In order for any virus to cause human disease it has to enter a cell – a lung cell, say – replicate, then leave the cell and go on to infect other cells: one viral particle enters, replicates ~1 million times, and each of those replicated particles attack other cells. The cycle continues and when enough of our cells are infected by the virus you get sick. And you stay sick until either your immune system makes enough antibodies to kill the pathogen or, if you’re lucky, there’s an anti-viral medicine you can take that kills it.
But what if, instead of attacking the virus on the backend of the disease process, you could prevent the virus from entering the cell in the first place?
The trick is to know what the viruses port of entry is and to somehow shut it down. With the coronavirus, we’ve known for some time that it docks at a protein port of entry called ACE2 (Angiotensin Converting Enzyme 2) that dots the surface of cells that line the mouth, airways and intestines, among others.
Researchers at the Univ. of Lethbridge in Canada (Igor Kovalchuk, MD, PhD, pictured above) have been studying the effects of cannabis on cancer since 2015. When they heard about coronavirus disease they reexamined their work to see if they had anything that might be of some help. And “Serendipitously, we noted that cannabis may also affect ACE2,” they said in their paper published last month.
So they designed a study that asked the question: Can high-CBD cannabis extracts be used to reduce the number of ACE2 protein receptors on the surface of cells that the coronavirus targets? In other words, can you reduce the number of viral ports of entry – the number of receptors – and thereby reduce the number of viral particles that get into the cell?
Answer: Yes, you can. The Lethbridge group found that select strains of high-CBD cannabis “significantly” reduced the number of ACE2 receptors on cells in the mouth, airways and intestines. As they told CTV News: “Cannabinoids decrease the number of [ACE2 receptors] by … 70 per cent, so it means the level of entry will be restricted. So, therefore, you have more chance to fight it.”
This “is a novel and crucial finding,” say the researchers. Importantly, their work could apply to other viruses as well:
Our results lay a foundation for further in-depth analysis of the effects of C. sativa on … COVID-19, as well as other viral diseases in which viruses use the ACE2 receptor as a molecular gateway.
And because the cells targeted by the coronavirus are quite accessible – in the mouth, airways and intestines – the researchers want to develop inexpensive and easy-to-use CBD-infused mouthwash, inhalers, oils and capsules for both clinic and at-home treatment.
As promising as all this is, the scientists point out a number of limitations with their work:
The results are strain specific. The Lethbridge team has developed over 800 different lines of cannabis and found that 13 of the 18 they tested lowered ACE2 levels to varying degrees. In other words, you can’t do this at home as there’s zero chance your local cannabis store will have one of the successfully tested strains.
Second, the high-CBD extracts were tested on human mouth, airway and intestinal tissue grown in the lab. This is SOP in medical research but only a necessary first step; animal and human studies need to follow.
Third, the CBD extracts were applied to the tissues to mimic applications by mouthwash, inhalers, oils, and capsules, but not – and this is crucial – application by smoking. In fact, the researchers caution that since “tobacco smoking increases ACE2 levels and exacerbates clinical outcomes of COVID-19, the effects of cannabis smoking on the levels of ACE2 expression should be carefully investigated” (italics added).
Notwithstanding the limitations the Lethbridge scientists are understandably elated: “We were totally stunned at first, and then we were really happy,” they told CTV News.
Here’s a brief video of the coronavirus-ACE2 docking complex. It references another therapeutic strategy, essentially putting ‘chewing gum’ on the coronavirus spike proteins so it can’t dock at the ACE2 receptor: