On March 1st, my friend and colleague, Marissa Carter, PhD emailed me a graph of her COVID-19 infection rate model. After seeing it, I put my mother in quarantine the following week. Her model turned out to be far more accurate than the Harvard model (or other models) – so when she sends me an email with permission to share it, you can bet it’s worth reading.
The Origins of the COVID-19 Virus – and What it Means for Us
It’s Hardly Natural
From the first cases, many aspects about COVID-19 have baffled us. The COVID-19 virus is so distant from its coronavirus cousins it’s got its own clade (that is, a genetic tree). For a virus that supposedly jumped from a pangolin (or bat or other animal) to a human in the Wuhan wet market, it sure doesn’t behave like a new zoonotic virus. This virus has been fully-formed from the get-go with a transmissivity (R0) approaching that of measles, and pathological characteristics approaching that of HIV and H5N1 avian influenza combined. So, I’m going out on a limb to suggest that this virus is the result of many years of gain-of-function testing, including ADE (antibody-dependent enhancement) research, in a Chinese lab in Wuhan. Perhaps it got there by accident, and the person it infected didn’t even know he or she was infected…
Extraordinary claims require extraordinary evidence, so let’s get started.
Start by reading this account.
Here’s my commentary on the above analysis:
- What’s the first big takeaway? Efficiency of binding. “It turns out that sections of the Wuhan Strain’s ACE2 receptor’s genes are unique… The odds that this concordance was bio-engineered into the virus are several orders of magnitude more likely than for this to randomly have evolved in nature, and is exactly the sort of process used to make the H5N1 Bird Flu airborne and highly pathogenic.” (My emphasis.) In other words, we’ve just boosted the binding efficiency of the C19 virus to the human receptor angiotensin‐converting enzyme 2 (ACE2) for host cell entry by a massive amount and created some backdoor entries for the virus.
- Second big takeaway: The antibody-dependent enhancement (ADE) mechanism is bad news for us, because all those people in which mild infection occurred are not only susceptible but with a new infection would likely experience poor prognosis with a strong probability of mortality. Worse, if the virus hibernates, which is common in many other bugs, such as HIV (long-term), or short-term because of viral swarms, any such patient would be a ticking time bomb, for themselves and others they can infect. This would have horrible implications for future waves months and years down the road.
- Third big takeaway: Vaccine implications. If this bug is in fact an escaped engineered virus, developing a vaccine to it is going to require a bnAB approach. We all know how (un)successful HIV vaccine trials to date have been. Given that lack of success, we can also imagine how many years it might take to develop a vaccine to C19. It’s not going to be the 12-18 months time frame that’s been bandied about in the popular press.
Today, the Chinese government imposed severe censoring of all COVID-19 research coming out of China. Does the Chinese government know something we don’t?
Does all of this constitute a smoking gun on the origins of the C19 virus? Perhaps not, but it’s darned close. If it is true, we can only hope that whoever engineered this virus carried out the gain-of-function research thoroughly. Otherwise, the two common strains we are seeing now won’t be the last, either.
Marissa J Carter MA PhD MAPWCA
Strategic Solutions, Inc.
37 Voyager Lane, Bozeman, MT 59718, USA