A discussion about COVID-19 vaccines originally written in April 2020 with a more recent update. If you need help with questions related to vaccination against COVID-19, if you need more information on the latest developments in vaccines against COVID-19, or if there is really a need to get vaccinated against SARS-CoV-2 for you personally, do not hesitate to get in contact with us.

An update from January 29, 2021: there are now effective vaccines based on new vaccination platforms.

Contrary to what we were expecting in April 2020, several large phase-3 trials from different companies showed that vaccines against SARS-CoV-2 are effective, including in those aged between 60 and 85.

The New Neander’s Medical on January 29, 2021:

Johnson & Johnson Announces Single-Shot Janssen COVID-19 Vaccine and reports on important data: “Complete Protection Against COVID-19 related Hospitalization and Death as of Day 28.”

The New Neander’s Medical on January 26, 2021:

Astra-Zeneca-Oxford did the most honest vaccine trials. In the vaccinated old: seroconversion=99%; ZERO hospitalizations and severe cases in phase 3 trials.

A discussion about COVID-19 vaccines and vaccination in general originally written in April 2020.

Due to immunosenescence, flu vaccination does not work in the elderly.

The seroconversion after a vaccine is only 11% in those aged 80 or above.
Based on Corsini et al., 2006 (1).

The senescent immune system (of the older people) displays reduced responsiveness, and this has to be overcome if therapeutic vaccination is to be of benefit for the patient.
Based on Corsini et al., 2006 (1).

For the same reason of immunosenescence, COVID-19 vaccines are unlikely to work in people aged 70 and above. And they are the highest-risk group. Why then bureaucrats are touting COVID-19 vaccines?

The propaganda machine and the bureaucratic figureheads are constantly repeating how important it is to have vaccines against the SARS-CoV-2 virus as soon as possible. The brainwashed masses are ready to inject themselves with anything. But will vaccines work in those who are in the high-risk group, that is, people aged 70 and above? The information on the currently available vaccines indicates that it is highly unlikely.

It is well established that normal aging is associated with an impaired immune response. Responses to preventive vaccination in the elderly are also reduced.

Corsini et al., 2006 (1):

The presently available influenza virus vaccine fails to generate protective immunity in 50% of old individuals.

In particular, the seroconversion after a vaccine is 50% from 60 to 70 years old, 31% from 70 to 80 years old, and only 11% after the age of 80.

Seroconversion can be defined as production of specific antibodies in response to an antigen.

Antigen is a substance that is capable of stimulating an immune response. Examples include parts of or substances produced by viruses or microorganisms (such as bacteria and protozoa).

Corsini et al., 2006 (1), used “seroconversion factor” to measure if there was a response to a flu vaccine administration:

The seroconversion factor was calculated as the ratio of the mean titer before vaccination:titer after vaccination.

Antibody titer means antibody level in a blood sample. Note that an increase in antibody levels after a vaccination against a pathogen or after an infection with a pathogen does not mean that you are protected from getting infected by the same pathogen in the future.

Below, there is a graph from the study by Corsini et al., 2006 (1), where you can see that the conversion factor in the elderly subjects was 1. That is, the level of antibodies to a flu virus remained the same before and after vaccination with a flu vaccine.

(A) Seroconversion factor of elderly and young subjects 18 days after vaccination. Source: Corsini et al., 2006.

Senescence of the immune system in the elderly and the challenges it poses to vaccination: a study by Corsini et al., 2006 (1).

Corsini et al., 2006 (1), investigated the functionality of the immune system in young and elderly subjects. It is interesting that the level of “anti-inflammatory”, “immunosuppressive”, cytokine IL-10 was correlated with the seroconversion after vaccine administration:

The production of TNF-, IL-10, and IFN-was evaluated after in vitro stimulation of whole blood with LPS and PHA. The optimal time and stimuli concentrations were identified in preliminary experiments for each cytokine. For TNF- production, cells were stimulated for 24 h with 1g/ml LPS, and for IL-10 and IFN-, cells were stimulated for 96 h with 1.2 g/ml PHA. The spontaneous release of all cytokines investigated as well as their plasma levels were below the limit of detection before and after vaccination.

Fig. 3.Seroconversion factor after influenza vaccination and its correlation with DHEA and IL-10. (A) Seroconversion factor of elderly and young subjects 18 days after vaccination. The seroconversion factor was calculated as the ratio of the mean antibody titer before vaccination:titer after vaccination. Each value represents the meanSEM. (B) Correlation between plasma level of DHEA and seroconversion. (C) Correlation between in vitro PHA-induced IL-10 production by human peripheral blood leukocytes and seroconversion. The correlation analysis of data was performed by linear correlation. The correlation coefficient, r, andPvalues are reported in the figure. Each dot represents a donor (n 66). Source: Corsini et al., 2006.

Corsini et al., 2006 (1), further shared their ideas on the immune system in the elderly and the challenges of the vaccination in this group. We insert an extended citation of the relevant passage below.

The senescent immune system displays reduced responsiveness, and this has to be overcome if therapeutic vaccination is to be of benefit for the patient. Although the defects are quite well-characterized, the molecular mechanisms, inducing and sustaining immunosenescence and ways to overcome them, are still to be explored in more detail. Substantial data from animal studies have demonstrated a stimulatory effect of DHEA on immune function. We previously demonstrated in vitro and in vivo that DHEA can restore the age-related, defective TNF- production in macrophages and mitogen-induced splenocyte proliferation [12]. May et al. [23] demonstrated that DHEA administration reversed corticosteroid and stress-induced inhibition of immune function, Loria et al. [24] showed that DHEA administration has a protective effect against systemic Coxsackie virus and Herpes simplex type 2 encephalitis, and Daynes et al. [25] found that it can enhance IL-2 production by activated murine T cells. In a limited clinical trial, it has been demonstrated that orally administered DHEA (50 mg/daily) to elderly men with low-serum DHEA safely activated several immune functions within 2–20 weeks of treatment, including B and T cell mitogenic response and PHA-induced IL-2 production, suggesting potential therapeutic benefits of DHEA supplementation in immunodeficient states [26]. On the contrary, although highly effective in sustaining the response to vaccination in aged rodents, a short course of DHEA treatment, 2 days prior and 2 days after vaccination, failed to improve the age-related, declined response to influenza vaccination in elderly human subjects [27]. Overall, too little is known about the effects of DHEA supplementation on the human immune system, and it is still premature to relate these findings to routine clinical applications. Nevertheless, in our investigation, higher baseline DHEA levels were predictive of better immunization against influenza and may suggest that DHEA supplementation may be beneficial. Other methods of increasing immune response in the elderly to influenza vaccine may include the addition of IL-2 to vaccine protocol, the use of liposome carriers or diphtheria toxoid adjuvants, or using alternative routes of immunization [28 –31]. Concerning the immune system functionality, age-related changes in cytokine production by immune cells are likely to contribute to the decreased antibody production seen after influenza vaccination in the elderly. Numerous studies have investigated the age-related change in cytokine production after specific and nonspecific stimulation, and contradictory results have been reported [32–34]. This may be a result of sample sizes, varying states of health and lifestyle, different stimuli, and culture conditions. Results from our investigation show decreased TNF-production, unchanged PHA-induced IFN-production, and decreased LPS-induced IFN-production in the elderly, together with increased mitogen-induced IL-10 production. IL-10 and TNF-are cytokines, which have complex and predominantly opposing roles in the activation of the immune response [35, 36]. The increased production of IL-10 in the elderly, observed in response to LPS and PHA, is likely to inhibit the maturation of APC, hampering, together with decreased TNF-production, their migration to draining lymph nodes, compromising the subsequent induction of the specific immune response. Furthermore, IL-10 can induce long-term, antigen-specific anergy in CD4 T cells. Thus, it is intriguing that the possession of an anti-inflammatory genotype (high IL-10 and low TNF-production) is increased significantly in male centenarians [37]. High TNF-production may be an important and necessary part of the normal host response to pathogens, but its overproduction may cause immune-inflammatory diseases and eventually death. An anti-inflammatory phenotype (high IL-10 production) may be highly advantageous in the last decades of life, owing to the chronic proinflammatory status, which develops in the subjects with age [37, 38]. Thus, it is tempting to speculate that the presence of “high IL-10/low TNF-” could be favorable in protecting against age-related diseases, particularly, neurodegenerative diseases [39, 40], but conversely, it could hamper the immune response to infections and vaccine. Overall, our study contributes to the understanding of the effects of age on innate and adaptive immunity, which accompany the response to influenza vaccine. It represents an important bridge between basic immune function and clinical immunology in the hope of generating an effective reconstitution to improve immune response in the elderly. The results obtained may contribute to define better strategies to improve the response to vaccination in the elderly and underlie the necessity to overcome immunosenescence at the moment of vaccination to obtain a better response.

Fig. 1. Hormone proﬁle of young and elderly subjects at the moment of inﬂuenza vaccination. (A) Plasma level of cortisol. (B) Plasma levels of DHEA. (C) Ratio cortisol:DHEA. Each value represents the mean SEM. Statistical analysis has been performed by unpaired t-test. The P value is reported in the ﬁgure. Source: Corsini, 2006.

Seroconversion after a vaccine administration does not guarantee protection against diseases.

Immunosenescence in the elderly is not the only problem with vaccines. The basic idea behind vaccines is interesting. But in practice, vaccines rarely work as intended. Thus, in the majority of children, there is seroconversion after a flu vaccine administration. But children are not always protected from flu infections.

Children vaccinated against flu had 440% higher relative risk to get infected with non-influenza respiratory viruses.

Cowling et al., 2012 (2), found that children vaccinated with trivalent inactivated influenza vaccine (TIV), had the same incidence of infection with influenza viruses as unvaccinated children (see the table below). Moreover, vaccinated children had 440% higher relative risk to get infected with non-influenza respiratory viruses.

Cowling et al., 2013 (2):

(TIV vaccinated) had an increased risk of biologically confirmed non-influenza infections (relative risk: 4.40; 95% confidence interval: 1.31-14.8). Being protected against influenza (???), TIV recipients may lack temporary non-specific immunity that protected against other respiratory viruses.

Cowling et al., 2012 (2), write that vaccinated children are “being protected from influenza”. We, however, do not see this from their data. The table below shows that there was no statistically significant difference in influenza infections between vaccinated and non-vaccinated children.

Incidence rates are from respiratory specimens collected from 115 participants aged 6–15 years who received trivalent influenza vaccine or placebo during 134 acute respiratory illness episodes. Abbreviations: ARI, acute respiratory illness; CI, confidence interval; TIV, trivalent inactivated influenza vaccine. a Incidence rates were estimated as the no. of virus detections or illness episodes per 1000 person-years of follow-up. ARI was defined as at least 2 of the following symptoms: body temperature≥37.8°C, cough, sore throat, headache, runny nose, phlegm, and myalgia. b In TIV recipients there were 4 detections with both rhinovirus and coxsackie/echovirus, and 1 detection with both coxsackie/echovirus and coronavirus NL63. c Including positive detections of coronavirus, human metapneumovirus, parainfluenza, respiratory syncytial virus (RSV). The ResPlex II multiplex array tested for 19 virus targets including influenza types A and B (including 2009-H1N1), RSV types A and B, parainfluenza types 1–4, metapneumovirus, rhinovirus, coxsackievirus/echovirus, adenovirus types B and E, bocavirus, and coronavirus types NL63, HKU1, 229E, and OC43. Source: Cowling, 2012.

Table 2. Incidence Rates of Acute Upper Respiratory Tract Infection Among 115 Participants Aged 6–15 Years Who Received Trivalent Inactivated Influenza Vaccine or Placebo. Abbreviations: ARI, acute respiratory illness; CI, confidence interval; FARI , febrile acute respiratory illness; TIV, trivalent inactivated influenza vaccine. a Incidence rates were estimated as the number of ARI or FARI episodes per 1000 person-years of follow-up. b ARI was defined as at least 2 of the following symptoms: body temperature≥37.8°C, cough, sore throat, headache, runny nose, phlegm, and myalgia; FARI was defined as body temperature≥37.8°C plus cough or sore throat. Source: Cowling et al., 2012.

The characteristics of the children that participated in the study by Cowling et al., 2012 (2, can be found in the table below.

Table 1. Characteristics of Participants and Duration of Follow-up. Source: Cowling et al., 2012.

Antibody-dependent enhancement of coronavirus infections.

From another post on this website:

SARS-CoV vaccine against Spike-protein potentiated infection of human immune B cells with SARS-CoV. Yet, a majority of vaccines in development target the same Spike-protein of the virus. It is possible that you will be forced to inject a “vaccine” that actually enhances infection.

A majority of SARS-CoV-2 vaccines in development as of March 2020 target Spike protein. Yet, this type of vaccine enhances infection in previous vaccine candidates for SARS-CoV-1 and animal coronaviruses. Source of the table: Amanat and Krammer, 2020 (3).

A 2011 study on SARS-CoV-1 vaccines: “aged mice displayed increased eosinophilic immune pathology in the lungs and were not protected against significant (coronavirus) replication”.

Immunisation against SARS-CoV-1 in aged mice does not work either. We discussed this in another post on this website. The post is linked below.

https://medical-en.nneandersphysiologicalliteracy.com/t-cell-mediated-immune-response-to-respiratory-coronaviruses/

DNA vaccines de facto turn humans into a new species. But they are not effective at clearing coronaviruses.

Channappanavar et al. (Stanley Perlman group), 2014 (3):

Although several groups demonstrated the presence of SARS-CoV-speciﬁc memory CD4 and CD8 T cells (after rDNA vaccine adminisration), very few studies have demonstrated their in vivo potential to clear virus.

More on this in the post on our website that we already linked above.

Conclusions: Billions are being spent on COVID-19 vaccines that are unlikely to work in the highest-risk group, those aged 70 and above.

Common Sense, Logical Thinking:

1. The group which is at the highest risk of SARS-CoV-2 infection are people aged 70 and above.

2. Vaccination does not work in the age group that is at the highest risk from COVID-19. Corsini et al., 2006 (1):

The seroconversion after a vaccine is 50% from 60 to 70 years old, 31% from 70 to 80 years old, and only 11% after the age of 80.

3. There are multiple other challenges related to vaccines against coronaviruses, for example, antibody-dependent enhancement (ADE) of the infection, immunopathology, weak protection and inability to clear viruses in vivo.

4. Why then billions are spent on vaccines, a solution that is highly unlikely to work against SARS-CoV-2?

A Test of Physiological Literacy.

1. There is an immune phenotype associated with longevity in older individuals. What is this phenotype? Namely, what are some of the cytokine levels that describe it?

2. Is the immune phenotype associated with longevity in older individuals more responsive or less responsive to vaccination?

3. Does low carbohydrate diet increase dehydroepindrosterone (DHEA) levels?

4. Is there any supplements that can incrase DHEA levels?

Selected references:

1. Corsini et al., J. Leukoc. Biol.80: 376–382; 2006.

2. Cowling et al., Clinical Infectious Diseases 2012;54(12):1778–83.

3. Rudragouda Channappanavar• Jincun Zhao• Stanley Perlman, Immunol Res (2014) 59:118–128.

COVID-19 vaccines are unlikely to protect those who are at a higher risk. A 2006 study: Vaccines fail to generate protective immunity in 50% to 90% of older individuals.

A short summary.