If I needed a tool, no, make it a multi-tool; something that has a knife, a can-opener, a saw, a file, a screw driver, and a small pair of pliers, I would choose furin. Only, this furin multi-tool works in the body in many different places doing many different things. And boy what a job it does. It is a special protein which is a member of a family of proteins called convertases also called endoproteases. They look like very different kinds of multi tools on a hardware store wall. An important point to remember is that a multitool has to be folded in one way for each job.
The problem with understanding furin is the way it has been discussed in the public press in semi-conspiratorial tones which totally miss the significance of this protein. Furin is an “off-topic” for most of the so-called main stream media. Even those scientists who point to it for its possible central role in Covid-19, still do not take the full round trip with this most mysterious and interesting protein. A multi-functional protein like this rapidly generates more questions than answers. Can we say we truly understanding the structure and function of this protein? Or are there features we still do not know about? The reality is that there is much much more to learn about furin.
Perhaps the best analogy is to think of the many complex proteins in your body as also having on-off switches. Furin is able to turn on otherwise non-functional proteins THROUGHOUT the body. That’s the clue, that’s the problem, that is what scientists should be studying very closely.
Why is furin important for Covid-19? The short answer is that Covid-19 cannot infect without furin. At least one paper from March 2020 acknowledged the peculiarity of furin in Covid-19. The link for the article includes the list of papers citing this paper since its publication. There are 424 subsequent citations in a year. That is a huge number. Very few papers get that many citations in a year. Yet, there is little discussion about the implications of furin in Covid-19. This article introduces the subject, and there will be follow-up.
Also, why is this furin site seen in other viruses such as HIV, and not corona viruses? It seems odd, something is out of place. Since it is not on other corona viruses, what is it doing there? The suggestion, no matter how sophisticated, no matter how much it relies on computer analysis and simulation, it is a huge stretch to suggest that you can create a functioning furin site through mutation and evolution. An underlying assumption is that furin is the resulting mutation most fit for functioning in a completely different virus. That too sounds like a stretch.
Some researchers have commented that furin on the spike protein seems out of place. One analogy is that a reading of a musical score. The general sequencing of coronaviruses reads like a collection of classical music pieces. But reading Covid-19 is like suddenly have some blues or rock and roll music interjected.
Another broad argument is that covid 19 is a chimeric virus. This is a more difficult argument because viruses normally mix and match different genes and gene variations, while remaining species specific.
To pose the question another way, could covid 19 work without furin. Research suggests not. But, then, how do other viruses infect in a similar manner without relying on furin? Furin’s basic role is to activate other kinds of proteins.
Covid-19 is said to bind to a cell surface receptor called ACE -2 (angiotensin converting enzyme-2). Furin presumably embeds the very tip of the spike protein. Again, furin is distributed throughout the body. So, furin is not unique to just viruses or spike proteins. Another point not adequately addressed is that furin may bind to receptors other than ACE-2. Given it’s nearly ubiquitous functions, that should not be surprising to know.
The suggestion that some sequence of viral mutations led to the identical recreation of furin in just the right spot on the spike protein is like saying you got damn lucky in Las Vegas, Damn Lucky.
In the next article we will explore the mathematics of a simple feedback model for mutation trending towards a certain function.
The more complex question involves being able to argue for a “furinome” in the body. Furin for internal cellular processes, furin for cell surface activities, furin for viral infectivity, furin for functionalization of otherwise inactive protein toxins, and possibly tumor progression. That is quite a disparate range of activities. It may also help explain the complex and inconsistent symptoms in whom the effects of Covid-19 linger.