Tag Archives: COVID 19

How long does the protection afforded by vaccination last?

Dr Robert HEss

Dr Robert Hess – 06/19/2021

How long does the protection afforded by vaccination last? This is a vital question that can only be answered when enough time has elapsed for results to come in.

There is one thing we can be certain of, however, namely that the protection afforded by vaccines does not live up to the claims made by their manufacturers. We strongly disagree with the assertion that “vaccine protection will remain at the same high level for approximately one year, so that we can get into an annual vaccination cycle like the one we have for influenza.” This is the reason why we set up our SARS-CoV-2 Antibody Profile Monitoring for Premium clients at the start of this year, measuring levels of SARS-CoV-2 antibodies as well as T-helper cells specific to SARS-CoV-2 and thereby covering both pillars of the immune response.

There are as yet no clinical studies to refer to, so we are in completely uncharted territory here. It is a matter of great concern to us that some of our clients who have been fully vaccinated for several months now appear to have built up little if any immune protection. In the circumstances, this monitoring of antibodies makes a lot of sense, and various scientific institutes have approached us to draw on our experience in this field.

Immune protection is, of course, also a subject of concern to the wider population, and many people, fearing that the immune protection they have gained from vaccination may already be weakening, are already asking for a third booster shot. The fact is that not a single scientific body has ventured an opinion on the matter. This means that Dr Robert Hess is entering completely new territory. We will not be making any general recommendations, as the individual situation of each client is different. The structure of each immune system is also highly individual with regard to natural immune response, vaccine-induced antibody levels and exposure to mutation events dependent on geographic location. We will therefore only make recommendations about booster jabs or next generation vaccines tailored to the individual client. We believe that it is simply impossible to devise a vaccination scheme in which the intervals specified are valid for everyone. This simply makes no sense. Consequently, a universal recommendation is completely out of the question.

Dr Robert Hess has also gained insight into the workings of the T-cells. First indications are that that they prevent severe infections, but not to the extent that has now been claimed in various scientific publications.

Furthermore, we also have to consider the special needs of so-called “low responders” or “non-responders” to the vaccines among our own clientele. We have to assume that such cases are more frequent than has been surmised so far. Low responders and non-responders are individuals who have acquired minimal or zero immune protection through vaccination. Among our clientele, we also have non-vaccinated Covid-19 survivors of whom around 25% have not built up any protection at all. This is a significant difference compared to measles, for example. The immunity of those who have recovered and those who have been vaccinated clearly decreases, and the curve falls away dramatically after about three months. The idea that there are people who cannot become infected has been absolutely refuted. Most people who have not been vaccinated will probably become infected at some point, but whether they end up as symptomatic or asymptomatic cases is another question. This is essentially what characterizes respiratory viruses in contrast to HIV, for example. There are people who are immune to the AIDS virus due to certain genetic polymorphisms which, by the way, we also measure as standard for our Premium clients. This is not the case with the novel coronavirus, unlike the Spanish flu, with which it is repeatedly compared: it has to be emphasized that the history of SARS-CoV-2 so far clearly points to each successive mutation event being more infectious and/or more dangerous.

The current prognosis of the Task Force of Dr Robert Hess still holds true: the pandemic is going to persist for a very long time, and the prospect that the virus will be with us forever is becoming more and more likely. This is because recovered and vaccinated individuals can still be carriers of SARS‑CoV‑2 and because the virus is mutation prone. There is also the potential for the animal kingdom to act as a reservoir for the disease – it is not yet known which animals can become infected with SARS‑CoV‑2 and spread the virus. From the case of the mink farms in Denmark, which we reported on in great detail a year ago, there are now very alarming statistics on how dangerous it is when animals also become infected. If we assume a similar regime as with influenza (bearing in mind that we have only moderate control over this less aggressive virus), then we will need to have an annual cycle of vaccination, because the previous year’s vaccines are never a perfect fit for the pathogens currently in circulation. This will definitely be the case with SARS-CoV-2 as well. Every year, the death rate from influenza in a medium-sized country such as Germany is around 10,000, sometimes even higher. In the more severe influenza years, for example on the American East Coast, the intensive care units are stretched to capacity. And if we add Covid-19 to the equation, hospital systems worldwide will have to be restructured.

As Dr. Robert Hess mentioned already, the level of protection depends on the sum total of antibodies, which obviously forms part of our monitoring. The antibodies are all directed against the spike protein, but not necessarily against the same regions. Many different types of antibodies are formed, which our monitoring classifies according to their effectiveness. In the case of a second infection, antibodies can even amplify the symptoms. However, the more antibodies there are in total, the greater the probability there will be some that also protect against mutations. The crucial question here is how high the antibody titer must be to protect against infection. In professional circles, we call this the “correlate of protection”, a figure that is usually defined by the WHO. Hepatitis provides a precedent: when the concentration of antibodies falls below a certain value, vaccination is called for; as long as it remains above that value, vaccination is not required. This is how the disease is managed. No such value exists for SARS-CoV-2, as no studies have been done on this so far. From our own SARS-CoV-2 antibody monitoring, we assume an average value of at least 3,000 BAU per mL, where BAU refers to binding antibody units with the relevant average efficacy classification.

Among the low responders and non-responders, there is a large group of people who take medications that suppress the immune system, or who have a donor organ and take drugs that prevent the immune system from rejecting it. This inevitably has the consequence of making pathogens difficult to fight off, but at the same time, the reaction to vaccine antigens is also weakened. This is a situation that affects patients who have to take anti-cancer drugs that affect the functioning of the immune system. Some of these medications can almost completely eliminate the B lymphocytes, which are important for the formation of antibodies. This is because the immune response occurs in several parallel pathways. The reaction to antigens produced to counter pathogens or derived from vaccination depends on how well the individual pathways work. One level is the antibody response, for which the above-mentioned B lymphocytes are indispensable. For example, rituximab, which is prescribed to alleviate certain types of cancer or arthritis, prevents the formation of B-lymphocytes and as such is a drug that needs to be taken into account here. Furthermore, there are steroids and antimetabolites that inhibit cell division and thus impair immune function in various ways. Added to which, there are the calcineurin inhibitors, such as cyclosporine and tacrolimus, which alter the T-cell response, namely that part of the immune response that may offer a certain long-term protective effect.

In non-responders with rheumatic diseases, their treatment usually involves a smaller number of immunosuppressive drugs. The dosage and effect are therefore less significant than with immunosuppression in organ transplant recipients or certain tumor patients. Nevertheless, a reduced effect is also to be expected here. The same applies to allergy sufferers who occasionally take antihistamines or use sprays and creams containing cortisone. There is definitely a reduced effect here, though by no means as drastic. We have already observed this with our Premium clients in the analysis of their antibodies.

In answer to the question of whether there is at least a T-cellular immunity in the case of a poor antibody response, we have evidence to support this, but not nearly as definitively as has been suggested in scientific publications over recent months. There have been indications that some immunity is gained, but at a far lower level than assumed. In our opinion, T-cells offer virtually no protection against actual infection, but they do make a severe course of disease less likely.

We already mentioned that we are working to build up T-cell specific immune response alongside antibodies. This development is eagerly awaited.

The question of whether mRNA or vector-based vaccines are preferable for the low-responder groups arises regardless of the reasons for their immune system deficiency. Ultimately, we have to assume that congenital immunodeficiency is a contributory factor with low-responders, irrespective of the risk groups just mentioned. This is confirmed for us on the one hand by the data derived from our own Premium clients, and on the other hand by the data that has come to us from the UK. To date, it has been shown that higher antibody titers can be expected after a first vaccination with an mRNA-based vaccine than after a first vaccination with a vector-based vaccine. As regards T-cell level, however, the situation is exactly the reverse: a higher value can be observed after a first vaccination with a vector-based vaccine. We should soon have the relevant data for the second vaccination. We see here that the combination of a first vaccination with a vector-based vaccine and second vaccination with mRNA can produce up to 10 times more antibody titers than if a vector-based vaccine is administered twice. As far as T cells are concerned, the combination of both principles also seems to be very effective. And that is why the best strategy for booster vaccinations has to be clarified with some degree of urgency. Our vaccinated clients have almost exclusively received an mRNA-based vaccine for both jabs.

Regarding the question of how a program of booster vaccinations might look, there are a couple of options available: on the one hand, a next-generation mRNA vaccine which also increases T-cell stimulation, and on the other hand (depending on the results in those affected), it may be possible to switch to a vector-based vaccine for the booster.

In conclusion, we can say that individualized vaccination schedules would be the optimal route to go down. I see it as my job to develop a long-term individual vaccination scheme.

According to Doctor Robert Hess, the Delta variant is not the dreaded super mutant

Dr Robert HEss

Dr Robert Hess – 06/18/2021

According to Doctor Robert Hess, the Delta variant is not the dreaded super mutant, but it may be a game-changer in a negative sense.

In various parts of the UK, incidences are rising sharply again; the seven-day rate, which has long been around 20 new infections per 100,000, has recently risen to over 90. Mass testing has now been started in the north-west of England and the vaccination campaign has been stepped up.

Delta has twelve genetic changes in its spike protein compared to the original Wuhan strain discovered in December 2019. However, it has no changes at positions 501 or 484 of the receptor binding site, which I are closely monitoring. These mutations have so far been detected on the Beta (South Africa B. and Gamma (Brazil P.1) virus variants and defined as escape mutations. In the case of the Delta variant, however, the relevant change is the L452R substitution in the spike protein. Initial experiments in the laboratory suggest that it significantly boosts binding to the ACE 2 receptors, making it more infectious on the one hand and more dangerous on the other. This means that the risk of infecting a person from the same household is 60% higher with Delta than with the previously dominant Alpha variant; in other words, it is much more easily transmissible. This is apparent not only from the increase in the number of cases but also from contact tracing. The percentage of infected contacts is higher at 12.5% than for persons infected with B.1.1.7 at 8.1%. Data from the UK also indicate that individuals who contract B.1617.2 are at greater risk of ending up in hospital than those who contract B.1.1.7. These statistics make it clear that Delta is not only more infectious, but also more dangerous.

In a study just published in the Lancet, medical experts looked at how effective the antibodies produced by vaccinated individuals are against the Delta variant. The good news is that everyone who received two doses of their particular vaccine developed antibodies against the spike protein of SARS-CoV-2. The bad news, however, is that these antibodies are clearly less able to neutralize the Delta variant than the wild-type virus by a factor of more than 5.8.

For those who have received only one vaccine dose, the effect was even more worrying. 21% did not neutralize the wild type very effectively. For Alpha it was 50% and for Beta (i.e. South Africa) it was as much as 75%. The antibodies produced by a single dose were to all intents and purposes ineffective against the Delta variant in 80% of cases. These findings are clearly at variance with the report issued by Public Health England in which it was stated on a purely empirical basis and without any clinical evidence having been gathered that double vaccination could prevent 96% of hospitalizations. We are deeply skeptical of this claim.

Another study from England with a much better design shows that effectiveness against the Delta variants is clearly reduced, with a single dose of an mRNA or vector-based vaccine protecting against a symptomatic course of the disease in only 34% of cases. By comparison, a single jab protects in 51% of cases caused by the Alpha variant. Efficacy is thus clearly reduced by the new variant. After two doses of an mRNA vaccine, protection against Delta is 88%, slightly lower than the 93% efficacy rate for Alpha. The equivalent rate for two doses of the AstraZeneca vector vaccine is 60% protection against symptomatic disease with Delta and 66% with Alpha. The UK government has already responded by postponing the lifting of all restrictions, originally planned for 21st June, by four weeks. This change was of the utmost urgency, as Prime Minister Johnson announced it immediately after the G7 summit. What has been dubbed “Freedom Day” has now been postponed to 19th July.

The UK is once again at the focus of our attention because, in the western world at least, it is “Delta land” par excellence and, at the same time, it is a leader in the field of gene sequencing. It therefore makes sense for other countries to closely observe what is happening there. The current scenario is also absolutely fascinating for us as scientists. Infections have increased in the UK by 64% in the last few weeks. In the worst-affected areas, cases are even doubling every week. The link between infections and hospital admissions has weakened, but it has not been broken. The number of people in intensive care units is also growing again. According to Public Health England, 91% of new cases are now caused by the Delta variant. Our prediction has been validated, and the race between mutations and vaccination is vividly illustrated here once again. How quickly can the vaccination program be implemented? How well will the vaccines work? And how soon will the next mutation emerge? What is still unclear are the numbers of Delta patients admitted to hospital who had been vaccinated. At the moment, we have three different figures which range between five and twelve percent, so we cannot say that the vaccines are forming a solid wall of defense against these mutations so far. We endorse the four criteria laid down by the UK for mapping the way out of the crisis.

1) the progress made by the vaccination campaign

2) the efficacy of the vaccines

3) the burden on the health system and

4) the risk posed by new mutations.

We predict that the fourth criterion will be the most challenging worldwide.

Looking carefully at the mutations observed in the Delta variant, it is clear that this is definitely not the dreaded super mutant that would ultimately render the entire vaccination strategy futile. It is only a foretaste of what may lie ahead.

Even in other countries that already have a high vaccination rate, such as Chile, the infection rate continues to rise, although the Delta variant has not yet made an appearance there. In Chile, they are still struggling to control the P1 variant. Due to the non-homogeneous vaccination regime in the country, where mRNA- and vector-based vaccines are being administered alongside protein vaccines from China, it is not yet possible to make a definitive comparison of their effectiveness against P1. Ultimately, we have to conclude that, even with a high vaccination rate, a reduction in the number of infections is nowhere in sight, especially as winter is now beginning in Chile.

In Israel, another country that we are observing closely, the vaccination strategy has paid off so far. However, gene sequencing there shows that the Alpha variant still has a monopoly. It remains to be seen whether further mutations will be introduced into the country.

In Moscow, which has taken on the status of “Delta city”, the rate of infection is also soaring and the number of patients requiring artificial respiration in intensive care units has risen sharply.

We are working on the assumption that the antibodies triggered by the vaccines currently in use are therefore less effective. It is possible that, with an overall higher antibody volume, Class 1 of the neutralizing antibodies (i.e. those with the highest efficacy) will also increase and consequently be more effective against the Delta variant. I measure these levels every three months for our Premium clients.

On 30th March 2021, the WHO Commission of Inquiry issued a statement

Dr Robert Hess

Dr Robert Hess – 06/01/2021

On 30th March 2021, the WHO Commission of Inquiry issued a statement to the effect that a laboratory accident as the cause of the pandemic was “extremely unlikely”. The skepticism we expressed at the time about their findings is now being vindicated.

The reevaluation of the surrounding circumstances by U.S. media, leading European scientists and even White House officials is not based on any new evidence, and nothing new has come to light, so we are more than surprised by the traction that the theory is gaining. At the same time, we take quiet satisfaction that our assessment at the time is now considered plausible by professional colleagues and by serious political institutions. What is supposedly new is in fact a republication of an article in the Wall Street Journal from November 2019 concerning three employees at the Wuhan Institute of Virology (WIV) who became so seriously ill with cold and flu-like symptoms that they had to be treated in hospital.

Just a fortnight ago, Science magazine published an article and open letter signed by 18 prominent experts calling for the investigation to be reopened. There is no smoking gun pointing to a laboratory leak, just as there is no proof that the virus has a natural origin. Consequently, the authors of the article have plumped for a 50:50 probability, compared with our odds of 60:40 in favor of a laboratory accident. And that is the order of likelihood we are standing by.

The authors of the Science article were stung into action by the official conclusions of the WHO Commission of Enquiry on 30th March 2021 which rated a laboratory accident as “extremely unlikely”. We strongly disagreed with that at the time and said so in no uncertain terms. We also expressed the view that this investigation was a farce. Even the WHO chief Tedros Adhanom Ghebreyesus has now voiced his own criticism, and that is quite astonishing, because ultimately he was the one who authorized the March statement. At the end of the day, it has to be conceded that the commissioners did not have access to raw data while they were in China, including information on previous patient samples from before December 2019, although they were allowed to visit some institutes and the possibility of a laboratory accident was given serious consideration. Tedros now admits that this investigation was inadequate. The mission was severely handicapped by the decision on the part of the Chinese government to “disinvite” colleagues with whom we work very closely, in particular the eminent German scientist Christian Drosten.

The commission itself had considerable internal conflicts of interest in its makeup. The team included Peter Daszak, head of the EcoHealth Alliance, a non-governmental organization that aims to protect health and ecosystems. In any serious investigation of a possible laboratory accident, Daszak would rank among the main suspects, because for many years the American worked together with the Chinese virologist Shi Zheng-Li. Supported by American funding that Daszak helped to source, Shi Zheng-Li was researching the coronaviruses found in bats; he captured them in the nearby caves and brought them to the Wuhan Institute of Virology over a period of 15 years. The aim of the project was first to clarify the origin of the SARS 1 pandemic and then to find out as much as possible about other potentially dangerous coronaviruses. So, the question arises: could the honorable intention to prevent a pandemic have been the trigger for the one we are now experiencing?

The theory of a laboratory accident is given added credence by the fact that the pandemic started in Wuhan. There is a general consensus that SARS-CoV-2 will originally have developed in horseshoe bats, a species widespread in Southeast Asia. But where did the virus make the crossover to a human or an intermediate host? At first, suspicion fell on a wild animal market in Wuhan. A conspicuously large number of the early patients had spent time there. However, further investigations revealed that there were also many patients among the early cases that had no connection to the animal market. The origin of the pandemic must therefore lie elsewhere. Wuhan is an ultra-modern metropolis, and it therefore unlikely that its inhabitants naturally come into contact with bats. She Zheng-Li found the closest relative of the SARS-CoV-2 virus in a mine in the southern province of Yunnan – 1,500 kilometers from Wuhan. This is only 86% identical to the novel coronavirus, meaning that decades of separate evolution have elapsed between the two viruses. However, it is conceivable that “patient zero” became infected with SARS-CoV-2 there or at some other location in China before traveling to Wuhan and spreading the virus in the city. However, there is a catch: if a virus jumps from one species to another, it can hardly happen overnight by a single change in the genome. Although an initial mutation can make the transition possible, the virus will at first be poorly adapted to the new host. Many further adaptations are necessary before a virus becomes so contagious that it can trigger a pandemic. In the case of SARS 1, which embarked on a short career as a pandemic in 2002, it has been possible to trace the many transformative steps, some of which involved viverrids as intermediate hosts. Traces of any such adaptation are missing for the SARS-CoV-2 virus. The genetic sequences recorded in the first patients at the end of 2019 are remarkably uniform.

The novel coronavirus seems to have come into the world out of nowhere as an already perfectly formed pathogen. It is possible, of course, that its evolutionary traces have simply not been found so far, or that China is keeping them under wraps. What is striking about SARS-CoV-2 is that, although it is no longer circulating among bats, it can infect various members of the carnivore group, including minks, cats and dogs. It is therefore conceivable that the virus adapted on large fur farms, for example among the fluffy tanuki from which China sources fur trimmings to supply the global fashion industry.

At this point, we have to ask ourselves why, after more than 18 months of mink, cats and dogs becoming infected through human contact, not a single animal-to-human retransmission has been recorded worldwide so far. This is yet another factor indicating a laboratory accident as the more likely cause.

We can pursue the matter further and explore the possibility that the evolution of SARS-CoV-2 took place in a laboratory, presumably at the Wuhan Institute of Virology. Viruses have escaped from such high-security facilities before. In 1977, for example, an unusual flu virus went around the world. It caused mild symptoms, mainly affected people under 26 and its genetic sequence was identical to a variant that last circulated in the 1950s. One possible explanation for this could be that old samples were used in vaccine development, thereby allowing the virus to escape from the laboratory.

There are six recorded cases of the SARS 1 virus having leaked out of laboratories in three countries – Singapore, Taiwan and China. In 2003, for example, a 26-year-old student at the Institute of Virology in Beijing became infected, blithely got on a train and traveled to her hometown 1,000 kilometers away. The student’s mother then became infected and subsequently died. The Chinese authorities quarantined around 1,000 people and were able to contain the outbreak. If SARS-CoV-2 also escaped from a laboratory, however, the question arises as to how it could have originated there in the first place. Various researchers have been looking for clues. The American scientific journalist Likus Walter describes the chain of evidence in particular detail in a report. However, we do not consider most of the points mentioned to be scientifically plausible. He thinks that She Zheng-Li was conducting so-called “gain of function” experiments in Wuhan. In experiments of this kind, virologists combine the component parts of different viruses to create new functions. The viruses can also become more infectious as a result. The intention of such experiments can be inferred from the research proposals submitted. In one case, She Zheng-Li published a successful experiment.

Wuhan has conducted at least one such experiment under the direction of Ralf S. Barec, one of the world’s leading coronavirus researchers based at the University of North Carolina. Barec and She Zheng-Li published a paper in Nature magazine in 2015 about a project in which they used the SARS 1 virus as the basic structure and added the spike protein of another coronavirus. The new virus was then able to infect human cells. Significantly, Barec is among the authors in Science magazine calling for a more rigorous investigation of SARS-CoV-2.

Any conclusion we might reach is necessarily subject to revision, because until China makes the data more transparent, all possibilities remain open, but in our view with a laboratory as the marginally more likely explanation. A virus database at the WIV with 22,000 entries was taken offline in September 2019, and initial assurances by some virologists that SARS-CoV-2 could not be a laboratory construct are now considered premature and untenable. As it later turned out, globetrotter Peter Daszak was behind an announcement to this effect that was published in the Lancet in February 2020. At the same time, there are certain features in the gene sequence of SARS-CoV-2 that give rise to speculation about possible human manipulation.

So, the debate is set to continue. The initial reluctance of the scientific community to be drawn into what looked like a conspiracy theory and to appear too close to the Trump administration has proved to be a good thing, as such considerations no longer need to temper or cloud their judgment. However, the view of the Dr Robert Hess SARS-CoV-2 Task Force is that the chance of the mystery ever being solved is slim. At the start of 2020, China imposed a gagging order, whereby no one in the country was allowed to say or publish anything about the origin of the virus. Nevertheless, there is a body of evidence to be found outside of China.

We believe that, if more information comes to light, it should be possible to deduce the origin of the pandemic by scientific means. At the same time, it is known that U.S. intelligence agencies, as well as other Western intelligence agencies, are beginning to trawl through human and electronic sources, which may eventually provide the basis for science to get to the bottom of the whole affair.

It is possibly also a matter of significance that the pace of mutation has accelerated in the last fortnight, which is due to the vaccination programs. As we have already pointed out many times before, the virus is forced by the vaccines to activate, adapt and optimize itself by means of escape mutations. Unfortunately, there is very little awareness or acceptance among political leaders that it is precisely the vaccinated population who should be tested because of this issue and that more sequencing should be carried out as part of the tests.

The latest variant to have been detected in Vietnam is ultimately a combination of the British and Indian virus strains. It disperses very quickly through the air, so that the viral load in the throat increases much faster after infection and thus spreads very strongly in the environment. This makes it much more contagious than the previously known variants. The race between virus mutations and vaccine development goes on …