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Varying progressions of SARS-CoV-2 infection
Host immune response and the severity of disease
About SARS-Cov-2 / COVID-19
COVID-19 is the name of the serious condition caused by infection of the SARS-CoV-2 coronavirus, an infection which has spread extensively enough for it to be called out as a pandemic by the World Health Organisation. The virus itself is novel in terms of being an entirely unfamiliar virus both to science and to the human immune system, both of which make it extremely challenging to control.
This is made worse by the fact that the virusis highly infectious - significantly more so than the original SARS-CoV-1 of 2003. Despite this virus killing many more so far than that original SARS infection, it is actually almost certainly much less lethal (although the actual case fatality ratio (CFR) will not be able to be calculated with any confidence for some time). Unfortunately this lower fatality is more than outweighed by its higher infectivity which is why the death toll continues to rise across five continents, already causing devastation for health services in Europe and North America, and now particularly threatening those countries with weaker health systems which it may well overwhelm.
How COVID-19 differs from TB
On the face of it there are some very obvious differences between the two pathogens.
TB is one of mankind’s oldest infectious foes, while SARS-CoV-2 is its newest.
One is a mycobacterium; the other is a coronavirus.
Current scholarship reckons that TB originated in humans and then passed to animals (as zoonotic or bovine TB), while the coronavirus originated in animal hosts (almost certainly from horseshoe bats) and has recently passed to humans.
One works painfully slowly; the other painfully fast.
One has a treatment that in most cases should still be effective; the other currently has none.
One is reckoned to be lethal if untreated in 50-70% of cases; the other in 0.5-4%.
One still regularly kills nearly 2 million each year (meaning that since the year 2000 at least 40 million lives have been prematurely lost to it); the other so far this year has killed at least 200,000 (though this number will inevitably rise further and this year’s total will end up being much higher).
One is numerically mankind’s most lethal infectious foe; the other isn’t (at least not yet…).
The modest but necessary budgets set by the global community for defeating TB are still being massively missed; the battle to defeat the coronavirus, meanwhile, is currently being bankrolled to the tune of possibly trillions of dollars.
This is a thought-provoking list of differences – but there are also some interesting similarities. Here are six which we think are significant because they particularly inform our thinking in relation to moxa:
Both diseases favour targeting the lungs but can also affect other organs catastrophically.
Successful control of both diseases depends on robust health infrastructures and widespread testing.
Despite one disease being so old and familiar and the other so new, the interaction between both pathogens and the human innate and adaptive immune systems are still not fully understood.
Developing effective vaccines to protect against both diseases is unquestionably extremely difficult.
Both are known to be able to sometimes re-infect those who have been confirmed as having recovered from it which threatens any goal of eradication of either.
And it seems that the most probable critical factor disposing towards a favourable outcome to an infection from either disease is a healthy functioning immune system.
These are important issues and each one, actually, directly relates to the critical issue of the host immune system.
Varying progressions of SARS-CoV-2 infection
The progression of a SARS-Cov-2 infection is highly variable. In the vast majority of cases the infection is defined as 'mild' - meaning that the symptoms may be barely noticed or may just result in a 'flu-like episode. In a minority of cases, however, the symptoms are severe enough to require hospitalisation, a significant proportion of whom require ventilation, around half of whom are currently dying, often from organ failure.
So what might determine this huge difference in the course of an infection? One thing, the WHO reports, is the relative size of the initial infection (which may explain why some otherwise healthy doctors and nurses on the front line sometimes succumb so catastrophically). The other factor the WHO identifies, is the quality and quantity of the host immune response to the infection.
Host immune response and the severity of disease
With this novel infection the body’s immune system recognises an invasive pathogen that is completely unfamiliar to it and (having done so) tries to deal with it as best it can - which is basically sub-optimally in comparison to a more familiar infectious pathogen which normally infects our species. If the immune system itself is already sub-optimal, however, this can make a big difference.
The WHO currently reckons that it does this by a combined process - firstly by developing specific antibodies which bind with the virus and disable it, and secondly by activating T-cells to destroy the host’s own cells which are already infected with the virus. Furthermore, the WHO suggests that there appears to be a complex balance between these two complementary actions which may well not just affect the severity of an infection and the quality of the recovery, but also the risk of reinfection.
Here's exactly what the WHO say about this:
“Most … studies show that people who have recovered from infection have antibodies to the Coronavirus. However, some of these people have very low levels of neutralizing antibodies in their blood, suggesting that cellular immunity [i.e. the T-cell response] may also be critical for recovery".
Can moxa help prevent serious SARS-CoV-2 disease?
Although the complexities of this disease are still far from understood, it is very clear that weaker immune systems make for increased vulnerability to severe life-threatening disease. In other words, a stronger immune system should reduce the risk of serious disease. Given our clinical experiences in Moxafrica we have good reason to believe that moxa may help bolster this host defence.
We published a blog on exactly this in the early stages of this pandemic, suggesting that moxa might help bolster the immune system and help reduce the risk of a life-threatening infection. A few more weeks of monitoring this disease has only increased our conviction that moxa really could help in several ways but, we need to explain what evidence we have to suggest this.
We originally found a fair amount of scientific reports (mostly in Japanese) that moxa can provoke a response in the immune system though for many reasons we’ve found it difficult to make totally coherent sense of it all. We’ve spent years attempting to clarify this and have written on it elsewhere.[i] But much more importantly we’ve also helped reveal primary research data suggesting that moxa may be able to protect people against infection from another infectious pathogen (drug-resistant tuberculosis), evidence that it both helps to prevent TB infections and also helps recoveries from MDR-TB after infection. What’s critical in respect of this coronaavirus is that we’re as certain as we can be that it does this by provoking a broad and low-level strengthening of the host immune system.
What’s also important is that all of this research has taken place where resources are poor (i.e. where it’s difficult to both diagnose or treat MDR-TB) – which, it must be said, is practically speaking generally the case currently with COVID-19.
So how might moxa help?
We’re still cautious about casually invoking similarities between host immune responses that are specific to TB and to COVID-19 especially since we've already identified some significant differences between them. So how sure can we be that moxa might help protect us if the disease spreads in the way many now fear that it will?
The truth is that we can’t be, but we’re also certain that it won’t harm as long as some simple rules are adhered to because moxa has been used for centuries and has a track record both of safety and ease of application. We can also add (and we want to stress this) that moxa appears to have a broad-spectrum low-level cumulative strengthening effect on the host immune system so doesn’t throw things wildly out of balance whilst developing effect. We are now satisfied that this effect works with a slow-burning disease like TB after an initial infection, although we recognise that we can’t be anywhere near so confident about how much it might help with a much faster-moving viral infection like COVID-19 (especially once the infection has developed into an acute phase and become dangerously symptomatic). But nevertheless our experiences have prompted us to ask some potentially important questions.
Might it help reduce the risk of initial infection? Or indeed (if this has failed, and infection does occur) might it help prevent the disease from progressing into a much more dangerous and life-threatening state? And perhaps more interestingly still, might it reduce the risk of relapse or reinfection?
Let’s take a look at both of these questions in turn.
General moxa when quarantining
Whether self-imposed or imposed by national authorities, quarantining is a logical and effective way of reducing a local epidemic. It also reduces individual risks of being infected and infecting others. Quarantines, or lock-downs, are put in place because there’s a known infectious pathogen stalking the neighbourhood (and they are being used now throughout the world) or because there’s a risk that you may already be infected and you might pass it on to anyone else.
Being quarantined, whether as a community or individually, can be scary. Currently the WHO recommendation if it's thought that you might be infected is that you should hole up for at least two weeks and wait it out to see if symptoms develop.
In such scenarios, whether holed up or locked down, doing anything that might potentially fortify your immune system would certainly seem to be a good idea. It makes sense to protect yourself as best you can against a dangerous infection that is out there in your neighbourhood (and you’ll be back out there again soon yourself); and you would obviously want to do all you can to minimise the risk that, if you are already infected and you do develop the symptoms, they turn out to be as mild as possible.
Potentials for preventing primary infections
Whilst it seems to be agreed that the virus initially starts infecting cells and replicating in the respiratory tract, no-one yet seems to have a clear picture of how most initial transmission of this new disease occurs - whether it’s mainly through inhalation, whether through digestion (by touching contaminated surfaces and then touching the mouth) - or any other route. Nor is there yet a clear picture about how exposed you actually need to be to the virus for a symptomatic infection to take root. (All routes for transmission are probably highly susceptible to environmental factors anyway, and there are existing highly variable reports of the virus’s infectious potential).
But what is already clear is that not everyone who is exposed to the virus ends up with active symptomatic disease (or even a measurable infection) and, given that this is a novel virus, this can’t be because some of us harbour existing sensitised antibodies that might instantly trigger immune cells to act against it and so stop an infection developing. It must be because of a less specific immune response (probably made by the ‘innate’ immune system).
We therefore suggest that those who’ve not developed the disease after exposure have done so because their existing innate immune system is somehow strong or broad-based enough to provide sufficient protection against this novel virus to prevent it replicating or creating havoc. (This is hardly a controversial idea – otherwise humanity would have died out a long time ago from the sorts of novel plagues that have intermittently appeared in previous centuries). So if moxa can fortify a host immune response, then maybe it really could help at this stage of infection. But we should immediately qualify this: not only are we not so sure about moxa’s impact on this more basic ‘innate’ part of the immune system, we also know that fortifying immunity with moxa is not a quick fix. The effects build slowly so expecting a quick protective effect from it against a fast-moving virus like COVID-19 is being too optimistic. Taking a longer-term perspective, however, (and this virus looks like it may be around for months if not years) then we think it could possibly help reduce the risk of a primary infection with long-term use.
Might moxa reduce the risk of an infection progressing into its more dangerous life-threatening phase?
This seems to be reasonable to suggest because those who contract the disease but only develop a milder form of it probably do so because their existing ‘adaptive’ immune systems are relatively stronger than those whose infection develops more seriously. This hypothesis is supported by existing reports that those who most often succumb to the disease appear to have existing lower adaptive immunity (i.e. the elderly and diabetics, etc.).
So, more so than in answering the first question, we suggest that regular moxa could fortify this adaptive immune system sufficiently to reduce the risk of more serious disease developing, potentially reducing occurrences of symptoms requiring hospitalisations and potentially leading to deaths.
Might moxa help prevent reinfections or relapses?
It's been reported that this disease has re-emerged in some cases who had already been defined as having recovered from a first infection; so might moxa help prevent the disease from re-emerging (whether it be by re-infection or relapse) if this phenomenon were found to be increasingly common as the pandemic continues and the number of recovered cases increases?
When we published our original blog we could only say that it seemed to be a reasonable question to consider - but that we knew far too little to say more on this. With the benefit of monitoring a further seven weeks of an unravelling pandemic, however, we now think that we can say a bit more.
The World Health Organization (WHO) is currently overseeing the global response to the coronavirus across the world (much as it has been continuously doing with the response to TB to date since its founding in 1948), and their recent statement on the interaction of the host immune system with the coronavirus has alarmed us.
This is not just because they are being cautious about any effective treatment or vaccine for the disease emerging soon – it’s because (as we'll see below) their statement is clear that there is still not enough substantial evidence for anyone to believe that people who’ve been infected and then recovered from Coronavirus can’t be re-infected by it.
This means that, unless an effective vaccine is developed (or the virus weakens) this virus could end up recirculating in the wider global community, whittling down those most vulnerable to it year-on-year as it does so. Thankfully we should also remember that the vast majority of infections are mild anyway so this certainly isn’t the Black Death. But if immunity acquired from an infection is difficult for an immune system to achieve, then it also means that developing any vaccine that has any long-term protection could be very difficult indeed.
Here is the statement the WHO made about the role of the immune system, including a critical final sentence about the risk of reinfection.
“Most … studies show that people who have recovered from infection have antibodies to the Coronavirus.” So far so good, but then they go on to qualify this as follows: “However, some of these people have very low levels of neutralizing antibodies in their blood, suggesting that cellular immunity [i.e. the T-cell response] may also be critical for recovery. As of 24 April 2020, no study has evaluated whether the presence of antibodies to SARS-CoV-2 confers immunity to subsequent infection by this virus in humans.”
The language used appears to be deliberately cautious but is also specific.
What appears to be suggested is that, if this combined response (of antibodies and a cellular immune response from the adaptive immune system) is broad, balanced and strong enough, it could provide sufficient resistance to recurrence of infection. Certainly so far only a small proportion of reinfections have been recorded but the WHO is equally clear that there are not enough studies available on the amount of neutralising antibodies after a patient’s recovery from Coronavirus to claim that presence of these antibodies alone are key to preventing reinfection anyway. In fact, the WHO have officially warned that the issuing of Immunity Passports based on positive antibody tests (something that many countries have been considering) could actually lead to continuation of transmission, so it would appear that they even consider it unlikely.
There is certainly already worrying evidence of reinfections (so far at least from Japan, China and South Korea, though none yet from Europe at the time of writing). These involve patients who have twice tested negative to the disease (and thus are defined as ‘recovered’) who then re-present with symptoms and test positive. It has been argued that this may happen because of false testing, or because of variabilities in virus shedding during what can be a lengthy recovery period, but there is clearly more to this or the WHO would have worded their statement otherwise.
In South Korea, for instance, there have so far been over 200 cases of reinfections reported with the number still rising – currently amounting to nearly 2% of ‘recovered’ cases. But a much higher proportion was identified in Guangdong in China where in one hospital 14% of patients who had recovered from the coronavirus still showed signs of it in later check-ups. These discharged patients were not showing renewed symptoms incidentally, and the tests were done from anal swabs, a method not widely used elsewhere, so the story is not exactly the same as the Korean, but it is still concerning.
Of course, all of these cases may not be reinfections anyway. They may rather be evidence of the virus never having been completely cleared by the immune response and thus constitute relapses. We can point out here that for us this has a certain resonance with the status of a latent (sub-clinical) infection with tuberculosis, where the mycobacterium lurks within the body (in the lungs generally) waiting for an opportunity to reactivate, often doing so when the immune system is weakened by other factors. It also resonates with the fact that with TB there are also many instances of relapses and reinfections because infection with the mycobacterium also does not necessarily confer long-term immunity, especially when immune systems are weak.
Adding further perspective on the potential of using moxa to preserve health
Unfortunately, we have to accept that too little is yet known about this new disease for us to be definite. No pharmaceutical treatment has yet been approved globally, and in fact the best treatment for it to date has been social distancing which is about as basic and low-tech as any public health response can get.
Whilst fully accepting that we cannot offer anything definitive, we still wonder whether we have something important and appropriate to add to this discourse, simply because of our decade of experience trying to tease out the historical reports of moxa’s usefulness in treating TB in Japan before any effective drugs were developed (i.e. in a similar situation to where we are with the coronavirus right now). This is because further clinical testing has led us to conclude, not just that moxa appears to help promote recoveries from TB (including from drug-resistant disease), but also that it appears to prevent reactivation of a latent infection into a potentially lethal acute phase. What’s more, we’re as certain as we can be that this occurs through moxa provoking a broad-spectrum low-dosed immune response that can be effective in controlling the replication of the pathogen.
So could it do the same with this pernicious new virus, by helping mediate the immune system to control it – specifically supporting promotion of those T-cells that the WHO reckon may be critical when antibody response is inadequate to prevent reinfection? (And might it also help in preventing a SARS-CoV-2 infection from becoming an acute COVID-19 condition in the first place?)
Both possibilities exist.
Which acupoints do we recommend using?
We are recommending carefully self-administering moxa on a daily basis at least for as long as this virus is around. Our preference is to use St36 and LI10, though we check out LI11 and LI4 for comparative tenderness as well and may use that instead on some days. There is more information on this here.
Why do we recommend daily moxa?
We recommend this simply because it is safe, and we strongly suspect that it may help control the severity of any SARS-CoV-2 infection (i.e. reduce the risk of it becoming a raging COVID-19 condition), or (if someone is already infected or believe that they may have been infected if there are no tests available) that it will help control the progress of disease. Finally, if someone knows or believes that they have been infected and recovered, then we believe that moxa may help prevent relapse from any possible surviving sub-clinical infection, or help prevent any further exogenous infection. In respect of all these three cases, doing daily moxa and maintaining good lifestyle choices is the nearest we expect to get to any sort of safe and effective vaccine in the next year and maybe longer.
Some specific and important caveats
1. We’re only talking here about small cone direct moxa, because that’s what we have harvested specific evidence for. This is the smouldering of tiny 1mg rice-sized cones of refined moxa on specific acupoints. (There are a lot of different methods of using moxa, and the fact is that we simply don’t have evidence for the other methods to make any claims about them – and, as importantly, we also know that this particular method is safe, quick to complete and effective.)
2. We are also sure that this simple therapy is best done on a daily basis (in other words enabling the slow low-level cumulative effect of the moxa to have the best chance of taking effect) and because of this we think that it should be begun as soon as possible and then continued daily.
3. There are few contraindications for moxa therapy when small cones are used, but common sense should nevertheless be applied, particularly if other health conditions already exist (so-called ‘co-morbidities’). Unfortunately, such co-morbidities are being reported to add to the risk of serious acute COVID-19 disease needing hospitalisation, so (like everything) careful weighing of risk may be important. We suggest that common sense should answer this quandry: if there are signs that any other condition that already exists might be getting worse, then moxa should be stopped and reviewed. Otherwise, proceed and let the effect develop.
We should add here, however, that if your immune system is severely compromised (by diabetes, for instance, or by HIV/AIDS) that moxa should be begun and continued more carefully being particularly careful of any signs of blistering, starting with only one or two cones on each point and monitoring accordingly.
4. Furthermore we do NOT recommend using moxa at all if there are any signs of a fever. In other words, if there are any signs that COVID-19 disease is provoking a high temperature in an acute phase, then moxa should be held back.
5. We also fully recognise that there are many other ways to help protect ourselves from this infectious pathogen, and recommend paying careful attention to any other suggestions emanating from either global authorities or other more local health providers. (We will certainly be doing this ourselves).
Moxafrica’s own evidence for recommending the use of moxa for preventing severity of disease
We have collaborated in clinical research on moxa for TB with partners in both Uganda and North Korea which have incrementally revealed evidence of improved recoveries with moxa used alongside existing treatments.
One study, however, particularly looked at preventing reactivation of TB disease from latency using moxa. The North Korean Ministry of Public Health compared daily moxa against daily drug therapy with isoniazid (which is the most widely used drug that’s approved for preventing TB in such cases), and the daily moxa compared well against the drug. The key finding here in respect of moxa for preventing COVID-19 was that they also reported a ‘positive trend’ of increased lymphocytes in the patients who used moxa suggesting that a moxa-provoked immune response was the mechanism at work.
This report didn’t just suggest that the effect was because of a generalised immune response in other words – it suggested that the immune response from the moxa includes a proportional increase in a component of white blood cells which are specifically useful for defending the body against viruses (including unfamiliar ones). This is one of the things that lymphocytes are known to do. So, while TB may be a bacteria and COVID-19 is a virus, we suggest that this is suggestive evidence that daily moxa might still help defend us against this new pathogen.
We also have to accept that we’ll have no immediate opportunity to access any better data on this to support our suggestions while this pandemic runs its course. We also suggest (as is the norm) that, if you can, you should consult a fully qualified medical practitioner before embarking on this therapy (although most physicians outside of East Asia will know nothing about it at all). Furthermore in lockdowns the simple act of consulting doctors may be very challenging.
In any case, our own research has taken us to corners of our world where such access is a luxury - which was one of the things that drew us to researching moxa in the first place (because we could see how appropriate it might be because of its simplicity and adaptability).
Sadly we are also acutely aware that for half of humanity the idea that either the technical diagnostics for this viral disease or the appropriate intensive care for acute cases infected by it will simply be unavailable. Ass such, the potential for this virus to create real problems for millions of vulnerable people is real, as is the potential for the virus to spread at scale in such under-resourced communities.
The ‘strengthen your immune system with moxa’ manual
Please feel free to download this manual, specifically recommending how you can support and strengthen your immune system with moxa. The manual is free to download, although we ask for donations to help support the Moxafrica charity. We also require that its contents are not distributed for any profitable purpose, but are happy if it is shared as widely as possible.
[i] We published the results of our research in two parts in the European Journal of Oriental Medicine in 2008 & 2009. This journal is unfortunately not published online, but links to each edition's contents can be found at: