Notes on homicide laws MN vs MO in context of Derek Chauvin Trial

The Derek Chauvin Trial (related to use of force in the attempted arrest of George Floyd and his subsequent death in custody) has become bogged down in complex issues of criminal law, included the definitions of the different kinds of homicide in Minnesota (a National Review Article describes these issues and the timeline of changes to charges, motions, appeals).

Most lay people are unfamiliar with these areas of law or how they differ state-to-state. I was, myself, surprised at how Minnesota defines 3rd degree murder and that it is not a lesser-included offense to 2nd degree murder but rather has a different, specific purpose. In support of debate, this post contains the definitions of related offenses in Missouri with links to equivalent offenses in Minnesota. The reader is encouraged to flip through the links and compare, particularly looking at the placement of terms I emphasize such as knowingly, recklessly, negligently, etc., as these are exactly the terms upon which legal cases turn. For general background and definitions, I particularly recommend Samaha's "Criminal Law, 11th ed." which is targeted at lay (non-attorney) readers.

The notes themselves are copied from my own Evernote entry which I created for personal reference:

RSMO 565.021.  Second degree murder, penalty. — 1.  A person commits the offense of murder in the second degree if he or she:

  (1)  Knowingly causes the death of another person or, with the purpose of causing serious physical injury to another person, causes the death of another person; or

  (2)  Commits or attempts to commit any felony, and, in the perpetration or the attempted perpetration of such felony or in the flight from the perpetration or attempted perpetration of such felony, another person is killed as a result of the perpetration or attempted perpetration of such felony or immediate flight from the perpetration of such felony or attempted perpetration of such felony. [This is "Felony Murder".]

  2.  The offense of murder in the second degree is a class A felony, and the punishment for second degree murder shall be in addition to the punishment for commission of a related felony or attempted felony, other than murder or manslaughter.

...

[ In MN, the equivalent is 609.19 ( https://www.revisor.mn.gov/statutes/cite/609.19 )

RSMO 565.023.  Voluntary manslaughter, penalty — under influence of sudden passion, defendant's burden to inject. — 1.  A person commits the offense of voluntary manslaughter if he or she:

  (1)  Causes the death of another person under circumstances that would constitute murder in the second degree under subdivision (1) of subsection 1 of section 565.021, except that he or she caused the death under the influence of sudden passion arising from adequate cause; or

  (2)  Knowingly assists another in the commission of self-murder.

  2.  The defendant shall have the burden of injecting the issue of influence of sudden passion arising from adequate cause under subdivision (1) of subsection 1 of this section.

  3.  The offense of voluntary manslaughter is a class B felony.

[MN equivalent is 609.20 ( https://www.revisor.mn.gov/statutes/cite/609.20 )]

RSMO 565.024.  Involuntary manslaughter, first degree, penalty. — 1.  A person commits the offense of involuntary manslaughter in the first degree if he or she recklessly causes the death of another person.

  2.  The offense of involuntary manslaughter in the first degree is a class C felony, unless the victim is intentionally targeted as a law enforcement officer, as defined in section 556.061, or the victim is targeted because he or she is a relative within the second degree of consanguinity or affinity to a law enforcement officer, in which case it is a class B felony.

RSMO 565.027.  Involuntary manslaughter, second degree, penalty. — 1.  A person commits the offense of involuntary manslaughter in the second degree if he or she acts with criminal negligence to cause the death of any person.

  2.  The offense of involuntary manslaughter in the second degree is a class E felony, unless the victim is intentionally targeted as a law enforcement officer, as defined in section 556.061, or the victim is targeted because he or she is a relative within the second degree of consanguinity or affinity to a law enforcement officer, in which case it is a class D felony.

[MN has only one Involuntary Manslaughter offense, 609.205 ( https://www.revisor.mn.gov/statutes/cite/609.205 )]

(MN) 609.195 MURDER IN THE THIRD DEGREE.

(a) Whoever, without intent to effect the death of any person, causes the death of another by perpetrating an act eminently dangerous to others and evincing a depraved mind, without regard for human life, is guilty of murder in the third degree and may be sentenced to imprisonment for not more than 25 years. [This is referred to as "Depraved Indifference Homicide"; we do not appear to have this in Missouri law.]

(b) Whoever, without intent to cause death, proximately causes the death of a human being by, directly or indirectly, unlawfully selling, giving away, bartering, delivering, exchanging, distributing, or administering a controlled substance classified in Schedule I or II, is guilty of murder in the third degree and may be sentenced to imprisonment for not more than 25 years or to payment of a fine of not more than $40,000, or both.

Missouri, Lesser-Included Offense:

565.029.  Lesser degree offenses in homicide cases — instruction on lesser offenses, when. — 1.  With the exceptions provided in subsection 3 of this section and subsection 3 of section 565.021, section 556.046 shall be used for the purpose of consideration of lesser offenses by the trier in all homicide cases.

  2.  The following lists shall comprise, in the order listed, the lesser degree offenses:

  (1)  The lesser degree offenses of murder in the first degree are:

  (a)  Murder in the second degree under subdivisions (1) and (2) of subsection 1 of section 565.021;

  (b)  Voluntary manslaughter under subdivision (1) of subsection 1 of section 565.023;

  (c)  Involuntary manslaughter in the first degree; and

  (d)  Involuntary manslaughter in the second degree;

  (2)  The lesser degree offenses of murder in the second degree are:

  (a)  Voluntary manslaughter under subdivision (1) of subsection 1 of section 565.023;

  (b)  Involuntary manslaughter in the first degree; and

  (c)  Involuntary manslaughter in the second degree.

  3.  No instruction on a lesser included offense shall be submitted unless requested by one of the parties or the court.

Minnesota Lesser-Included Offense:

609.04 CONVICTION OF LESSER OFFENSE.

Subdivision 1.Lesser offense prosecution.

Upon prosecution for a crime, the actor may be convicted of either the crime charged or an included offense, but not both. An included offense may be any of the following:

(1) a lesser degree of the same crime; or

(2) an attempt to commit the crime charged; or

(3) an attempt to commit a lesser degree of the same crime; or

(4) a crime necessarily proved if the crime charged were proved; or

(5) a petty misdemeanor necessarily proved if the misdemeanor charge were proved.

Subd. 2.Conviction; bar to prosecution. A conviction or acquittal of a crime is a bar to further prosecution of any included offense, or other degree of the same crime.

EO Threatens Schools Who Will Not Let Men in Women's Sports

I wonder why it is so hard for people to grasp the simple concept that men do not belong in women's sports? That this discriminates against women who fought hard to have these sports in the first place? Why willful indifference to girls like Selina Soule who are displaced by men unable to compete in male sports?

<<The conservative Alliance Defending Freedom has filed a federal complaint on behalf of a Connecticut high school student, Selina Soule, who failed to quality for the New England regionals after losing a race to two biological male students who identify as girls.

“In fact, one of the athletes who displaced Selina previously competed against other male athletes in the winter 2018 season and failed to advance in boys’ indoor track events,” the ADF said. “It wasn’t until that athlete began competing in girls’ events during the 2018 spring season that the dominance began. This biological male now holds more than 10 records within the state of Connecticut that once belonged to 10 different girls.”>>

If Biden carries out his threat to cut federal funding for schools who do not go with him off the cliff, we, as a state, should take him up on it, and for better reasons than this: after being incompetently thrashed around first by No Child Left Behind then by Common Core, it is clear that the federal behemoth-- and the large corporate curriculum cartel it feeds-- having too much influence on education is bad for our children no matter who is in the Oval Office, no matter who is in Congress. DC Republicans have often been just as eager to expand federal power over our schools, especially when it expands budgets for corporate handouts. At exactly the time that more and more education resources become ubiquitous, low-cost, or even free, inpouring of federal money and the imprimatur  of thoroughly-captured standards boards has lead to inflation of education costs and consolidation of vendors.

This Biden EO is just the latest symptom of a deeper problem both parties created. If we do not have control of our own children's education, we will always be held hostage to corporate profiteering or misplaced ideological rubbish imposed from the top.

This is just one more place where it is past time Missouri minded its own business... and told others to mind theirs.

Capitol Riot Officer-Involved Shooting

This page will organize a set of sources and commentary on the Officer-Involved Shooting during the 2021 US Capitol Riots on 6 January in which Alisha Babbitt was killed. The intent here is to have these sources and links in one place for ease of discussion and debate, including analysis of police use of force involved by myself or by others. Gathering sources will come first and commentary will be added later. It will need to be reorganized as I go.

Version 0.4: 15 January 2021 (Added a number of links including more videos and more background on Babbitt.)

Disclaimer: This page and any commentary on it is my own and not an official statement of any organization. There are clearly both political and non-political issues here (or, at least, some issues which should not be political). A subset of these issues, those dealing with use-of-force and the shoot/no-shot decision separated (as much as possible) from the political context, will be discussed using these sources at the 11 January meeting of the Lawrence County Sheriff's Auxiliary. This page, however, does not represent that discussion. The use of force analysis will almost certainly have to change over time in any case as more information is known, so no such analysis could be definitive at this time. Clearly, the videos linked here are going to contain graphic content and this discussion will be of a violent subject: if you do not wish to be exposed to such content, do not continue.

What Are the Questions?

Let's start out with a decent framing of the questions. LegalInsurrection does a decent job in "Video of Shooting Death of Ashli Babbitt Raises Questions About Use of Deadly Force". Deciding on major questions (and dispensing with less useful questions) should guide inquiry and gathering of sources. The primary issues I am interested in here are:

* Was the individual officer's use of force correctly made and justified?

* Who actually made the choice? Was it the individual officer or did he act in response to an order given? Or was the choice part of a mission parameter/rule of engagement? (e.g. "Do not fire unless the barrier is breached, but do not permit protesters to enter this lobby.")

* Why was the officer who made the shoot/no-shoot decision put in the position of having to make that choice? In other words, were other failures made in the larger response which might have prevented the necessity of fatal confrontation. Potential "lessons learned" are crucial for security planning in future events in this crazy political climate.

* What larger liability might apply to others involved in illegal activity (i.e. the Felony Murder question)

* What were the actual and perceived physical threats presented by Babbitt and the larger incident?

Questions which I do not feel are terribly useful:

* Was what Babbitt did wrong/illegal? The answer to this question is rather obvious and there can be little doubt that climbing a broken barricade was not a lawful or peacable act. The further intentions of the deceased cannot be gauged and, as she is deceased, there is no question of further punishment.

* Did Babbitt "deserve to die"? This is often too ill-defined a question to answer and too wrapped up in political/ideological perceptions. It is clear that her act was willful, illegal, and dangerous. There is no reason to suppose that she was unaware that her actions were risky and might lead to injury or death. Nor does answering such a question change the fact that she did, in fact, die whether she "deserved it" or not.

Videos of the Shooting

Information on the Capitol Riots is frequently taken down. There is no guarantee that the following sources will continue to exist indefinitely. Please inform me of broken links in comments (or better sources) and I will attempt to fix them. The video of the incident itself are crucial for looking at use-of-force questions.

Heavy.com commentary with Twitter link to the original Sulivan video: https://heavy.com/news/ashli-babbitt-video-capitol-shooting/ This video is the first one widely shared but shows little context and it is not easy to get a sense of the space around the incident. The LegalInsurrection link above also has the same video.

Two videos with commentary by the Washington Post showing a different viewpoint than the Sullivan video and more context before the shooting: (MSN link) This link also contains a map of the Capitol showing the area of interest.

 

Bell?ngCat's "The Journey of Ashli Babbit" has several video links in one place, including a link to a YouTube video which combines and sinks four videos into one. 

TheResistance has a 44-minute video showing the entire progression from entry into the Capitol to the Officer-Involved Shooting.

The question of the shoot/no-shoot decision is more complicated than justification. There is also a larger safety question involved. Training and policy typically dictates discharging a weapon only with a clear target and clean background. As can be seen from these videos, the "background" to the shot was quite complicated and rapidly changing, something which may be hard for people to appreciate if they have not stood behind a gun (in training or a live incident) and had to try to make such a decision. To the left of the barrier (facing into the lobby, opposite to the shooter's perspective) were more protesters and people filming (whether or not 'protesters'). To Babbitt's right were Capitol Police staging on the descending stairwell. Behind the doors in the lobby were more Capitol Police and officials sheltering. Behind the frontline of protesters were other protesters who may not have presented an immediate threat and, seemingly, other police. Any weapon discharge might potentially hit friendly, neutral, or unknown targets. It is possible that the shooter had (or perceived) a background which was only momentarily clean, while Babbitt was elevated above others and before she made it into the lobby proper. Only at that moment (arguably) could a round aimed at Babbitt at an upward angle avoid striking others. This may have determined the timing of the shot; any additional video or information to this question may be very important.

Legal Commentary

The question of whether what Ashli Babbitt did was illegal is clear (it was not) and moot (she is dead and therefore there is no point in charging her with a crime). The incident has larger implications for the use-of-force inquiry into the shooting and the potential charges for others who were present. This section will gather some relevant commentary as I find it.

A discussion of Felony Murder  in the context of the Capitol Riot and the death of Ashli Babbitt. Includes definition of Felony Murder, references DC statutes, and looks through the circumstances of her death in that light.

Ashli Babbitt

Some background on Ashli Babbitt from Heavy.com and NYPost. Also some (limited) information about past charges for property damage and a restraining order. Bell?ngCat has a detailed article, "The Journey of Ashli Babbitt" describing the chnages in political views over time from Obama supporter to Trump supporter to QAnon.

John Sullivan

Sullivan is a controversial individual because he recorded the first widely-distributed video of Ashli Babbitt's death while standing in the Capitol nearby. Sullivan is not a Trump Supporter (nor does he appear to be a member of Antifa) but from Insurgence USA, an organization for "racial justice and police reform" who is decidedly anti-Trump. So, ineveitably, the question arises: what was he doing in the Capitol and what were his motives? This link from PJ-Media includes a number of other links discussing this question and the more general question of who might or might not have been associated with Antifa. It also includes a video of Trump Supporters stopping someone who is (claimed to be) Antifa from breaking into a Capitol window. It is clear, therefore that the situation may have been complex and more research is needed on who was there, why they were there, and just what they thought they were doing.

Tea Time: What is a crumpet, anyway?

Tea and crumpets. It is a phrase many of us have heard, conjuring images of steaming Earl Grey served in porcelain cups and overstuffed armed chairs. But what is a crumpet? Recently, I dug up a recipe and made a batch.

 

Crumpet rings, tea is whistlin'; On the cake, butter's glistening. We're humming a song as we munch along...

A "crumpet" is a griddle cake, something like a cross between a pancake and an English muffin. Unlike a pancake, crumpets are yeast-risen and fluffy, big foamy bubbles form the "nooks and crannies" that absorb plenty of warm butter and jam. Crumpets are grilled on one side only at first and toasted before serving. They are an old English tradition, going back in some form for centuries, first fomally mentioned by the Bible translator, John Wycliffe, in the 14th century and later described in closer to the their current form by Elizabeth Raffald in "The Experienced English Housekeeper" in the 18th century [Oxford Online Reference Library].

The ready-to-cook batter is much too soft to stand on its own while cooking, so the crumpets are formed in metal rings, crumpet rings. Good crumpet rings are stainless steel and double-rolled to present a smooth, easy-to-clean surface for consistent crumpet extraction. Most people don't have them, however, and it's not like you can just pick them up at an typical American store. Canning jar lids are not at all ideal, but they do (mostly) work. (They probably offend some deep-seated English taboo, so exercise caution. I have no idea how a Brit would resond to them being served with hot coffee, either...)

My crumpet adventure started with a recipe from the Daring Gourmet. I was with the in-laws and made a double batch. I did not double the salt. So, the ingredients list ended up being:

• 4 cups of flour, sifted. Half of this was recently ground, half store-bought because I ran out of fresh.
  
• 1 teaspoon salt
• 2 cups warm milk
• 2 tablespoons active dry yeast
• 2 teaspoons sugar
• 2 cups warm water
• 1 teaspoon baking soda

As instructed in that recipe, the batter is made in two stages, first making and rising a spongy dough, then beating in more liquid and resting for 30 minutes. The recipe specifically states not to worry about beating all of the lumps out when mixing the batter: you want some variation in texture. The rising process is very important to getting the big bubbles in the batter (you can see this in my picture of crumpets on the griddle). On this particular day, my wife was also baking, so the area was nicely warm for the rising and it doubled in size fairly quickly. Your mileage may vary. Proof your yeast and go by actual rising, not the clock-time.

The rings are necessary to get the batter to stand up enough to get decently-thick crumpets. The canning jar lids are not ideal and take some fiddling. I used a mix of narrow and wide mouth rings because that is what my inlaws had in the cupboard. I found that it was best to fill them 2/3rds full with batter on the hot, greased griddle. Preheat the griddle until a droplet of water dances. The crumpets expand when cooking and will overflow if the ring is overfilled. The crumpets are flatter and kindof crispy when underfilled. They have a pleasant, yeasty aroma while cooking.

Grease the rings well! I used cooking spray, again, because it was what I had on hand. When the rings were not greased well, underfilled or overfilled, I suffered Crumpet Extraction Failure (CEF). I had to force the cooked crumpet out and then had to try to quickly scrub and regrease the ring for the next batch. This was a substantial pain-in-the-you-know-what. When the rings were filled correctly and greased well, the crumpets dropped right out, even with the threads in the rings. When you are still learning, you probably want to have a large stock of clean rings handy, preferably the wide-mouth ones. That way, when CEF occurs, you can just set it aside temporarily and grab a clean ring.

The Crumpet Extraction Falure (CEF) condition. Avoid this. Have spare rings in case you do not avoid it.

Since some of the crumpets were to be served right away, I toasted them right on the hot griddle after everything was done. Turn up the heat a bit for proper toasting. The crumpets made with wide-mouth rings fit in a slot toaster, the small ones not safely. In civilized places, crumpets are supposed to be served cut in half (half-moons, not sliced like English muffins!). Again, this worked well for the larger rings, not so well for the smaller. The crumpets were slathered with butter and optionally homemade strawberry jam or honey, served with tea. They were a big hit with our teenage daughter who is now angling for me to make more.

The doubled recipe made 30 crumpets of mixed sizes. I found that the leftovers were best stored in brown paper because they were otherwise retaining too much moisture.

Some people do all kinds of unnatural things with crumpets, including topping with ham and cheese, curry, etc. Diehards stick to butter and jam or honey. Or just butter.

Exocytosis, Stage Left: Coronavirus strategies for spreading infection

On a cellular biology level, learning about SARS-CoV-2 opens up a micro-world of epic struggles: stealth and trickery, strategem and counter, adaptation and (usually) survival. This is an early stab at the fifth panel for the redo of Bat Soup: the Graphic Novel in which we attempt to teach really tough biology concepts in a fun way. In this panel, we show the strange ways the virus spreads itself once it successfully enters the cell, takes over its machinery, and  forces the ribosome to start transcribing its proteins to make copies. When I have it where I want it, I will do the final copy on an 11"x14" Bristol Board where I will able to get finer detail with a less cluttered layout.

Endocytosis: In previous panels, we show the dastardly virus using a disguise to evade the immune system to successfully approach the cell. Its spike protein is initially rotated downward and harder for the immune system to recognize. The virus makes use of a host pro-protein such as furin to properly align the spike protein at the S1/S2 boundary so it can activate the ACE2 receptor to make entry into the cell (endocytosis).

Snippet from Panel 1

Infiltration and Replication: Once inside, the coronavirus then makes further use of existing human proteins such as cathepsin to unpack its payload and start transcription of its own proteins encoded in its RNA genome. At about 30,000 basepairs, these SARS coronavirus are among the largest and most complex RNA genomes known. So, now that the virus has taken over the cell's fabrication facility, a fleet of new virus particles is being constructed!

So what happens next? Most (lay) descriptions of viral replication just say that the virus causes the cell membrane to rupture so it can surge forth and infect more cells. With most viruses, there is more to it than that and, anyway, with the SARS viruses, particularly SARS-CoV-2 it takes a very different path-- mediated by the "non-structural proteins" in its complex genome which is only partly understood. Programmed cell death, "Apoptosis", does likely happen, but the virus has already spread by then and it is done for a much more cunning reason (which we'll get to in Panel 6).

In the meantime, though, in Panel 5: the viral horde is unleashed.

Bat Soup, the Graphic Novel, Panel 5 concept sketch

The Endoplasmic Reticulum: A long time ago in a galaxy far away when I tutored Cell Biology to make a little side money for college, the Endoplasmic Reticulum and the viral transcription process was something most people seemed to have trouble with. It's extraordinarily complicated, and we are still learning. But I always found it helped to picture it like an WWII-era industrial complex, tiers of concrete and banks of windows (some of them are broken out) rising, the ribosomes stuck to the sides. This is the Rough ER, where the magic of protein synthesis and folding happens. I then picture the Smooth ER, where lipid synthesis happens (the stuff that makes cell membranes, among other things), as rising stacks because they are round and smooth like chimneys or pipes. The nucleus is a walled-complex just beyond the factory.

This is the structure the virus has taken over. The ribosomes start decoding RNA sequences: cytosine, guanine, adenine, and uracil, and stringing together chains of amino acids, the building blocks of proteins. But finished proteins aren't just strings of amino acids (AAs), they are complex 3D structures. The Endoplasmic Reticulum is where those chains of AAs are folded into completed structures like enzymes or hormones... or the shell of a new virus particle.

Exocytosis: Once the viral structure is fabricated, the replicated RNA strand is placed inside and the whole assembled inside smooth-walled vesicles small bubbles inside the cell which are made out of pieces stolen from the Endoplasmic Reticulum. The result is little packets of virus-laden food service condiment packets (extra spicey!) being arrayed inside the cell. But the virus does not have to burst the cell open to escape. At the command of virus-provided S-proteins, pores form in the surface of the cell and merge with the smooth-walled vesicles, pouring virus into the intercellular space (the spike protein once more disguised) where they can find more cells to infect. This is "exocytosis".

Synctium: But, this virus has another trick for avoiding the immune system, particularly deep in the lungs: it doesn't have to leave the cell to spread. The hostage cell starts leaking S-proteins into the intercellular fluid. The S-proteins cause the cell membranes of nearby cells to merge together. Long multinucleated cells called "synctium" start to form which share the same cytoplasm-- and the same viral infection! As we will see in future panels, the cell, including these multi-nucleates mega-cells, can end up dying several different ways.

This cycle of formation of mega-cells, their destruction, and the body's attempt to heal and regrow tissue is a big reason the virus can cause such massive tissue damage and scarring inside lung tissue. The immune response often makes the situation even worse. Understanding how it works and why some people get away with minimal damage may be a key to effective treatment of severe cases.

Bat Soup, the Graphic Novel - How SARS-CoV-2 enters a cell

Holy pandemics Batman, it's a graphic novel!

Today we get a quick dose of microbiology and an explanation of how Bat Soup, 2019-nCoV, SARS-CoV2, (whatever you wish to call it, see a note about disease names at the bottom!), gains access to a cell and starts to infect a human host.

The more basic information people know about this disease, the more tools they have to interpret the news reports (which are often very poorly done by people who know no more than you do). This gives you a chance to make rational decisions, maybe understand what to fear and what not to. My background is described at the top of the Bat Soup for the Soul: Teaching with Coronavirus article I wrote previously.

This particular virus uses a vulnerability in the Angiotensin Conversion Enzyme 2 (ACE2) found in many human cells and, in particular, epithelial cells (lining) in the lower lung. This is the same receptor used by SARS-CoV, but quite different from MERS-CoV, the common flu, etc.

Note here that there are plant compounds or "phytochemicals" which also bind weakly to this receptor and may inhibit (temporarily block) viral activity. Host receptor blockage by phytochemicals or synthetic compounds is a hot area of antiviral research. The object, of course, is to find something which inhibits the virus without itself causing damage to humans. There are actually a substantial number of naturally-produced compounds which might do the trick with COVID-19. None have been clinically proven yet, though a few had some potential effect in studies with the original SARS outbreak in 2004 or show antiviral activity in vitro (in a test tube) or an animal model.

 

 

The coronavirus really does look a bit like a hairy ball (that is where it gets its name), but I have used a tiny bit of artistic license here.

 

The ACE2 receptor is part of the Renin-Angiotensin System, or RAS. The RAS regulates a number of important body functions, including respiration, heart rate, blood pressure, and kidney function.  Some of you make take medications which target angiotensin or the ACE (Angiotensin Conversion Enzyme, part of a set of related functions with ACE2). These medications, called ACE inhibitors, may cause or indicate potential complications for Bat Soup, but this is still being researched. In any case, the virus, in addition to hijacking the cell for its own purpose, causes collateral damage to the RAS and complications throughout the body of the human host.

 

After gaining entry into the cell and using its own machinery to replicate, the cell dies and releases more virus particles to spread further. The human body has mechanisms to try to detect and destroy these hijacked cells before they release a virus cargo (also used to fight tumors) a cytokine called TNF (Tumor Necrosis Factor). When the immune system overreacts, cytokine's go crazy attacking everything in site, causing cell damage, inflammation, viral pneumonia, etc. in what is referred to as a "cytokine storm". It is though by many researchers that the cytokine storm may be triggered as a tactic by the virus, like causing a large-scale riot to cover up a break-in in a particular building. The chaos caused by the cytokine storm permits further and faster infection and may become deadly in its own right but is very hard for modern medicine to treat.

This is, of course, a very simple attempt at explaining a complex topic. More references are included below for the adventurous reader to explore further.

References

• Buhner, S. H. (2013). Herbal Antivirals: Natrual Remedies For Emerging and Resistant Viral Infections (e-book). Massachusetts: Storrey Publishing. Retrieved from https://www.scribd.com/book/176719013/Herbal-Antivirals-Natural-Remedies-for-Emerging-Resistant-Viral-Infections
• Includes an in-depth section on SARS, the ACE2 receptor, and potential phytochemicals, including sources, studies, and preparations. Extremely in-depth material, but the best one-stop source for plant compound antiviral activity, research, and practice.
• Chen, H., & Du, Q. (2020). Potential natural compounds for preventing 2019-nCoV infection Hansen. Preprints.Org, (January). Retrieved from https://www.preprints.org/manuscript/202001.0358/v1/download
• Wan, Y., Shang, J., Graham, R., Baric, R. S., & Li, F. (2020). Receptor recognition by novel coronavirus from Wuhan: An analysis based on decade-long structural studies of SARS. Journal of Virology, (January). https://doi.org/10.1128/JVI.00127-20
• Bat Soup for the Soul: Teaching with Coronavirus describes disease models and spread statistics to the non-epidemiologist with graphical illustration.
• The Confusing World of Disease Mortality Statistics in Simple Numbers

If you want to learn more about the general mechanisms of viruses (e.g. influenza), there is an excellent online Virology 101 course/podcast with plenty of diagrams and examples (free).

An Explanation of Names

When it was originally discovered, this virus, which was found to belong to the general family of the coronavirus, was simply labelled 2019-nCoV or "2019 novel coronavirus", novel, here, meaning simply previously unknown and poorly understood. As more about the virus was learned, it was renamed to SARS-CoV-2, formally signifying that it was closely related (but not identical to) the SARS outbreak of 2003-2004. The disease the virus causes is called COVID-19 (Coronavirus disease of 2019).

The two names can be a little confusing, but it is similar to HIV/AIDS: the human immunodeficiency virus (HIV) causes AIDS. Most of the time, the names can be used interchangeably unless you wish to make it clear that you specifically mean either the virus itself or its disease in humans. "Coronavirus" is often an acceptable shorthand as long as it is clear that it potentially refers to more than one virus which affect both humans and animals.

I started using the nickname "Bat Soup" before a formal name had been decided on, based on the urban myth (almost certainly not true) that the original victims got the virus from eating undercooked bat soup. In any case, this tiny virus has put many people in "deep soup".

The Confusing World of Disease Mortality Statistics in Simple Numbers

2b/~2b: 'How Many?' is the question!

There is a lot of confusion and debate over mortality figures for novel coronavirus (COVID-19, formerly 2019-nCoV). Most people see the numbers but do not understand how they are derived and therefore may be confused on how to compare numbers from different outbreaks or even the same outbreak on different days or different sources.

As discussed in my previous article, "Bat Soup for the Soul: Teaching with Coronavirus", the simple answer to how deadly this new virus is is that it is a good deal less deadly than SARS-CoV was and a good bit more deadly than the seasonal flu (but affects somewhat different age-groups--- out of scope for this article). At the same time, it is markedly more transmissible than SARS was and somewhat less transmissible than the flu. So, bottom line is that it does less damage on an individual basis than SARS but already has affected many more individuals (and continues to do so). Similarly, it is likely to spread less effectively than the flu but hurt more of the people it does infect (especially the elderly).

[Version 1.1 20200311: corrected typo in equation. Thank you CEMV!]

Less Deadly Is Not Always 'Good'

In general, we often see that less deadly diseases spread faster for the simple reason that people who get quickly and desperately sick do not tend to want to run around and spread disease! When someone has only mild symptoms or takes longer to get sick, they have opportunities to pass the infection to more people. But let us take a quick look at how the mortality figure is derived and why estimates may differ very sharply. We will walk through the math but with deliberately very simple numbers to start:

Let's say you have an outbreak with 20 people infected. At the time we measure, there are 5 fatalities, 5 serious cases, 5 recovered cases, and 5 mild cases. What is the fatality rate?

The quick answer is to divide 5 fatalities by 20 total cases for 25%:

5/20 = 0.25 = 25%

This is more or less the type of number often published for COVID-19. At this moment, using Johns Hopkins' tracker, you get:

4,373 deaths / 121,564 total cases = 0.35981047 or 3.6%

Don't put ANY stock in that specific number because it will be different by the time you read this. If you take this number at different times over the outbreak, the number varies somewhat, and the numbers published by various clinicians or regional authorities vary a great deal because they are taking numbers from their specific populations. Depending on what numbers you use, you can get anywhere from 0.7% to almost 8%, for instance, from different phases of the outbreak in China (according to WHO's report on the Joint Mission to China at the end of February).

OK, so why are people arguing about this? Why are some people saying the number is "wrong" or "likely wrong".

Well, there are a couple of issues with using this number reflexively.

 

Crude Mortality versus Completed Cases

First, the number is subtly wrong from the way most people think of the probability of dying from a disease. The number above is really what is often referred to as "crude mortality" because it includes uncompleted cases. What does that mean?

In our first set of numbers, we have 10 people, 5 serious cases and 5 mild cases, who have neither recovered nor died (yet). Presumably, they will do one or the other eventually. When looking at past epidemics, like the final numbers for the SARS outbreak in 2004, every case is completed because no one is still walking around actively infected with SARS-CoV-1! So let's fix the number by only including completed cases:

5 deaths / (5 deaths + 5 recovered) = 0.5 = 50% (!)

Ten people total in our example have either died or recovered, so that goes on the bottom. With the other ten people we simply do not know (yet) what will happen. Hopefully that makes sense so far. Mortality calculated from completed cases will tend to be higher for an active outbreak versus a past outbreak, so one must take some care comparing typical actively reported numbers versus historical. But it takes time during an outbreak to get statistically meaningful numbers of recovered cases, so crude mortality is usually what you get.

To take real coronavirus numbers further, we get:

4,373 deaths / (4,373 + 66,239) =  0.061929984 or 6.2%

This is usually what people are really thinking of when they ask "If I am in fact infected, what is my chance of dying once the disease runs its course?" As you can see, it is worse than the crude mortality frequently published. If only two of the serious cases later die and the rest recover, you will see yet a different (lower) number. But wait...

How Many People Actually Get the Disease?

The number you get is clearly heavily influenced by the number of cases of infection you use in the first place. Is this number "correct"? Well, probably not, and how much it is off is a matter of great debate. What happens if you are "infected" but have a mild case (or maybe do not even notice) and never get tested? You won't be included in the numbers at all. Going back to our simple example, if we say that the mild cases are simply never noticed, we get:

5 deaths / 15 cases = 0.333... or 33%

This number is higher than our initial 25%, but we know it does not actually reflect reality. So, let us say that instead of 121,564 cases of COVID-19 world-wide (the confirmed case count from above), we actually have one mild or asymptomatic case for each confirmed case, someone running around who may think they merely have a cold or whatever. Then we get:

4,373 deaths / 121,564*2 total cases =0.1798641 or 1.8%

Well, that looks better, doesn't it? This is the kind of thing you will see in many estimates of COVID-19 mortality, depending on what they use as their guess of how many mild or asymptomatic cases there are. In theory, the unknowns could affect the death count as well (two of the confirmed cases in Washington state were diagnosed postmortem), but we tend to be a bit better at noticing when someone actually keels over as opposed to when they just have a sniffle for a day or two.

Getting Actual Numbers

So, how does one figure out which number is the "correct" number to use for actual cases? How do you account for what you do not know?

Well, people guess from various disease models based on past outbreaks or on detailed numbers from one part of an outbreak. But the tried-and-true method is to swab and test everything that moves throughout a community (at least on a random sample basis) to find out how many people running around have the disease but have not actually showed up at a hospital. China, after a very rough beginning, has started to do this and, as a result, their case-counts, while initially sketchy, are a great deal more reliable. They did actually find unreported cases lurking around the community, mild cases, cases mistaken for something else, people afraid to report, etc., but not that many. South Korea has also done extensive testing around their outbreak (and, interestingly enough, their mortality figures are closer to 0.7%, at the low end of what China found).

The US has done very little of this at all and has suffered from a chronic shortage of test kits. Numbers for our domestic outbreaks (and consequently, estimates of mortality in the US) are therefore extremely poor. Presumably, if we actually had the foggiest clue how many people were infected, our mortality figures would be much lower than they appear. But we just do not know--- and cannot until the test kits catch up, which they are starting to do as of this writing on 11 March.

Be aware, then, if you use global case-counts and deaths, you are getting a mixed bag of both good data and bad data. That results in a number which--- well, it isn't wrong, it is a calculation, and it is what it is, but--- may not be very reliable from predicting the future. Using numbers from countries or regions we know have better data may give better results, but then you have to ask yourself whether the results China gets in their health system or South Korea in theirs will apply equally to the US population and our health system. Roughly, perhaps, but never exactly. HIV spread very differently in European populations than in African populations to what turns out to have been a genetic leftover from bubonic plague: that stuff happens and is inherently unpredictable.

Conclusion

So, what then? What conclusion can we solidly make?

Well, we come back to the beginning: "a good deal less deadly than SARS-CoV was and a good bit more deadly than the seasonal flu". (And, by the way, this virus seems to leave (most) children (<20 years) alone, and that is rather interesting, isn't it?)