex (left) can be converted to a graph (middle) to analyze how its parts relate to one another.

The more we learn about the universe, the more we see that it is a product of design. Indeed, for quite some time now, many scientists have recognized that the universe is finely-tuned for life. There are many parameters that govern how things happen in the universe, and they all have the characteristics of being just what they need to be for life to flourish. An electron, for example, is precisely as negative as the proton is positive, despite the fact that they are very, very different particles. If the charges were off by as little as one billionth of one percent, the resulting electrical imbalance in molecules would make even very small objects too unstable to form.1 The most obvious explanation for such fine-tuning is that the universe has been designed for life.

Now, of course, if you don’t want to believe that the universe is a product of design, you can offer any number of desperate alternatives. Perhaps we are just very fortunate. After all, if the universe weren’t designed for life, we wouldn’t be here to study it, so the very fact that we can discover these relationships tells us that the universe just happened to evolve into one that appears to be finely-tuned for life. You could also suggest that there are a ridiculously large number of universes out there. Most of them don’t have life, because they don’t have the proper parameters. However, if there are many, many universes, there’s a high likelihood that at least one will have all the right parameters, making it appear to be finely-tuned for life. You could also argue that there are actually a lot of combinations of parameters that might work for life; we just don’t know them. In that case, the universe’s apparent fine-tuning is an illusion.

While I think the scientific data clearly demonstrate that the universe is designed, I have always said that the most obvious case for design can be put forth by biology. Even the simplest life form on this planet is more complex and well-engineered than anything made by human technology, and most of the biological world makes our best inventions look positively crude by comparison. Well a reader (Victor Ferreira da Silva) sent me a paper in the secular, peer-reviewed literature that claims to have confirmed this fact.

Continue reading “Another Peer-Reviewed Paper Favoring Intelligent Design”

Dr. Fauci, Americans Believe Science, but They Don’t Believe Many Scientists (For Very Good Reasons).

Dr. Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases (click for credit)
Dr. Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases and one of the lead members of the White House Coronavirus Task Force was recently on the US Department of Health and Human Services’ podcast, which is called “The Learning Curve.” It exists so people can hear from experts in the department, learning what those experts are doing and what they think you should know. Obviously, Dr. Fauci was on to discuss the COVID-19 pandemic.

While some of what he said on the podcast was valuable, he made one statement that shows he is completely out of touch with most people in the United States:

One of the problems we face in the United States is that unfortunately, there is a combination of an anti-science bias that people are — for reasons that sometimes are, you know, inconceivable and not understandable — they just don’t believe science and they don’t believe authority…

Now, of course, you can always find people who don’t believe science for a variety of reasons. In my experience, however, they are few and far between. The majority of people in the United States hold science in very high regard. For example, Scientific American recently conducted a poll that found 90% of the people they surveyed wanted science to have a significant influence on society. An additional 7% wanted science to have some influence, which leaves a mere 3% that wanted science to have no influence at all. This is consistent with what I see around the nation. Most people believe science, some are skeptical, and very few think it has no value.

If people in the United States believe science, why does Dr. Fauci think they don’t? Because he is confusing science with scientists. As a scientist myself, let me put this very bluntly: In general, you can trust science. However, you cannot trust many scientists. Why do I say this? The Scientific American article linked above gives one reason: Many scientists have values that conflict with the majority of people in the United States, and those values affect how they interpret the science they know. For example, when a scientist doesn’t recognize that this world is a product of design, he or she will be led to all sorts of false conclusions. When the scientist communicates those false conclusions as if they are absolute fact, many reasonable people end up distrusting him or her.

But the Scientific American article linked above misses the more important reason people don’t trust scientists. It’s because scientists regularly make statements that they claim are absolutely true, but eventually, those statements are shown to be false. I highlighted a recent example a year ago. Visitors to Glacier National Park were told that computer models indicated the glaciers they are admiring will be gone by 2020. Well, it’s 2020, and the glaciers are still at the park. So what did the scientists do? Did they admit to their mistake? No. They quietly removed the signs, hoping the mistake would go unnoticed. In this day and age, however, such things rarely do.

The nonsense about the glaciers isn’t an isolated example. Time and time again, scientists make pronouncements and even take action based on ideas that they claim are absolutely true, but end up being utterly false. It was thought for a long time that the human appendix was a useless remnant of evolution. This silly notion was believed by surgeons, so many would remove the appendix from a patient having abdominal surgery, even if the appendix was entirely healthy. We now know that the appendix is an important lymphatic organ, and people without an appendix are more likely to have difficulty recovering from certain intestinal diseases. Tonsils are another example. It was once common practice to remove inflamed tonsils rather than treat the inflammation with medicine, because tonsils were supposed to be a leftover vestige of evolution. People who were unfortunate enough to be treated by someone who believed such nonsense (me, for example) are much more likely to suffer from respiratory, allergic, and infectious diseases. The fact that scientists routinely make definitive statements which are later shown to be wrong is so well-known that it is the subject of comedy routines.

In the end, scientists have themselves to blame when it comes to people not believing their pronouncements. They have betrayed the public trust too many times, because they have forgotten that by its very nature, science is tentative. Thus, it cannot be used to make grand pronouncements of absolute truth. Scientists have to realize that they are not priests. They are people who have expertise, but that expertise is based on a method of inquiry which routinely produces false conclusions. Rather than making grand pronouncements about the “truth,” they should show people the evidence and explain how they interpret the evidence. If they don’t communicate science that way, the public has no choice but to distrust them.

Did This Bird Go Extinct and Re-Evolve? I Doubt It.

A flightless Railbird on the Aldabra atoll in the Indian Ocean (click for credit)

Over the past few days, several people have sent me articles like this one, which makes a rather fantastic claim:

The Aldabra white-throated rail bird was declared extinct, a victim of rising sea levels almost 100,000 years ago.

However, the flightless brown bird has recently been spotted – leaving scientists scratching their heads as to how – and why – the species has come back to life.

What do you conclude from reading that? The article seems to be saying that no one had ever seen this bird before; it was only known from the fossil record. Now, however, living versions of it have been seen, and how they came back from extinction is a mystery. Unfortunately, like many “science news” stories, this one distorts the science to the point that it is deceptive and misleading.

The science that is being distorted comes from a study published last year. A responsible article that describes the study can be found here. While the study and the responsible article don’t distort the science, I do think the conclusion that they draw is not the only one consistent with the data.

Let’s start with the bird that is being discussed. It’s the Aldabra white-throated rail, whose scientific name is Dryolimnas [cuvieri] aldabranus. It lives on the Aldabra atoll in the Indian Ocean and is nearly identical to white-throated rails (Dryolimnas cuvieri) found in other parts of the world, like Madagascar. However, the ones on the Aldabra atoll cannot fly, while the others can. As a result, the flightless birds on the atoll are considered a subspecies of the version that can fly.

While we cannot say for sure, the generally-accepted origin story for the Aldabra white-throated rail is that normal white-throated rails landed on the atoll, and since there were no predators there, they stayed. Since they didn’t need to fly anymore, they evolved into flightless birds over several generations. This makes sense, because when a population of organisms doesn’t need a particular biological trait, mutations can degrade those traits without affecting survivability. In addition, DNA is so incredibly well-designed that over the course of generations, it can “turn off” genes that are no longer used in order to save energy. As a result, it makes sense that these flightless birds are descendants from birds that could originally fly.

Why do these articles discuss the birds being extinct at one point? Because the authors of the scientific study looked at the fossil record of the atoll. Using scientifically-irresponisble dating methods, they came to the conclusion that the atoll was completely underwater about 140,000 years ago. When they looked at fossils they interpreted to be older than 140,000 years, they found two bones that seem identical to the corresponding bones in the Aldabra white-throated rails that currently live on the atoll. Thus, they conclude that these flightless birds lived on the atoll before it went completely underwater.

Well, since the birds couldn’t fly, the authors assume that they all died when the atoll was underwater. However, in fossils that they interpret as being deposited after ocean levels decreased and the atoll was no longer underwater, they found another bone that looks similar to the corresponding bones in white-throated rails that can fly. However, it is heavier and more robust than what is found in those birds, but still lighter than what is found in the flightless Aldabra white-throated rails. In other words, it seems to be “in between” the bone of a normal white-throated rail and a flightless white-throated rail. To them, that gives “irrefutable evidence” (their words) that the Aldabra white-throated rails evolved twice: once before the atoll went underwater, and once after.

While their interpretation of the evidence makes sense and is consistent with all the known data, their case is certainly not “irrefutable.” First, you have to assume that they are interpreting the fossil record correctly. There is a lot of evidence to indicate the earth isn’t anywhere close to 140,000 years old, and if that evidence is correct, then their entire explanation is wrong. Also, even if the earth is as old as these scientists want to believe, the authors’ explanation is not the only one consistent with the data. We know that flightless animals can move from place to place on floating mats of vegetation. This is called “rafting,” and it is used by both evolutionists and creationists to explain the worldwide distribution of certain animals. If the atoll flooded like the authors think, the flightless birds could have survived by rafting. What about that one bone that is “in between” the two subspecies? There are natural variations in all bones. A “more robust” bone from a normal white-throated rail can be explained by natural variation within a population of normal white-throated rails.

The main reason I am writing about this is not to argue with the authors. It’s to point out the deceptiveness of articles like the one I quoted at the beginning of the post. As I have said many times before, do not believe the things you read in the popular press when it comes to science. Most “science journalists” are profoundly ill-equipped to understand science, and usually quite poor journalists as well.

Lichen Hid This Secret From Scientists for More Than 140 Years!

The colorful splotches on this rock are lichens, which we now know are a mutualistic association between THREE different organisms (photo copyright Kathleen J. Wile)

For more than 140 years, scientists have taught that lichens are the result of a relationship between a fungus and an alga (singular of algae). The fungus gives the lichen most of its visible characteristics and provides a protected place for the alga to grow. In exchange, the alga does photosynthesis and shares what it makes with the fungus. In other words, the fungus provides housing for the alga, and the alga provides food for the fungus. This is a form of symbiosis, in which organisms of different species exist in a long-term relationship. Since both organisms benefit in this symbiosis, it is called a mutualistic symbiosis, one of the most fascinating aspects of the biological world (see here, here, here, here, here, here, and here, for example).

Despite the fact that lichens have been studied for more than 140 years, there has always been one nagging mystery: The relationship cannot be recreated in a lab. Lichens can be found in all sorts of ecosystems, but no matter what you do with the fungus and the alga, you cannot get them to form the same relationship in a laboratory setting. A recent study might explain why. The authors of the study analyzed two different species of lichen, Bryoria fremontii and Bryoria tortuosa. They are easily distinguished from each other, since the first is dark brown, while the second is yellow. However, recent studies have indicated that the fungus and alga in each are the same. How is it that two lichens can be so different when their fungus and alga are the same? That’s what the authors wanted to find out.

They decided to look at the specific genes that were actually being used by the two species. After all, even if both lichens have the same fungus DNA and the same alga DNA, it’s possible that one lichen uses one set of genes more than the other lichen, and perhaps that could explain the differences between them. However, their initial analysis indicated that both lichens used essentially the same set of genes. That’s when they decided to think “outside the box.”

When doing a study like this, you have to decide what gene products you are looking for. They had limited themselves to the genes found in the fungus and the alga that were known to exist in the lichens. They decided to change their analysis to include all known fungus genes. When they did that, they found that genes from an entirely different fungus were also being used by the lichens! That fungus is a type of yeast (specifically from genus Cyphobasidium), which is very different from the fungus that was already known. The authors did some very difficult microscope work and confirmed the presence of the yeast in the lichen. In addition, they did the same genetic tests on many different species of lichen, and they found the yeast genes in the vast majority of the lichens that they studied. As a result, the authors suggest that the vast majority of lichens are made up of at least three different species. Here is how they conclude their paper:

The assumption that stratified lichens are constructed by a single fungus with differentiated cell types is so central to the definition of the lichen symbiosis that it has been codified into lichen nomenclature. This definition has brought order to the field but may also have constrained it by forcing untested assumptions about the true nature of the symbiosis. We suggest that the discovery of Cyphobasidium yeasts should change expectations about the potential diversity and ubiquity of organisms involved in one of the oldest known and most recognizable symbioses in science.

While this discovery in and of itself is remarkable, it is also an excellent illustration of how assumptions can put blinders on science. Why haven’t these yeasts been discovered in more than 140 years of lichen study? Partly, because they are well-hidden. To confirm the presence of the yeast in the lichen required some rather detailed microscopic analysis. In addition, when you are doing genetic analysis, you have to decide what to search for, which means your results will be limited by that decision. However, here’s the main reason: No one was looking for them. Since the assumption that lichens are mutualistic symbioses between two different species was so ingrained in biological thought, no one ever considered looking for a third, until these authors decided to “think outside the box.”

I wonder how many more scientific discoveries are waiting on other scientists who are willing question old paradigms and look for things that no one else has been looking for!

Please…Discard the Dogma!

Evolutionists have dogmatically insisted that pseudogenes are genes that were broken by mutation and are now useless. Some are now pleading with their colleagues to actually look at the data.

It always troubles me when I read other scientists who ignore the data in order to cling to their cherished dogmas. As a scientist, I know that this holds back the progress of science. As a result, I was heartened to read three scientist calling on their colleagues to abandon evolutionary dogma when it comes to pseudogenes. If others heed their call, we will most certainly learn more about DNA.

What am I talking about? Let’s start with what a pseudogene is. It is a region of DNA that looks like a known gene, but is different enough that it can’t do what the known gene does. As a result, it has become evolutionary dogma that pseudogenes are “broken” genes – genes that became non-functional due to duplication and mutation. Here, for example, is how the Encyclopedia of Genetics definitively describes a pseudogene:

A pseudogene is a nonfunctional genomic region that originated by duplication of, and is still homologous to, an ancestral gene.

In other words, a pseudogene is the result of a gene being copied and then broken. Creationists have long argued that pseudogenes are functional; they just don’t function the way evolutionists expect them to. The three authors of the paper I mentioned above have arrived at that same conclusion (at least for many pseudogenes), and they are asking their colleagues to pay attention to the data and do the same.

To emphasize the point that this evolution-inspired dogma is wrong, they list many pseudogenes that have been demonstrated to have an important function. They then make this important statement:

The examples of pseudogene function elaborated on here should not imply that pseudogene functionality is likely to be confined to isolated instances.

In other words, you can’t say that the known functional pseudogenes are exceptions to the rule. There are enough functional pseudogenes to call into question the assumption that they are mostly non-functional.

At the same time, however, these authors are cautious:

The purpose of this article is not to discard the pseudogene concept or to suggest that all pseudogenes are functional. The majority of currently annotated pseudogenes are neither robustly transcribed nor translated. Such regions fit well the original descriptions of pseudogenes as ‘similar, but defective’. Rather, we argue that their labelling as pseudogenes is not constructive for advancement of understanding of genome function and misdirects experimental design.

In other words, the authors are simply telling their colleagues to follow the data. Do not assume that a pseudogene is non-functional just because it has been identified as a pseudogene. Instead, investigate it to find out whether or not it actually is. The progress of science is hindered when you assume non-functionality because of the way the sequence has been identified.

I not only completely agree with that sentiment, I would also add this: following any dogma (evolutionist, creationist, or other) hinders the progress of science. Scientists should be willing to follow the data wherever they lead. Unfortunately, such scientists tend to be the exception, not the rule.

Are Hydroxychloroquine and Azithromycin Effective Against COVID-19?

Dr. Didier Raoult, French physician and microbiologist who thinks he has an effective treatment for COVID-19 (click for image source)
Two weeks ago I wrote about a possible treatment for COVID-19, the pandemic disease that is affecting most of our lives. It has been championed by French physician and microbiologist Dr. Didier Raoult. So far, he has written two papers about it (here and here). I was excited about his initial report, and I was hoping for a serious follow-up study. When I saw that he had written a second paper, I eagerly read it. Unfortunately, it wasn’t the serious study that I had hoped for. Nevertheless, it has gotten some media attention and seems to have influenced the FDA, so I decided to share my thoughts on it.

The results seem very exciting. He and his colleagues treated 80 patients with the malaria-fighting drug hydroxychloroquine and the antibiotic azithromycin. They note that they saw “clinical improvement” in 78 of them. One of the other two (an 86 year-old patient) died, and the other (a 74 year-old patient) was still in intensive care when the paper was written. While that sounds really good, there are a couple of “red flags” that make me hesitant to think that the treatment is as effective as it seems.

The first problem is that there is no control group. In a serious medical study, there needs to be a similar group of patents who do not receive the treatment. The treated group can be then measured against the untreated (control) group. Without that, it is very difficult to determine what the actual effect of the treatment is. Of course, I understand why there is no control group. Dr. Raoult wants to save lives. He thinks his treatment is effective, so he wants to give it to as many people as he can. He would have to “withhold” his life-saving treatment from some people so that he could have a control group, and that could lead to more deaths. I can understand why a physician would shudder at that idea.

However, the control group is important, because we really have no idea what would have happened to the 78 people who recovered had they not been given the treatment. While we still don’t know, the fatality rate of this disease is thought to be 1-2%. In 80 people, then, you would expect only one or two (0.8-1.6 to be precise) deaths, so this group of patients has the fatality outcome we expect had there been no treatment at all.

Now, of course, Dr. Raoult and his colleagues did more than just track whether or not the patients died. They tracked the amount of virus in each patient’s nasal cavity and found that the amount of virus dropped significantly for most of them. Once again, that sounds nice, but without a control group, we simply don’t know whether or not that was because of the treatment.

The second problem is the profile of patients who got the treatment. They mostly seemed to have a mild case of the disease. Only 15% had fever. Only 53% showed signs of lower respiratory tract infection. Worse, 5% showed no symptoms at all. Once again, it isn’t surprising that most of these patients recovered – most of them fit the profile of people who are expected to recover.

There is a third problem. A scientific study has been done in China with a control group. It is very small, and I can’t read it, since it is in Chinese. However, based on a Forbes article, the study had 30 patients. Half were given hydroxychloroquine, and half were not. That study showed no significant difference between the control group and the treatment group. Thus, if that study is correct, hydroxychloroquine is not an effective treatment for COVID-19.

Now, of course, that study didn’t include the antibiotic, so it’s possible that Dr. Raoult’s treatment is better than the treatment assessed by the study. It’s also possible that because of problems with the Chinese study’s design (small number of patients and no placebo, for example), the Chinese study is wrong. From a scientific point of view, then, we simply do not know whether or not Dr. Raoult’s treatment (or hydroxychloroquine by itself) is effective against COVID-19.

Nevertheless, the FDA has approved using hydroxychloroquine and other, similar drugs to treat COVID-19. This is probably a good plan, since the risks of using the drugs are low. However, until serious, controlled studies are done, we have no idea whether or not they are doing any good.

A Possible Treatment for COVID-19

A transmission electron microscope image of the coronavirus SARS-CoV-2. The spikes surrounding the virus make it look like a crown, which is where it gets its name. (click for credit)

While countries are scrambling to prevent the spread of COVID-19 (the disease caused by the new coronavirus), doctors are trying to find the best treatment for it. In three separate studies, a surprising candidate has been found: the anti-malarial drug chloroquine. In a letter that was published on February 19th, three Chinese scientists reported that more than 100 patients were given the drug. Based on the patients’ responses, they write:

…chloroquine phosphate is superior to the control treatment in inhibiting the exacerbation of pneumonia, improving lung imaging findings, promoting a virusnegative conversion, and shortening the disease course…

The authors also report that there were no adverse side effects noted in the patients.

A report in Spanish (translation here) concurs. It discusses both the results seen in patients and the results of experiments where primate cells are infected with the virus and then treated with chloroquine. The conclusion is as follows:

Chloroquine can both prevent and treat coronavirus in primate cells…According to South Korean and China human treatment guidelines, chloroquine is effective in treating COVID-19. Given chloroquine’s human safety profile and existence, it can be implemented today in the U.S., Europe and the rest of the world.

Finally, a study published in the journal Nature confirms that when primate cells are infected by the virus that causes COVID-19, both chloroquine and an antiviral drug known as remdesivir were effective at fighting it. The researchers state:

Our findings reveal that remdesivir and chloroquine are highly effective in the control of 2019-nCoV infection in vitro. Since these compounds have been used in human patients with a safety track record and shown to be effective against various ailments, we suggest that they should be assessed in human patients suffering from the novel coronavirus disease.

Now, of course, these studies are far from conclusive. However, I expect that doctors will judiciously test the treatment on patients who volunteer for it. Hopefully, that will allow us to learn more. Perhaps an effective treatment is on the horizon!

More Thoughts on the New Coronavirus

An infographic adapted from one produced by the CDC (click for larger version)

A few readers have sent me questions regarding the coronavirus that is spreading across the world, so I thought I would make a post answering those questions and providing some resources you can use to deal with the issue. Please note, however, that I am neither a medical doctor nor a biologist. As a result, I don’t claim any expertise on the matter. However, there are some misconceptions about the virus that are easily cleared up, and there are some facts that anyone who can understand the scientific literature should share.

First, a few facts. The term “coronavirus” refers to a very large group of viruses that circulate mostly among mammals and birds. However, some are able to infect people. Most coronaviruses that infect people produce mild illnesses, but some (like this one) produce potentially fatal ones. The coronavirus that is in the news right now is one that has not been seen before. This is not unusual. When an animal is infected with two different versions of the coronavirus, they can mix together, producing a new (usually called “novel”) coronavirus. This particular novel coronavirus has been charmingly named SARS-CoV-2, and it causes the disease referred to as COVID-19. Because of that, it is sometimes referred to as the “COVID-19 virus.”

The reason it has been given the name SARS-CoV-2 is that its genetic sequences indicate it is very similar to the virus that caused the SARS outbreak of 2003. Based on that sequence, it is thought that the virus originated in bats, but it might have passed through another animal (possibly a scaly anteater) before infecting people. Most importantly, there is strong evidence against the idea that it was genetically engineered. This is because the way it infects people is quite different from what would have been predicted given our current knowledge about these viruses. In other words, it is very hard to believe that anyone knowledgable enough to engineer a virus would purposefully make the genetic sequences that end up allowing the virus to be so good at infecting people.

The illness caused by this virus is flu-like, but it is much more serious than the flu. The death rate caused by the flu changes from year-to-year, depending on the strains that circulate. However, on average, the flu has a death rate of about 0.1%. That means for every 1,000 people who get the flu, 1 will die. Even though that is a low death rate, a lot of people get the flu. As a result, millions of people die from the flu every year. We don’t know the death rate for this new virus, since we don’t really know how many people have actually been infected, but the best estimate so far is that the death rate is about 2%. That means this virus is thought to be 20 times more deadly than the flu virus.

Second, the resources. The infographic above has been adapted from one that was produced by the CDC. The university at which I teach has asked all its professors to post this electronically as well as wherever students might be found. It is basic, but nevertheless, it does contain some helpful information. This link will take you to the latest information regarding where the virus has been detected, how many people have been infected, and how many people have died.

In general, the best way to avoid being infected by this virus is to avoid other people and avoid going to places where it has been found. The virus spreads most effectively when an infected person is within a few feet of an uninfected person. However, it might also be transferred by surfaces. If someone sneezes on a surface and someone else touches that surface, the virus can be transferred to the hand. Then, if that person touches his or her mouth, nose, or eyes, it is possible for the virus to begin an infection. Thus, you need to wash your hands a lot and avoid touching your eyes, nose, and mouth in between washings.

The most important thing to remember is that while the illness caused by this virus has a death rate that is thought to be about 2% on average, it is significantly higher for elderly people, people who are already sick with something else, and people with weakened immune systems. Thus, if you show any of the signs of the illness (fever, cough, shortness of breath) and think you might have been in contact with someone who has the virus, you should seek medical help.

While there are several groups working on a vaccine to prevent the spread of the virus, the earliest a vaccine could possibly be ready would be at least a year from now. My guess, given that I am anything but an expert about these things, is that it will not be needed. The disease seems to have already plateaued in China, and I expect other countries to be a bit better at reducing the spread. Thus, I expect that the spread of the disease will slow down significantly before a vaccine can be approved for use. I could easily be wrong about that, however.