(1) Are we going to shut down every time this many people start dying? Tons of people die from multiple illnesses every year.
No, we’re not going to shut down every time this many people start dying.
There are individuals that spend the entirety of their careers tracking infectious diseases. There are people that dedicate their time tracking existing known infectious pathogens and diseases, looking for mutations in known pathogens, and tracking disease patterns that may suggest new pathogens have entered the human landscape and could potentially affect the population at large. Those folks usually work and the national and international levels – they are telling us COVID-19 is different.
Let’s take a look at influenza.
According to CDC estimates, between 01-Oct-2019 and 28-Mar-2020, there have been a range of 24,000 – 63,000 influenza deaths in the United States. This is based on data that the CDC collects yearly and publishes on a weekly basis. If you’re so ever interested in looking at some of this data, you can go here (I’ve used this on previous flu studies I’ve worked on and continue to use it):
If influenza kills a lot of people every year, why is COVID-19 such a big deal? There’s a series of reasons: (1) This past flu season doesn’t seem to have had a novel/new stand of Influenza (there might be new strands that appear in the future that have the potential to become epidemic). SARV-CoV-2 (the virus that causes COVID-19) is novel/new coronavirus in humans. (2) We have a lot more influenza tests available and continuously work to make better tests. (3) We have an influenza vaccine. A new one is released every year based on what scientists think would be applicable for that season. One of the many reasons we track influenza, is because a new strand of influenza could appear in our landscape. Influenza could become pandemic, but it hasn’t in quite some time. (4) There are ways to manage and mitigate the symptoms of influenza (ie. Xofluza) and we’re constantly working on research to find more treatments. (5) Scientists think that COVID-19 is “deadlier” than influenza (Johns Hopkins Medicine, Coronavirus Disease 2019 vs. the Flu) (6) All the advances we’ve made in understanding (and tracking) influenza over the years, make it so that everyone in our population doesn’t get sick with the seasonal flu all at once. It happens over time, for a particular season.
I’d like to highlight that Seasonal Influenza and COVID-19 are caused by different kinds of viruses. There might be some similarity in the symptoms presented (though they are also distinct) , but they’re not caused by the same pathogen. Seasonal Influenza viruses and Coronaviruses are different. Below, I’ll be sharing some images of Seasonal Influenza Viruses vs Coronaviruses.
Long story short: If we had a vaccine or treatment against SARS-CoV-2 (the virus that causes COVID-19), chances are we’d see a smaller curve rather than the spike we’re seeing – the incidence rate in cases would likely look different over time. By people getting sick over time, hospitals wouldn’t be overburdened, scientists could continue to monitor the data, and research would continue. Unfortunately, to date, there is no vaccine nor any treatments for COVID-19 – just treatments that can mitigate the symptoms.
Also, in the future we should probably invest more into pandemic preparedness (governmentally, economically…a restructure of our healthcare system).
(2) Is this virus made in a lab?
Scientists don’t think so. Livescience published an article highlighting some of the reasons why scientists don’t think the virus is man-made (The coronavirus did not escape from a lab. Here’s how we know.) Additionally here’s a paper from Nature that may be of interest: The proximal origin of SARS-CoV-2. (For clarification SARS-CoV-2 is the virus that causes COVID-19, the disease).
Some highlighted items:
“Here’s why: SARS-CoV-2 is very closely related to the virus that causes severe acute respiratory syndrome (SARS), which fanned across the globe nearly 20 years ago. Scientists have studied how SARS-CoV differs from SARS-CoV-2 — with several key letter changes in the genetic code. Yet in computer simulations, the mutations in SARS-CoV-2 don’t seem to work very well at helping the virus bind to human cells. If scientists had deliberately engineered this virus, they wouldn’t have chosen mutations that computer models suggest won’t work. But it turns out, nature is smarter than scientists, and the novel coronavirus found a way to mutate that was better — and completely different— from anything scientists could have created, the study found.
Another nail in the “escaped from evil lab” theory? The overall molecular structure of this virus is distinct from the known coronaviruses and instead most closely resembles viruses found in bats and pangolins that had been little studied and never known to cause humans any harm.
“If someone were seeking to engineer a new coronavirus as a pathogen, they would have constructed it from the backbone of a virus known to cause illness,” according to a statement from Scripps.
Where did the virus come from? The research group came up with two possible scenarios for the origin of SARS-CoV-2 in humans. One scenario follows the origin stories for a few other recent coronaviruses that have wreaked havoc in human populations. In that scenario, we contracted the virus directly from an animal — civets in the case of SARS and camels in the case of Middle East respiratory syndrome (MERS). In the case of SARS-CoV-2, the researchers suggest that animal was a bat, which transmitted the virus to another intermediate animal (possibly a pangolin, some scientists have said) that brought the virus to humans.
In that possible scenario, the genetic features that make the new coronavirus so effective at infecting human cells (its pathogenic powers) would have been in place before hopping to humans.
In the other scenario, those pathogenic features would have evolved only after the virus jumped from its animal host to humans. Some coronaviruses that originated in pangolins have a “hook structure” (that receptor binding domain) similar to that of SARS-CoV-2. In that way, a pangolin either directly or indirectly passed its virus onto a human host. Then, once inside a human host, the virus could have evolved to have its other stealth feature — the cleavage site that lets it easily break into human cells. Once it developed that capacity, the researchers said, the coronavirus would be even more capable of spreading between people.” (Source)
(3) “Some treatments that scientists make cause cancer.”
First, cancer is a chronic illness rather than an infectious disease. There is no “one pathogen” we can point to that “causes it”.
I think the word “cause” is a very strong word to use when talking about cancer. A better way to refer to a carcinogenic agent, is by saying that the agent increases the likelihood of cancer in (insert population). This is because not everyone exposed to a carcinogenic agent will develop cancer. Cancer is super complex and there is no “one cause”.
In regards to “treatments causing cancer” – that’s a little bit of a stretch. I have a series of additional questions to statements such as the one written above. I need clarification – are we talking about potential treatments that are being tested in clinical trials or are we talking about treatments already in the market?
Since I don’t have that additional context, I can only explain the clinical trial process. When scientist have a new drug they think might be helpful in treating a disease, they have to submit an application to a regulatory body requesting to test the product. The regulatory body assesses the application, takes ethics into consideration, and then decides whether a new drug (or investigational product) should be tested in humans. The purpose of clinical trials is to observe and collect data on how a product behaves in humans. In clinical trials, they typically look at how toxic an agent may be, to determine the correct dose, how the human body metabolizes it, potential adverse events and effects, how it interacts with other medications an individual may be taking, how it affects individuals with a particular medical diagnosis, among other variables… there’s usually a ton of data collected. This data is collected because if the product appears to be promising and eventually makes it’s way into the market, the package insert for that particular product needs to have a warning with the potential “side effects” or what could potentially happen to individuals that take a particular treatment. Have you ever had a conversation with a doctor or pharmacist about the side effects you may experience from taking a medication? That information comes from data collected in clinical trials.
Now, if in the process of a clinical trial, a product is found to be toxic (the definition of toxic varies from product to product), then that trial will be closed down. No further testing will be conducted. This is why there is always an informed consent process in clinical research. So that someone getting involved knows what the potential risks and benefits are for using a particular investigational product (these risks/benefits vary from trial to trial). Clinical trials are not to be confused with clinical care. The clinical trial process is looking for treatments that can be potentially used for clinical care. It’s important to note that the products tested in clinical research are investigational -chances are not all of them will work, so the testing is looking for which ones might.
I won’t go into further details about how, often, in treating disease there is no “one cure” – it’s a bit more complex than that. Doctors/healthcare providers have to consider a multitude of factors before they treat a patient/recommend medications. For now, I think the point I’m trying to make here is that clinical trials are used to see how a product behaves in humans to see if it can be used in the context of clinical care.
Have a great weekend.