SARS-CoV-2 Archive -

Dr Robert Hess: Long Covid After Vaccination

Dr Robert Hess – 03/23/2022

Dr Robert Hess: Long Covid After Vaccination

In rare cases, coronavirus vaccines may cause Long Covid–like symptoms.

As mentioned the symptomatology of this condition can be very similar to the side-effects and possible long-term consequences of vaccination. While preliminary data suggests that getting yourself vaccinated significantly reduces your risk of succumbing to Long Covid, there have also been cases where vaccination has caused Long Covid-like symptoms – and for a lengthy period of time.

We always take a balanced view, so that our clients are optimally informed and can weigh up the available information accordingly. There are no official figures, nor have there been any large-scale studies on this phenomenon as yet, but the symptoms, the link to vaccination and the accounts given by those affected are currently being investigated by the National Institute of Health (NIH) and other researchers around the world.

Previous studies have been too limited in scope and have not allowed 100% conclusions to be drawn about whether any of the vaccines have caused some rare form of long-term health problem and, if so, by what mechanism.

Long Covid-like symptoms such as fatigue, brain fog, insomnia, headaches, blood pressure fluctuations and various others are currently being investigated for a possible link to the administration of a COVID-19 vaccine. A number of scientists and research institutes are looking into this matter, among them neuroimmunologist Avindra Nath, clinical director of the Neurological Diseases Institute of the U.S. National Institutes of Health (NIH). In the specialist journal Science, he posited “temporal associations” between vaccination and Long Covid symptoms, but he would not be drawn on whether there was an “etiological association” (i.e. a causative link). Studies conducted by Nath on around 30 case reports have so far remained unpublished, but publication is expected soon.

Much remains unclear about Long Covid, especially the cause of its non-specific symptoms. It is broadly assumed that there is an underlying persistent immune dysregulation, in other words a defective immune response. Some candidates for further research are beta-interferons, immunoglobulins, mini blood clots and autoantibodies.

The Science article also explores the role of autoantibodies – their importance is recognized not only in acute CoV infection, but also in Long Covid. According to recent studies, autoantibodies can be detected up to six months after infection, and as Harald Prüss, a neurologist at the German Center for Neurodegenerative Diseases (DZNE) and at the Charité Hospital in Berlin, writes in an as yet unpublished paper, they are capable of damaging brain tissue.

Experiments on animals have suggested that antibodies targeting the SARS-CoV-2 spike protein – the same protein that many vaccines use to trigger a protective immune response – could cause collateral damage. While searching for antibody therapies for COVID-19 in 2020, Harald Prüss and his colleagues discovered that, of the 18 antibodies they identified with strong efficacy against SARS-CoV-2, four also attacked healthy tissue in mice – an indication that they could trigger autoimmune problems.

Initial clinical data point in a similar direction. Last year, researchers testing people infected with SARS-CoV-2 found unusually high levels of autoantibodies, which can attack the body’s own cells and tissues. In the May 2021 issue of Nature magazine, immunologists Aaron Ring and Akiko Iwasaki and their colleagues at the Yale School of Medicine reported finding autoantibodies in acute COVID-19 patients that were targeting the immune system and brain. They are now investigating how long the autoantibodies persist and the extent to which they can damage tissues. In January of this year, Cedars-Sinai Medical Center cardiologist Susan Cheng and protein chemist Justyna Fert-Bober reported in the Journal of Translational Medicine that autoantibodies can still be present up to six months after infection, although the researchers did not link their persistence to long-term symptoms.

To find out whether such autoantibodies harm humans, scientists at the German Center for Neurodegenerative Diseases (DZNE) are testing cerebrospinal fluid from Long Covid patients for antibodies that react to brain tissue obtained from mice: if there is indeed a reaction, these antibodies could also attack human neural tissue. Prüss and his team have published a paper in which they describe finding autoantibodies in at least one third of these patients, which are capable of attacking mouse neurons and other brain cells.

In August 2021, a group at Northwestern University reported in an advance publication that, in patients with neurological complications after COVID-19, a subset of T cells is persistently activated, similar to how it would be in persistent SARS-CoV-2 infection, suggesting an aberrant immune response or a lingering virus.

Scientists investigating possible side-effects are faced with a dilemma: their work risks stoking opposition to vaccines that currently seem to be “safe and effective” (this statement cannot be made with 100% certainty. After all, we have only been vaccinating for about 2 years and we are therefore rather cautious with these statements). “You have to be very careful about associating COVID-19 vaccines with complications,” Nath cautions. “People can draw the wrong conclusions. The implications are enormous.” Complex and persistent symptoms like those experienced by most sufferers are even more difficult to study, because patients often don’t have a clear diagnosis.

At the same time, understanding these problems could help those who currently suffer from them and, if a link is found, help in the development of the next generation of vaccines, perhaps identifying the ones that pose a high risk of serious adverse events. “We shouldn’t be averse to adverse events,” is how William Murphy, an immunologist at the University of California, sums it up. In November 2021, he suggested in The New England Journal of Medicine that an autoimmune mechanism triggered by the SARS-CoV-2 spike protein could explain not only the Long Covid symptoms but also some rare vaccine side-effects, and he called for more basic research to investigate possible links. He also maintains that it is more important to reassure the public that everything is being done in research to understand vaccines than to just say everything is safe, an assertion that we also endorse.

In the meantime, many affected people feel they have been let down by the health care system. The issue is sadly neglected, poorly defined and also politically sensitive, so family doctors and hospitals have not yet taken any initiatives. Many would like to see a network of specialist outpatient clinics for people with Long Covid and Long Covid-like symptoms, sharing their knowledge and experience.

Long Covid symptomatology after vaccination seems to be rare so far. Nevertheless, this is a topic that needs to remain in focus and be subjected to greater in-depth investigation. Overall, there are still too many unknowns and therefore there are currently no approved and effective therapies on the market. Nevertheless, we are able to take preventive action. We have already adapted our prophylactic measures in this regard, and we will also revise our supplements. We are one step ahead in this regard and we have put together effective options exclusively for our clients.

If you have any questions about Long Covid or specific symptoms, please do not hesitate to contact your consultant. We will continue to monitor this issue closely and to update our knowledge.

Dr Robert Hess: Managing the Covid-19 aftermath

Dr Robert Hess – 03/07/2022

Dr Robert Hess: Managing the Covid-19 aftermath: Detox of the spike-protein.

Two full years after the pandemic began, it is now time to consider our next moves. In order to maintain a clear overview, I placed great emphasis on accurate documentation and ongoing information exchange right from the start. This meticulous approach, together with insights from science and research findings, enabled us to make precisely tailored recommendations for our clients. In the last few weeks and months, we have been gathering up loose ends and shifting our focus to appropriate preventive measures as well as preparations for the aftermath of the Covid-19 pandemic. In addition to shortening test intervals and adapting diagnostic methods, we will now also review the composition of our supplements to ensure that they are likewise optimally adjusted to the individual pandemic-related circumstances of our clients.

The focus of our prophylactic supplement program and of the measures we are taking for the COVID-19 aftermath is primarily on the spike protein. The spike protein, which is not only a component of the SARS-CoV-2 virus but also produced in our bodies as a result of vaccination, can circulate in our bodies and damage cells, tissues and organs. It is our view that “detoxing” the body of spike proteins as soon as possible after infection or vaccination can protect against damage from residual or circulating spike proteins. Various international committees have been drawing up guidelines and collating information on how to remove viral and vaccine-induced spike proteins from the body. The lists of herbal medicines and dietary supplements together with the information on them were compiled in collaboration with international physicians, scientists and health practitioners.

COVID-19 infection, COVID-19 vaccines and spike protein damage are all relatively new phenomena, so the guidelines have been based on established and recent medical research as well as the clinical experience of international physicians. The respective guidelines will be updated on an ongoing basis as new knowledge and findings emerge. We will review the guidelines, herbal medicines and dietary supplements, as well as other measures and, as appropriate, incorporate them into our program and adapt them individually for our clients.

What exactly is the spike protein?
The SARS-CoV-2 virus first identified in Wuhan has spike protein on its surface. The spike protein is also found in all SARS-CoV-2 variants. In a natural infection, the spike protein is the component of the virus that allows it to enter the cells of your body. One region of the protein, called S2, binds the viral envelope to the cell membrane. The S2 region also has the effect of making the SARS-CoV-2 spike protein easily recognizable to the immune system, which then produces antibodies that attack and bind to the virus.
Spike proteins are also produced by the human body following vaccination against COVID-19 and function in a similar way, in that they can fuse with cell membranes. It is not yet entirely clear to what extent spike proteins formed by vaccination interact with our immune system, as they are produced in our own cells, but this does not necessarily mean that an immune response cannot also be triggered. Misdirected immune responses (i.e. the inability of our immune system to distinguish between virus-related and vaccine-produced spike protein) could have devastating consequences and damage healthy cells in our body.

Why should I consider a spike protein detox?
Recent research has linked viral spike protein to negative effects and consequences, such as blood clots, brain fog, pneumonia, and heart muscle inflammation. A Japanese-led biodistribution study examining the Pfizer/BioNTech vaccine also demonstrated that the vaccine particles had reached various tissues throughout the body within 48 hours of vaccination and did not remain at the injection site, with high concentrations found in the liver, bone marrow and ovaries. New evidence also shows that the spike protein may interfere with the ability of our cells to repair DNA. All of the above taken in the context of Long Covid prompted us to focus more on this issue. Taking preventive action in this area could be of tremendous benefit on multiple levels.

If you have had side-effects after being vaccinated or if you suffer from Long Covid or Long Covid-like symptoms, the “Spike Detox” is one of the best ways to tackle your symptoms. Even if you have not experienced any of the above phenomena and have ever been vaccinated or infected with COVID-19 (with or without symptoms), this is relevant to you. Spike protein induced by a natural infection or alternatively a COVID-19 vaccine has high potential to damage our cells, so it is important to take steps to detoxify the body as much as possible.

What is the purpose of the Spike Detox?
General measures such as heat therapies, sauna sessions and hot baths, are good ways to detoxify from spike protein. Intermittent fasting, a dietary measure that stimulates the body’s autophagy ability, can also be helpful in this context. This is essentially a recycling process that takes place in human cells, whereby cells break down and recycle components. By means of autophagy, the body eliminates damaged cell proteins and can destroy harmful viruses and bacteria resulting from an infection.

The right diet is, of course, also essential here, the consumption of pro-inflammatory foods should be avoided, and it also makes sense to aim for a low-histamine diet. The daily intake of important multivitamins and minerals is essential – we already cover this with our personalized supplements.

The targeted spike protein detox primarily refers to four different components, which we will discuss in more detail below:

– the spike protein
– ACE2 receptors
– interleukin 6 (IL-6)
– furin

“Protein-binding inhibitors” impede the binding of the spike protein to human cells, while others neutralize the spike protein, rendering it potentially incapable of causing damage to human cells.

Spike protein inhibitors: prunella vulgaris, pine needles, emodin, neem, dandelion leaf extract, ivermectin

Spike protein neutralizers: N-acetylcysteine (NAC), glutathione, fennel tea, star anise tea, pine needle tea, St. John’s wort, comfrey leaves, vitamin C

Ivermectin has been shown to bind to the spike protein, potentially preventing it from binding to the cell membrane. A number of naturally occurring plants – including pine needles, fennel, star anise, St. John’s wort, and comfrey leaves – contain a substance called shikimic acid that may help neutralize the spike protein. Shikimic acid is also believed to counteract the formation of blood clots. Pine needle tea has a strong antioxidant effect and contains high concentrations of vitamin C, which has a key role to play in neutralizing toxins.

What are ACE2 receptors?
ACE2 receptors are found in the cell wall, in the epithelial and endothelial lining of lungs and blood vessels, and in blood platelets (thrombocytes). Spike protein binds to ACE2 receptors, and it is thought that variable concentrations of spike protein can bind and adhere to our ACE2 receptors, blocking their regular function in various tissues. In addition, the “stickiness” of the spike protein at the ACE2 receptor could cause the immune system to attack healthy cells and possibly trigger autoimmune diseases.

Substances that can naturally protect ACE2 receptors: ivermectin, quercetin (with zinc), fisetin

There is evidence that, when ivermectin binds to an ACE2 receptor, this prevents the spike protein from binding to it.

Why attack IL-6?
Some natural substances support the detoxification process after infection by acting on interleukin- 6. It has been scientifically proven that cytokines such as IL-6 are present at much higher levels in individuals who have been infected with COVID-19 than in those who have not. IL-6 has also been used as a parameter for measuring the progression of COVID-19 cases. In 2021, a meta-analysis using worldwide datasets showed a correlation between IL-6 levels and the severity of COVID-19 disease and demonstrated that IL-6 levels were inversely related to the number of T cells in ICU patients.

IL-6 inhibitors (anti-inflammatories): Boswellia serrata (frankincense) and dandelion leaf extract

Other IL-6 inhibitors: black cumin (Nigella sativa), curcumin, fish oil and other fatty acids, cinnamon, fisetin (flavonoid), apigenin, quercetin (flavonoid), resveratrol, luteolin, vitamin D3 (with vitamin K), zinc, magnesium, jasmine tea, spices, bay leaves, black pepper, nutmeg, and sage

Several natural, plant substances are used in antiviral therapy. The plant pigment quercetin has been shown to have broad-spectrum anti-inflammatory and antiviral effects. Zinc acts as a powerful antioxidant that protects the body from oxidative stress, a process associated with DNA damage, excessive inflammation and other harmful effects.

What is furin?
Furin is an enzyme that cleaves proteins and makes them biologically active.
Furin has been shown to cleave the spike protein, allowing the virus to enter human cells. There is a furin cleavage site on the spike protein of COVID-19, which is thought to make the virus more infectious and transmissible. Furin inhibitors could therefore prevent cleavage and thus activation of the spike protein.

Furin inhibitors: rutin, limonene, baicalein, hesperidin

Many of these measures and detox options are already part of our program. All further suggestions and research results will be reviewed in the coming weeks for our clients and, if we consider them to be necessary, safe and prophylactic, they will be individually incorporated into the supplements. It is therefore of enormous benefit that we are up to date regarding the infection, recovery and vaccination situation of each client. If you have any further questions or if we do not have all the information about your individual situation, please do not hesitate to contact your consultant.

Dr Robert Hess: In rare cases

Dr Robert Hess – 02/28/2022

Dr Robert Hess: In rare cases, coronavirus vaccines may cause Long Covid-like symptoms.

As mentioned on Long Covid and potential risk factors, the symptomatology of this condition can be very similar to the side-effects and possible long-term consequences of vaccination. While preliminary data suggests that getting yourself vaccinated significantly reduces your risk of succumbing to Long Covid, there have also been cases where vaccination has caused Long Covid-like symptoms – and for a lengthy period of time.

Long Covid-like symptoms such as fatigue, brain fog, insomnia, headaches, blood pressure fluctuations and various others are currently being investigated for a possible link to the administration of a COVID-19 vaccine. A number of scientists and research institutes are looking into this matter, among them neuroimmunologist Avindra Nath, clinical director of the Neurological Diseases Institute of the U.S. National Institutes of Health (NIH). In the specialist journal Science, he posited “temporal associations” between vaccination and Long Covid symptoms, but he would not be drawn on whether there was an “etiological association” (i.e. a causative link). Studies conducted by Nath on around 30 case reports have so far remained unpublished, but publication is expected soon.

The Science article also explores the role of autoantibodies – their importance is recognized not only in acute CoV-2 infection, but also in Long Covid. According to recent studies, autoantibodies can be detected up to six months after infection, and as Harald Prüss, a neurologist at the German Center for Neurodegenerative Diseases (DZNE) and at the Charité Hospital in Berlin, writes in an as yet unpublished paper, they are capable of damaging brain tissue. Experiments on animals have suggested that antibodies targeting the SARS-CoV-2 spike protein – the same protein that many vaccines use to trigger a protective immune response – could cause collateral damage. While searching for antibody therapies for COVID-19 in 2020, Harald Prüss and his colleagues discovered that, of the 18 antibodies they identified with strong efficacy against SARS-CoV-2, four also attacked healthy tissue in mice – an indication that they could trigger autoimmune problems.

In August 2021, a group at Northwestern University reported in an advance publication that, in patients with neurological complications after COVID-19, a subset of T cells is persistently activated, similar to how it would be in persistent SARS-CoV-2 infection, suggesting an aberrant immune response or a lingering virus.

Long Covid symptomatology after vaccination seems to be rare so far. Nevertheless, this is a topic that needs to remain in focus and be subjected to greater in-depth investigation. Overall, there are still too many unknowns and therefore there are currently no approved and effective therapies on the market. Nevertheless, we are able to take preventive action. We have already adapted our prophylactic measures in this regard, and we will also revise our supplements. We are one step ahead in this regard and we have put together effective options exclusively for our clients. Next we will report on how to best protect yourself from long-term effects and just how useful a “detox” of the spike protein can be.

If you have any questions about Long Covid or specific symptoms, please do not hesitate to contact your Consultant. We will continue to monitor this issue closely and to update our knowledge.

Dr Robert Hess: Long Covid risk factors

Dr Robert Hess – 02/15/2022

Dr Robert Hess: Long Covid risk factors now identified.

According to the latest figures, between 10 and 30 percent of all persons who test positive for SARS-CoV-2 go on to develop long-term symptoms that can last for weeks, months or potentially even years. These can vary greatly depending on the severity of the disease, the age of the patient and his or her medical history. When – or indeed whether – those who suffer so‑called “Long Covid” can expect their symptoms to clear up is unclear, and there is as is as yet no treatment for the condition that does more than just alleviate symptoms. A U.S.-based research group has now identified four factors that significantly increase the risk of Long Covid.

In order to derive a more complete picture of Long Covid and to better define the term, an international team of researchers has analyzed data from a large-scale survey of covid-specific symptoms, involving 16 studies conducted in different countries around the world. The researchers found that there were no fewer than 55 long-term effects associated with COVID-19. Most of these effects are classic clinical symptoms such as fatigue, headaches, joint pain, anosmia (olfactory disturbance), ageusia (lost sense of taste), muscle weakness, depression and cognitive impairment (i.e. concentration and memory problems). However, long-term effects such as respiratory problems and hair loss, as well as diseases such as myocarditis, the onset of diabetes mellitus and thromboembolism, have also been observed.
In some cases, these long-term effects also overlap with vaccination side-effects. It is therefore is important to take into account the point in time when the symptoms first manifested themselves. Some patients infected with SARS CoV 2 are at greater risk of developing Long Covid than others. Triggers for the syndrome have previously included advanced age, severe obesity and underlying pulmonary/coronary conditions. Gender also appears to play a role: the research concludes that women are disproportionately affected by fatigue syndrome as a long-term consequence of infection.

Recent studies suggest that people who have been hospitalized for COVID-19 are significantly more likely to suffer from long-term sequelae. In this group, no fewer than 76 percent of patients were still suffering from Long Covid symptoms six months after discharge.

A team of researchers led by Yapeng Su at the Institute for Systems Biology in Seattle has now identified four additional risk factors for Long Covid. For the purposes of their research, the team followed almost 300 patients from their initial COVID-19 diagnosis through convalescence (two to three months after diagnosis) in an in-depth multimicroscopic longitudinal study. The subjects, whose age ranged from 18 to 89 years, had contracted COVID-19 in 2020 and early 2021. Consequently, the results cannot be extrapolated to the Omicron variant.

The patients were quizzed about more than 20 symptoms considered typical of Long Covid, such as persistent fatigue, shortness of breath or cognitive impairment (see above). Of those who reported three or more symptoms, 95 percent had one or more of the four risk factors identified in the study:

1) a high viral load in the blood at the onset of infection, as evidenced by high levels of viral RNA;

2) the presence of certain autoantibodies which are directed against the patient’s own immune system, have the capacity to aggravate an infection and also occur in rheumatoid arthritis or other autoimmune diseases (COVID-19 sufferers can form a large quantity of such antibodies, which are detectable up to six months after the acute illness and are evidently involved in the development of Long Covid syndrome);

3) reactivation of the Epstein-Barr virus (EBV) which is responsible for triggering glandular fever, a disease that many people become infected with at a young age (EBV can lie dormant in the body for very many years and become active again during systemic illness, in much the same way as the herpes virus);

4) the presence of diabetes mellitus (Type 2).

More than 60 percent of those examined in the study exhibited two or more of the typical symptoms. Autoantibodies were found in two-thirds of them, and no other factor played such a significant role. Diabetes, high viral load and EBV were each identified in one third of the sample. Typically, however, more than one factor was present at the same time, and the combined effect therefore proved decisive. These findings could now open up new approaches to the treatment of Long Covid.

Preliminary data from Israel indicates that vaccination against SARS-CoV-2 inhibits the development of Long Covid syndrome. In the specific case of Israel, the vaccine administered was exclusively of the mRNA variety. This was found to not only reduce the risk of severe disease but also to make long-term sequelae following vaccine breakthrough less likely. Data from individuals who contracted SARS-CoV-2 relatively early in the pandemic suggests that vaccination could also reduce the risk of Long Covid: persons who became infected after previously receiving the BioNTech/Pfizer vaccine were significantly less likely to report typical long-term symptoms (e.g. fatigue and persistent exhaustion) than those who were unvaccinated at the time of infection. In fact, vaccinated people were no more likely to complain of certain symptoms than people who had never contracted SARS-CoV-2. The results of the study are preliminary, however, and the peer review process has yet to be carried out.

As mentioned in our last Keynote, we will now be incorporating these risk factors into our prophylactic program and updating it with regard to Long Covid symptomatology in addition to vaccination side-effects. Thanks to our C-19 saliva testing and antibody monitoring last year, we have already managed to collect all specific data in this regard for our Premium clients, which puts us one step ahead. We will be shortening the intervals between tests for clients with a higher risk profile and introducing even more targeted diagnostic methods.

Dr Robert Hess: Updates and Revises

Dr Robert Hess – 02/04/2022

Dr Robert Hess: Updates and Revises Section 4 of its Prophylactic concept.

In the current circumstances, it is more important than ever to maintain a clear overview. The number of vaccinations and infections, the virus variants in circulation and the available vaccines, the course taken by an infection, possible side-effects and the administration of various drugs against severe COVID-19 – these are all factors that make our efforts to provide comprehensive protection more complex, requiring close attention and detailed documentation. Protection of the organism as a whole remains our priority, which is why we are now broadening the scope of our prophylactic concept and scheduled check-ups.

In the last two years, our immune system has been through a lot – it has had to adapt and evolve, to adjust and play a supportive role in meeting the new challenges of either infection with COVID-19 or injection with an mRNA vaccine. To complicate matters, a pandemic is a fast-moving and generally unpredictable state of affairs that may drag on over months and years. Right at the start of the COVID-19 pandemic, I placed great emphasis on accurate documentation of the vaccination and infection status of my clients in order to ensure that data is systematically processed and that possible sequelae are spotted. The information we have gathered will now be evaluated and incorporated into our amended prophylactic program.

With this specific focus on prevention, we aim to identify and monitor potential long-term effects of SARS-CoV-2 infection. Long covid and post-covid are both sequelae of the disease, but they describe a very broad and elusive picture of diverse symptoms. As the pandemic has progressed, it has become increasingly clear that infection with SARS-CoV-2 can have long-term health consequences, even if the course of the disease itself is mild or is asymptomatic and therefore goes unnoticed. For this reason, I pay special attention to the sequelae of COVID-19 with the aim of defining these terms more precisely for our clients in the future.

At the same time, we also have to consider the possibility that certain symptom manifestations might instead be associated with vaccine damage and the long-term consequences of repeated vaccinations. More and more studies are producing information about the effects of the spike protein and about endothelial damage. However, we are surprised that there are no large-scale studies on possible carcinogenic effects or immunomodulatory changes so far. We will continue to keep this on our radar.

This specific focus on prevention in relation to the COVID-19 pandemic also shifts attention to the internal organs, where we are primarily looking at the kidney, liver, coronary arteries and the bronchial and neurological systems. Likewise, our prophylactic recommendations will also cover the relevant techniques and diagnostic methods. For example, we consider echocardiography (ultrasound examination) in cardiac and coronary artery diagnostics as no longer sufficient for our requirements and would therefore favor diagnostics based on a cardiac MRI scan.

In conclusion, I would like to inform my clients that we now intend to shorten the intervals for preventive care planning. This has the advantage that continuous monitoring of our clients and the availability of individualized data allows us to intervene at an early stage and thereby prevent damage in the long term.

Dr Robert Hess: Best medication yet?

Dr Robert Hess – 01/20/2022

Dr Robert Hess: Best medication yet? Paxlovid a potential gamechanger

Paxlovid received emergency approval in the USA just before Christmas, and it got the all-clear for use in Europe as early as January. This new medication could help reduce the number of people who fall severely ill with COVID-19, but supply shortages and manufacturing problems are so far hindering widespread distribution.

Taken early enough after a diagnosis of COVID-19, paxlovid could dramatically reduce the risk of severe illness. Its manufacturer, Pfizer, claims that the likelihood of hospitalization or death for high-risk patients following an infection is reduced by almost 90 percent. Many in the medical profession are now hoping for its rapid and widespread deployment. Indeed, Germany and other European countries will probably begin using paxlovid before it is officially approved by the European Medicines Agency (EMA). However, it will not be clinicians who administer paxlovid to their patients. Ideally, the drug will avert the situation where infected patients have to go to hospital in the first place. It will therefore be prescribed primarily by family doctors. In our opinion, the great advantage of Paxlovid is its convenience and ease of use, i.e. as a tablet that infected individuals can take at home.

Paxlovid is an antiviral medication against COVID-19 consisting of two substances. The actual active ingredient, newly developed by Pfizer, is called nirmatrelvir. This inhibits 3CL protease, a molecule that Sars-CoV-2 needs to replicate in body cells. This mechanism of action has a major advantage: the gene segment that codes for this protease is only changed at one site in Omicron compared with Delta. We therefore have reason to believe that paxlovid is also effective against the new variant. And according to Pfizer, its effectiveness has also been indicated by initial laboratory tests. The other active ingredient contained in paxlovid is ritonavir, a substance that is also used in the treatment of HIV. Ritonavir ensures that nirmatrelvir is broken down more slowly and can therefore act for longer. The two elements are dispensed as separate tablets in the package of paxlovid. Infected patients who are deemed eligible for the drug must take two doses of nirmatrelvir and one of ritonavir twice a day for five days.

Paxlovid has been dubbed a potential gamechanger the basis of interim study results published by Pfizer at the beginning of November 2021. In mid-December, the company then issued a further announcement confirming these initial good results. According to the report, the drug is highly efficient in averting the need for emergency treatment and/or in preventing death among COVID-19 patients with mild or moderate symptoms who have not yet been hospitalized. In high-risk patients, paxlovid reduced the relative risk of hospitalization or death by almost 90 percent.

While only five of 697 people in the paxlovid test group required emergency treatment within four weeks (equivalent to 0.7 percent), among those who received a placebo, 44 out of 682 (equivalent to 6.5 percent) had to be admitted to hospital. Nine test subjects from the placebo group died from COVID-19, while there were no coronavirus deaths in the paxlovid group. These results apply to subjects who took paxlovid within three days of symptom onset, according to the news release. However – and this is very good news – Pfizer reports that efficacy is just as good when the first tablet is taken within five days of symptom onset. This considerably extends the window of opportunity.

Unlike molnupiravir, another antiviral drug we reported on a few weeks ago, estimates of paxlovid’s efficacy have not been downgraded. Merck & Co, the company that manufactures molnupiravir, had initially claimed that its product reduced the relative risk of severe COVID-19 by approximately 50 percent, but a subsequent review of the study results showed only a 30 percent reduction.

Based on everything we know so far, paxlovid looks the best of the available options. However, we must remember that there are still no published trial data. Pfizer has submitted its results to a medical journal for publication, but they are not yet open to public scrutiny. In order to better assess paxlovid, we require far more data, for example identifying the type of patients who most strongly benefit from treatment with the drug. The over-65s, who are automatically at greater risk due to their age, accounted for only 11.4 percent of the test subjects in an interim evaluation, and people over 75 made up only 2.9 percent of the sample. Furthermore, only unvaccinated individuals participated in the study. Since most of my clients are vaccinated, it is also important to see how effective paxlovid is among this population.

In terms of side-effects, paxlovid performed relatively well in the study. Apart from the more or less “usual” side-effects of drugs, such as diarrhea or vomiting, there were no unforeseen adverse reactions. The bigger problem with paxlovid is likely to be from another source, namely drug-drug interactions (DDIs).

The ritonavir component of paxlovid ensures that the actual active ingredient nirmatrelvir is broken down more slowly and can therefore take effect over a longer period. This happens because ritonavir inhibits an enzyme complex in the liver that is used to metabolize and break down many drugs in the body. And this, in turn, can cause these drugs to remain in the body in excessive concentrations. Other mechanisms associated with paxlovid consumption can also cause certain drugs to be broken down more quickly than normal, so that they work either inadequately or not at all. These interactions affect a wide variety of medications, but especially those prescribed for cardiac arrhythmias, antidepressants, cholesterol-lowering drugs, anticoagulants and certain antibiotics. We would therefore ask our clients to inform us in advance in the event of infection and a proposed course of paxlovid. We will then check and reconcile possible interactions with other medications.

And what about vaccination status?
The Pfizer study initially included only high-risk unvaccinated volunteers. Another study is currently analyzing the effectiveness of paxlovid in low-risk unvaccinated individuals and in vaccinated people with breakthrough infections. Nevertheless, vaccinated people will also be eligible to receive the medication.

The bigger problem in this context is availability and the inevitable triage scenarios, especially in the United States where doctors are already complaining about supply bottlenecks.

The U.S. government procures paxlovid centrally and allocates supplies to federal states where local health officials decide on distribution and on the guidelines to be issued to doctors. However, supplies have already been exhausted. The city of New York, for example, received about 1,300 paxlovid treatments at the end of December, but according to a spokesperson for Alto Pharmacy, which distributes the city’s supplies, these were used up within a week. We are reliably informed that New York City currently has no paxlovid in stock. Last Tuesday, the U.S. government doubled its paxlovid order, though we don’t expect supplies to last until April.

So while it is relatively easy to get a vaccine, there is likely nowhere near enough paxlovid to treat every at-risk individual who becomes infected. Manufacturing the drug also takes time, because producing the nirmatrelvir component is a complex multi-step process that takes months. Pfizer plans to produce up to 120 million units of paxlovid by the end of 2022. This sounds like a lot at first, but given the global demand, it is a drop in the ocean.

And it is not only paxlovid that is suffering from supply shortages. There are also problems with the procurement of proven monoclonal antibody therapy. Throughout most of the pandemic, monoclonal antibodies – a treatment generally administered intravenously in hospitals or clinics – have been the primary intervention for recently infected patients. The two most common types of monoclonal antibodies (casirivimab/imdevimab and etesevimab/bamlanivimab) do not work well enough against the Omicron variant. There is a third antibody treatment, sotrovimab, manufactured by GSK and Vir Biotechnology, that is effective against Omicron. However, the U.S. government had ordered only about 450,000 treatment units to date, many of which have now been used or have not yet been distributed to the state governments. On 12th January, the U.S. government announced in a press release that it had ordered an additional 600,000 units of sotrovimab.

Paxlovid can only become a gamechanger and GSK’s MAB therapy can continue in a supportive role if these treatments are made as widely and easily accessible as possible. Currently, the system only favors those who have the time, energy and knowledge to seek out treatments.

We will continue to share our assessment of the situation with you. If you find yourself in the situation of needing paxlovid or MAK therapy, please contact us beforehand so that we can talk through all the options and tailor them to your individual circumstances.

Dr Robert Hess: Weekly Omicron Update

Dr Robert Hess – 12/20/2021

Dr Robert Hess: Weekly Omicron Update

Our Situation report in the run-up to Christmas

The Omicron variant continues on its triumphant march around the globe. According to the World Health Organization, the mutant has already been detected in 89 countries, and more are being added to the list every day. Even in places with high immunity rates, the spread is rapid, and the number of confirmed Omicron cases is doubling every one and a half to three days in some countries. If it continues at its current rate, Omicron will be the prevalent form of SARS-CoV-2 in Europe in around two to four weeks. The UK is one of the first countries to be hit hard – Omicron is already the dominant form there, constituting 60% of new cases. Worryingly, a new study from England does not give much hope for the new variant leading to a significantly milder course of disease.

How well a person is protected against Omicron depends on many different factors, for example age, previous illnesses and underlying conditions, vaccination status and length of time since last dose administered. The risk of infection has risen dramatically in Europe, where the transmission rate of Omicron is between 2.5 and 4.3 times that of the Delta variant. For individuals without a basic level of immunity, this presents a huge problem. But it has now become apparent that even double vaccination does not provide sufficient protection against Omicron. The immunity afforded by antibodies against the variant is significantly weakened, as has been confirmed by several recent studies.

According to these studies, double vaccination offers almost 70% protection against the disease taking such a severe course that hospitalization is required. However, the level of protection against actual infection is generally significantly lower than with other variants – some studies estimate it to be as low as 33%.

How will the booster jab perform against Omicron?
Many scientists and virologists warn against inflated expectations and are agreed that even a third dose of vaccine will not provide 100% protection against infection. Although the protection against Omicron increases from a double to a triple vaccination, it is still 4.8 times lower than with the Delta variant. Despite the public exhortations from politicians to the effect of “Get vaccinated and all will be fine again”, this is patently not so. We conclude this from cases of triple-jabbed individuals who have become infected and then gone on to infect others. Particular caution is advised for those who come into contact with high-risk groups.

To predict the growth of the Omicron variant and estimate the degree of immune escape, scientists in the UK analyzed data from all PCR-confirmed SARS-CoV-2 cases in England and published them a few days ago. The results revealed that hospitalization and asymptomatic infection indicators were not significantly different for Omicron, suggesting that there little change in severity compared with Delta. On the one hand, this means that Omicron does not cause worse disease or have higher severity than Delta, but on the other hand, it also means that it is not milder than Delta, as had been initially hoped.

The conclusion we draw from this is that the role played by vaccination status is significantly reduced in terms of immunity to Omicron. The weighting previously given to vaccination is substantially lower than before, so it is now all the more important to take general measures to optimize the immune system. We would therefore once again urge our clients to adhere even more strictly to the recommendations made by us. This includes the personalized elaboration of concepts and measures, as well as the intake of the individually adjusted supplements for the modulation and optimization of the adaptive immune system.

We expect that Delta will have been largely supplanted by Omicron in most countries of Europe by mid to late January 2022. In the United States, this may take a little longer, but it is also the inevitable outcome. It is not yet possible to form a definitive opinion about what will happen in the next few months, with so much being in the realms of speculation, but for the first time, the Omicron variant holds out the theoretical prospect of worldwide herd immunity.

Dr Robert Hess: Weekly Omicron Update

Dr Robert Hess – 12/11/2021

Dr Robert Hess: Weekly Omicron Update

Teams of researchers around the world are working hard to understand the new Omicron variant of the coronavirus. It is the most highly differentiated among the five variants that have so far qualified for the World Health Organization classification “variant of concern” since the pandemic began.

The number of cases in South Africa has risen rapidly to nearly 20,000 per day since the country first reported the discovery of Omicron two weeks ago. In the weeks leading up to that, the number of COVID-19 cases in the country had remained relatively low, even though only 26% of the population was fully vaccinated. With a vaccination rate of under 30% and many South Africans having most likely been infected naturally at some point, it will be interesting to see if the same rapid rise in cases occurs in countries with a high take-up of mRNA vaccines.

There are three important questions, the answers to which will indicate the likely impact of Omicron on countries around the world. How transmissible is this new variant of coronavirus?
How well is it able to evade the antibodies and T‑cells that make up the immune defenses of both the vaccinated and unvaccinated? And what is the probability that an infection with Omicron will be severe, resulting in the hospitalization and possibly death of an infected person?

How easily does Omicron spread?
The Omicron variant spreads more readily than the original “wild type” SARS CoV-2 virus first identified in Wuhan. This is already evident from the numbers coming in from all around the world. How easily Omicron spreads compared to Delta is not yet clear. According to a study by Professor Hiroshi Nishiura of the Health and Environmental Sciences Department at Kyoto University in Japan, who specializes in mathematical modeling of infectious diseases, the Omicron variant of COVID-19 is 4.2 times more transmissible in the early stages than Delta – a finding that is likely to confirm fears about the contagiousness of the new strain.
Furthermore, scientists believe that anyone infected with Omicron can transmit the virus to others, even if they are vaccinated or have no symptoms.

Will Omicron cause more severe disease progression?
More data is needed to assess whether Omicron infections – especially reinfections and breakthrough infections in individuals who are fully vaccinated – cause more severe disease or death than infections with other variants. There are fears that Omicron could cause more damage around the world than Delta, and the WHO has warned that outbreaks with “severe consequences” could occur. However, the surge in cases in South Africa following the emergence of the variant in the country has not yet led to hospital overload, so there is currently a degree of confidence that Omicron will not trigger more severe courses of the disease. However, it is important to note that the first reported cases involved university students – younger people whose lifestyle exposes them to greater risk of infection – so it will be days to weeks before the severity of the Omicron variant is fully known. There is no information as yet to suggest that the symptoms associated with Omicron are different from those of other variants.

Do vaccines work against Omicron?
The current crop of vaccines are expected to offer a certain percentage rate of protection against severe illness, hospitalization and death due to infection with the Omicron variant. Studies are being conducted around the world to establish the actual level of protection. Moderna and Pfizer/BioNTech are currently testing their existing vaccines against the Omicron variant with a view to modifying them if the results should prove disappointing.

To study the effectiveness of a vaccine against a particular variant of Sars-CoV-2, researchers typically carry out what are called “neutralization tests”. They look to see how many antibodies a vaccinated person has in his or her blood that can bind to the viral variant and thus eliminate it. However, the true protection status of vaccinated persons cannot be completely determined in this way; clinical studies involving several thousand volunteers are needed, or evaluations of the speed at which the disease is spreading.

Last Wednesday, Sandra Ciesek, a virologist at Frankfurt University Hospital, published initial results showing a significantly reduced antibody response to the new Omicron variant. According to Ciesek, the data lends weight to the suggestion that the development of a vaccine specially adapted to Omicron is the way ahead. On Tuesday, South African experts had already presented similar data showing a weaker antibody response to Omicron in vaccinated individuals. Researchers at the Africa Health Research Institute in South Africa released preliminary data on the effectiveness of the BioNTech/Pfizer vaccine against Omicron. The results suggest that the viral variant escapes the antibody response of twice-vaccinated individuals, whereas a third booster jab neutralizes the new variant. Antibody levels against the Omicron variant are as high after booster vaccination as they are against the wild type after two doses. In vaccinated individuals who had also been infected at some stage, a substantial antibody response was also measurable.

Scientists emphasize that Omicron still relies on the same biological mechanism as the other corona variants to attack human cells. Consequently, T-cells and antibodies continue to have a protective effect. If it turns out that the efficacy of vaccines against Omicron falls below 50%, then this variant would come under our definition of a “super mutant”. We will present scenarios for this again as more data become available.

Breakthrough infections in people who are fully vaccinated can still be expected.

Will therapies and treatments work against Omicron?
Scientists are seeking to determine how well existing treatments work against COVID-19. Because of Omicron’s altered genetic profile, it is likely that some treatments will remain effective, while others may be less so.

What are the vaccine manufacturers saying?
On Wednesday, Moderna CEO Stephen Hog announced that his company could have a COVID-19 booster vaccine targeting the Omicron variant tested and ready for approval in the USA as early as March. Moderna said in a statement that booster vaccines with genes that specifically target mutations in the newly discovered Omicron variant would be the fastest way to address the reduction in vaccine efficacy which the variant is expected to cause. The company is also working on a multivalent vaccine that would target up to four different coronavirus variants, including Omicron.

Moderna, as well as Pfizer/BioNTech, have already started to work on the further development of their vaccines. How long it will take for these to be approved is as yet unknown. Given previous guidance from the U.S. Food and Drug Administration, which requires mid-stage clinical trials, the process could take three or four months. According to Stephen Hoge, the Omicron-specific boosters will not realistically be ready for rollout until March or possibly the second quarter – unless, of course, the FDA changes its guidance on the data needed for approval.

One dilemma we currently face is whether to recommend a booster jab with one of the existing vaccines or to wait. And how can we prevent the emergence of more virulent pathogens in the future?
The data on the risk posed by the Omicron variant is gradually building up and becoming clearer. Nevertheless, based on what we know so far, booster vaccinations provide relatively good protection, if not against an actual infection, then definitely against severe disease. Moreover, this is for the moment our only proven effective weapon in the fight against the virus. Scientific opinion is that an x-fold reduction in neutralizing activity does not necessarily mean that a vaccine is x times less protective. The actual loss of immunity is much less, and the triple vaccination is the best protection we have.
New vaccines are not expected until after the winter wave washes over the northern hemisphere, so politicians continue to push the booster programs. However, if the FDA and other regulatory agencies change their rules, the process of approving a new, more effective vaccine against Omicron could be significantly accelerated. We expect to have more information and data on this in the run-up to Christmas, so for now, we are adopting a wait-and-see approach, especially for our clients who are under no particular time pressure as regards boosting and are reasonably well placed in terms of antibody count and T-cell immunity.

Another matter that concerns us is how new mutations and vaccination regimes should be dealt with in the future. Some scientists believe that vaccines and the mass distribution of them in industrialized countries could lead to the emergence of even more virulent pathogens. Conventional wisdom holds that natural selection eliminates highly lethal pathogens, as the death of the host greatly reduces transmission to other persons. Vaccines that keep the host alive but still allow transmission could therefore enable highly virulent strains to circulate in a population. The data that we have accumulated so far shows that vaccines against diseases that do not prevent transmission can create conditions that favor the emergence of pathogen strains capable of causing more severe disease in unvaccinated hosts.

Importantly, most vaccine experts agree that current vaccines still protect against severe disease and death in the event of Omicron infection. Thus, we are not left completely defenseless. However, once again, timing is critical here in deciding whether to boost now with one of the vaccines already available or to wait and boost with a next-generation vaccine. We know from our private sources that vaccine adaptation will be on a far greater scale than previously assumed. In addition, the definition of “fully vaccinated” status will be expanded from double vaccination to triple vaccination. We will be weighing this carefully over the next few weeks and will keep you updated.

We wish to reiterate that my Premium clients can contact us at any time if they have any concerns regarding booster vaccination or vaccination status or if a change is pending. We only give out highly individual recommendations in this regard – a refinement in procedure that is currently gaining more and more relevance.

Dr Robert Hess: How do viruses interfere with the p53 pathway?

Dr Robert Hess – 12/06/2021

Dr Robert Hess: How do viruses – and more particularly SARS-CoV-2 – interfere with the p53 pathway?

We look at the strategies employed by viruses against this tumor suppressor gene.

Since the onset of the pandemic, research has been conducted into the extent to which SARS-Cov-2 affects the p53 tumor suppressor gene and its pathway. Two widely published studies from 2020 and 2021 have provided interesting insights into this, revealing the molecular strategies by means of which viruses such as SARS-CoV-2 target the p53 function. It is also interesting to compare the combat strategies of other viruses with those of SARS-CoV-2, and we will also briefly discuss this below.

Virtually all viruses have evolved strategies and molecular tools to disable and/or control cell regulatory mechanisms in their hosts that might otherwise impede replication, dissemination or persistence. To this end, viruses have evolved specific proteins to target cell decision centers that regulate cell proliferation and survival as well as the innate immune response mechanisms used by cells to defend against viral infections, for example interferon-gamma-mediated antiviral responses.

Among these decision centers and mechanisms, the p53 tumor suppressor protein plays an important role. This stress-inducible factor can directly and indirectly command a variety of signaling pathways that control DNA replication and repair, cell proliferation, programmed cell death, metabolism and innate immune responses. This broad spectrum of suppressive effects makes p53 a highly “legitimate” target for many different cancers which seek to inactivate it by mutation, deletion or other mechanisms.

The p53 protein was originally discovered as a cellular target of the large T antigen (LT) of the oncogenic Simian Virus 40 (SV40). Over the years, a number of studies have identified an astonishing variety of molecular devices employed by each known viral family to hijack, control or impair the functionality of p53. In persistent oncogenic viruses, such as the human high-risk papillomaviruses (HPV 16, 18, 31, 45), these devices are so specific and powerful that they permanently inactivate p53 functionality and produce an oncogenic effect. Non-oncogenic viruses also produce proteins that interact with p53 or p53 regulators, thereby confirming that control of p53 is an essential mechanism to support efficient viral replication, propagation and in some cases persistence.

In this article, we briefly summarize the current state of knowledge regarding the mechanisms by which viruses interfere with the p53 pathway and the consequences that flow from this. We then discuss the evidence to date on how SARS-CoV-2 attacks the p53 pathway and look at the potential functional impact of this disruption on replication, pathogenesis and the potential long-term consequences of infection.

VIRAL STRATEGIES FOR THE CIRCUMVENTION OF P53
Seen from the perspective of a virus, the presence of an active p53 in the host cell represents a threat that must be neutralized or circumvented in order for the virus to go about its business of replication and propagation. The most immediate challenges posed by p53 are stress-induced programmed death of the host cell and induction of innate or adaptive immune responses of the antiviral kind. Programmed cell death – primarily through apoptosis – is a radical protective response at cellular level that effectively destroys the viral host cell. The p53 protein acts as a stress-activated switch for many pro-apoptotic pathways, so by seizing command of this switch, the virus ensures that it can control the survival and lifespan of its host cell.

The mechanisms chosen by individual viruses to the detriment of p53 depend on cell tropism, propagation cycle, and modalities of latency or persistence. In the next section, we give examples of three strategies that viruses use to target the p53 pathway: Hit and Run, Hide and Seek, Kidnap and Exploit. The name given to each of these strategies describes how the virus exploits the host cell for its own replication and propagation purposes and reveals the perfect adaptation of the virus to a particular ecological niche.

Hit and Run
Exemplifying the Hit and Run strategy is the influenza virus (IAV), a member of the Orthomyxoviridae family of RNA viruses and one of the most common agents of human respiratory infections. Speed is of the essence for IAV, as the time available to it for the cycle of infection, replication, and reproduction is very short. This cytolytic virus triggers host cell apoptosis to promote the release of virions from infected cells. It therefore employs the unusual strategy of attacking p53 to activate its ability to trigger programmed cell death.

Hide and Seek
This viral strategy comprises two sequential phases: first, the attenuation of p53 functions (hide) and second, the positive mobilization of p53 (seek) to support the virus at different stages of its life cycle. A typical example of such a hide-and-seek strategy is HIV-1, a lentivirus that latently infects CD4 lymphocytes and causes a loss of T-helper functions that in turn leads to AIDS. HIV-1 has evolved several proteins that target p53 either early or late in the viral life cycle.

Kidnap and Exploit
This strategy is a somewhat more sophisticated form of Hide and Seek in which the virus manipulates p53 with a whole range of molecular tools, not only to attenuate the antiviral effects mediated by p53, but also to exploit p53 as a factor that controls and facilitates viral replication. Examples of this strategy include members of the Herpesviridae family, such as herpes simplex virus 1 (HSV-1) and Epstein-Barr virus (EBV). Infection with HSV-1 is often asymptomatic: it manifests itself mainly as benign herpetic skin and mucosal lesions, but due to its persistence in neurons, the virus can also cause latent, recurrent infections.

HOW DO SARS-COV VIRUSES INTERFERE WITH THE p53 PATHWAY?
Information on how SARS-CoV-2 targets and manipulates the p53 pathway is still sparse and limited. However, the information we have for SARS-CoV-1 is more detailed. Given that the two viruses are approximately 89% genomically homologous and share many similarities in their infection and pathogenesis mechanisms, it is reasonable to speculate that both viruses use similar molecular mechanisms to target and circumvent p53.

The observations summarized above underscore the fact that SARS-CoV viruses, like most other virus families, have evolved and developed molecular tools that are well adapted to targeting p53 and its signaling pathway. The strategy followed by these viruses shares similarities with the kidnap-and-exploit strategy described above for EBV and HSV1. The distinguishing feature of this strategy is the hijacking of p53 by viral antigens that initiate alternative pathways for the degradation of p53, thereby not only impairing the suppressor functions of p53 but also protecting it from regulation under stress conditions. This mechanism shifts p53 from its normal cell response pathway to a viral response pathway, allowing the virus to bypass components of the p53-controlled pathways or even use them to its own advantage. How this mechanism affects the pathogenesis of SARS-CoV infections and, in particular, the progression of Covid-19 remains a matter for conjecture for now. Two scenarios can be considered:

1) p53 could serve as an antiviral factor that limits SARS-CoV virus replication and reproduction. Consequently, the rate and extent of virus replication might depend on how efficient it is in causing p53 degradation.

2) In parallel with the impairment of p53, SARS-CoV viruses also set in motion molecular programs that lead to oxidative cell and DNA damage and have the potential to hyperactivate p53, resulting in rapid and massive apoptosis. This mechanism could be a contributory factor in the severe lung inflammation and respiratory distress seen in severe forms of Covid-19. Again, p53 could act as a regulator, with the extent of cell and tissue damage depending on the intensity of the p53-mediated responses.

Placing these two scenarios in sequence, one can speculate that SARS-CoV tools (e.g. nsp3 or RCHY1) rapidly switch off p53 function upon infection, thus protecting the virus from innate immune responses and allowing replication. As replication and virus production begin to decline, p53 again becomes available for activation by DNA damage and other stress response pathways of the cell. At this point, the host cell has accumulated considerable oxidative damage, causing p53 to enter a hyperactive state. This, in turn, may contribute to setting in motion a sequence of events that leads to severe inflammation and tissue damage.

Further investigation is needed to determine whether restoring and normalizing p53 activity could be an accessible and affordable objective for Covid-19 therapy. To us, this seems to be a promising target, and we endorse the focus on p53 and its pathway. Further studies are already underway, and we continue to stay on top of the latest developments. The methylation of p53 genes is already central to the epigenetic monitoring of our Premium clients, with review and analysis taking place every three months. The current direction taken by pandemic with regard to SARS-CoV-2 and its impact on p53 further increases the need for monitoring. My traditional focus is on cancer prevention, and since the beginning of the pandemic, we have also become deeply involved in immunology. We are therefore following the fusion of these two areas of research with great interest.

Dr Robert Hess: Update on Booster jabs and vaccine breakthroughs.

Dr Robert Hess – 11/26/2021

Dr Robert Hess: Update on Booster jabs and vaccine breakthroughs.

Infection rates in Germany, Austria and the Netherlands have risen to a new and worrying high. Hospitals have had to postpone planned surgical procedures, and intensive care units are rapidly filling up. The situation in Germany is unfortunately a forerunner of what is likely to happen in the United States soon. The UK had the unwelcome distinction of being ahead of the curve in Western Europe, although the rate there now seems to be leveling off. We expect the current fourth wave will hit the USA in a few weeks. There are two main reasons for this: firstly, waning vaccine efficacy paired with vaccine breakthroughs, and secondly, the slow progress being made by the booster vaccination campaign. More and more studies are showing what we already concluded a few weeks ago, namely that the protection afforded by the vaccines is declining at a rapid rate and that antibody counts are also falling fast.

Eleven months ago, there was great jubilation at the test results from a study conducted by BioNTech which showed that their vaccine had a 95% success rate against infection with the SARS-CoV-2 virus. Not long after, Moderna reported a similar impressive result. This was all the more encouraging, because the FDA had set a modest efficacy threshold of only 50%. Since then, billions of people have been vaccinated against the coronavirus, and numerous studies have confirmed the high protective effect in practice.

Unfortunately, it is now clear that even a double dose of vaccine is not going to be enough to end the pandemic. There were indications of this relatively early on when the initially high antibody titers in the blood of vaccinated individuals dropped again just a few months after they had received their second dose. In Israel, which had vaccinated its population earlier and faster than any other country, the infection curve rose steeply again in the summer, but this has since been flattened out and brought under control by the booster vaccination roll-out.

In Germany, too, it is primarily unvaccinated Covid-19 patients who are occupying beds in intensive care units, but the number of breakthrough infections is also rising. This does not come as a complete surprise from an immunological perspective, as we know that vaccine protection gradually wears off after approximately six months.

Large-scale analyses from different countries now reveal the extent to which vaccine protection declines over time. Scientists in Israel recently published the results from their analysis of cases involving vaccinated adults who had contracted Covid-19 between 11th and 30th July. These showed that individuals who had been vaccinated seven months earlier were at twice the risk of infection as those who had been vaccinated only five months earlier. A study by Pfizer also reached the same conclusion.

An analysis from Sweden produced an even more unpleasant surprise. The research team there found that protection against infection was no longer detectable at all seven months after vaccination and that even protection against hospitalization was down to only 42 percent. Another study from the UK made a comparison using the case-control method. According to this observational study, protection against infection two months after vaccination was 96 percent compared to the placebo group. Five to seven months later, however, it had dropped to 84 percent. Data from the USA also show the diminishing effect.

The effectiveness fades particularly quickly in the elderly, whose immune system responds more weakly anyway. And people in this most at-risk group are precisely the ones whose protection depends on vaccination administered more than six months previously.

With a large proportion of its population now triple-vaccinated, Israel seems to have broken the fourth wave. A recently published analysis shows the effect of the booster campaign, with protection for recipients of the third dose now restored to a highly satisfactory 93-percent level.

The data we have gathered had already indicated the dwindling protection afforded by the vaccines, and what we already suspected has now been confirmed by the latest analyses and studies. The third jab is not “just” a booster per se, but rather complements the vaccination series. According to our data, a third dose of the vaccine finesses immunity and completes the vaccination protection. The antibodies after a third shot are usually in a range that cannot be achieved by just two. This means that, even if vaccine efficacy slowly declines again after a third dose (and it will), it does so from a higher baseline and thus probably more slowly. We are working on the assumption that “fully vaccinated” status will soon no longer apply to those who have had only two doses. How policymakers and governments react to this remains to be seen.
Vaccine breakthroughs are becoming an increasingly acute problem, and booster vaccination is currently the only way to tackle it. The more people, especially the elderly, receive booster vaccinations, the more we will be able to flatten out the wave. In our opinion, countries that have a vaccination rate below 70% and in which the population received their first and second vaccinations early are at a disadvantage in this scenario. The recommendations we make to our clients will continue to be on an individual and, above all, laboratory-dependent basis. This means that we look at the overall picture of antibody quantity and quality, T‑cell immunity and general immune system status. Our recommendations are therefore not country-dependent and may therefore not necessarily be in accordance with national rules and regulations.

We expect that the future will bring more opportunities to recommend full protection against Covid-19. Although vaccination is currently our main pillar of defense, we expect that other methods such as approved antiviral drugs, more effective antibody therapies and differentiated vaccination regimens will be increasingly incorporated into the protection program in the near future.

Tag Archives: SARS-CoV-2