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Nov 9 • 134 tweets • 38 min read
/🧵II. Why is health not “binary” (alive vs. seriously sick / dead)?

This thread is part 2 of 7 of the mother thread #FreshStart2PublicDebate.

It is about a nuanced understanding of health in terms of a complex state and about the effect of SARS-CoV-2 infections.
/ The state of health involves, for example, the state of the microbiome and it is characterized by a degree of inflammation / oxidative stress, and it is defined along the spectrum of aging / senescence.
/ Here is for revisiting the risks associated with a #SARSCoV2 infection.

The risks can be approached by dividing the time span after an infection into three phases:

The acute phase after infection
The 12 week window post-infection phase
The long term phase (3 months +)
/ Public health responses have been mainly if not exclusively focusing on phase 1: the acute phase of infection. This will become apparent already from the fact that the main aim appears to lie in avoiding ICUs from being overrun.
/ The risk of severe disease and death within the framework of the first (acute) phase of being infected has been strongly lowered from a ballpark figure of 1% IFR to one of 0.1% IFR thanks to powerful vaccines.
nature.com/articles/s4385…
/ If there were only the acute phase to consider, one might opine that science and politics have fulfilled their duty. Covid-19 may now, in as far as the acute phase is concerned, be less lethal than Influenza on a population-based level.
/ In other words, one might consider the risk of severe disease after an infection to have become a risk within the realm of what might be considered ordinary risks of life. Of course, this phrasing s is not supposed to belittle tragic fates of individuals and their loved ones.
/ Some people conclude that SARS-CoV-2 is now less dangerous than circulating human Influenza. And this is where the discussion ends?

Hang on.
/ The main risks resulting from infection arise after the acute phase. During the second phase (the 12 weeks post-infection), a peak in risk for pulmonary embolism (thrombosis)
bmj.com/content/377/bm…
/ strokes and heart attacks, thromboses, and other severe complications arises.
sciencedirect.com/science/articl…
/ The second phase (the 12 weeks post-infection) has been coined the window of “medium covid” by @BenMazer. After the medium covid window, the mentioned risks drop off significantly.
theatlantic.com/health/archive…
/ The 12 week window is also a risk after breakthrough infection despite existing pre-(cross-)immunity. In other words, being vaccinated and/or having been infected before is not a sufficient protection.
nature.com/articles/s4159…
/ This thematically leads up to what is probably the biggest concern: the mid and long term aftermath of an infection with SARS-CoV-2. The risk in this phase lies in post viral syndrome, PASC (post acute sequelae of SARS-CoV-2), or also colloquially known as #LongCovid.
/ According to the @WHO, research shows that approximately 10%-20% of infected individuals in 2020/2021 went on to develop prolonged symptoms that may be #LongCovid.

who.int/news-room/ques…
/ There does not appear to be a relationship between the initial severity of infection and the likelihood of developing #LongCovid
/ The RKI (Robert Koch institute, the German federal government agency and research institute responsible for disease control and prevention) estimates that 10% of the infected individuals develop #LongCovid.
/ #LongCovid is a generic term covering many different forms of post viral syndrome. Typicl symptoms are cough, chronic exhaustion, lung damage, inflammation, reactivation of latent viruses (EBV, Herpes viruses, etc.), immune dysregulation, etc.
nature.com/articles/s4159…
/ @fitterhappierAJ conjectures that immune dysregulation caused by #SARSCoV2 covers the following three aspects:

1. The hyperactivation of many T cells, which can prematurely age the immune sysytem;
2. The exuberant function of hyperactivated T cells, which can then cause organ damage; and

3. The exhaustion of hyperactivated T cells, which implies they aren’t winning the battle against viral proteins they are supposed to defeat.
/ Changes in T-cell activation and exhaustion are notable in non-hospitalized patients. Moreover the evidence suggested “a prolonged period of immune dysregulation” after infection.
ncbi.nlm.nih.gov/pmc/articles/P…
/ The following study of patients recovering from acute disease after hospitalization found exhausted T cells and a deranged immune profile. ncbi.nlm.nih.gov/pmc/articles/P…
/ The blood profiles of patients suffering from #LongCOvid comparing them to healthy controls reveal immunological dysfunction persisting for eight months after mild to moderate” infection including indicators of “chronic T cell activation and potentially exhaustion.”
/ Moreover, people with #LongCovid were found to miss naive T cells,
pubmed.ncbi.nlm.nih.gov/35027728/
/ Even after mild disease during the acute phase of infection, the blood clot risk is higher post infection.
news-medical.net/news/20221027/…
/ Cardiovascular disease is a major post acute sequela. heart.bmj.com/content/heartj…
/ As of August 2021, a metastudy estimated the global number of people that experienced #LongCovid to be 248 million.
medrxiv.org/content/10.110…
/ In autumn 2022, the assumption is an estimated 144 million people live with #LongCovid.
jogh.org/2022/jogh-12-0…
/ In view of the extent of the number of people experiencing #LongCovid, one may coin the rapid increase of patients that are disabled from carrying on with their daily lives and, sometimes, with work, the great #MassDisablingEvent.
jamanetwork.com/journals/jama/…
/ It appears fair to state that the current generation of vaccines appear to provide insufficient protection against developing #LongCovid after breakthrough infection.
/ Insufficient protection against #LongCovid:
nature.com/articles/d4158…
/ Insufficient protection against #LongCovid:
medrxiv.org/content/10.110…
/ Current generation vaccines do not offer sufficient protection against #LongCovid. Studies revealed that #LongCovid sufferers that had received 2 doses of mRNA vaccines produced higher levels of IgG against Spike.
/ Without vaccines, #LongCOvid sufferers had higher IgG against nucleocapsid.
/ #LongCovid affects children and adolescents. The following metastudy based on 21 studies found that the prevalence in 80,000 children and adolescents was 25.24%.

medrxiv.org/content/10.110…
/ The World Health Organization has repeatedly warned about #LongCovid. Here is an example:
theguardian.com/society/2022/o…
/ There have been warnings from Anthony Fauci, for example: theguardian.com/society/2022/o…
/ There are by now an extensive database available on #PASC / #LongCovid:
/ Another library on PASC / #LongCovid can be found here:
/ What about reinfection (sequelae of SARS-CoV-2 reinfection)?

The following study is based on about 250´000 people with first infection, about 39´000 people with reinfection and 5.4 million non-infected controls.
/ People with reinfection exhibited increased risks of all-cause mortality, hospitalization, and several pre-specified outcomes than people with first infection only.
researchsquare.com/article/rs-174…
/ There have in fact been warnings about the cumulative risk of developing #LongCovid from reinfections from the WHO.
businessinsider.com/who-official-i…
/ Chris Goodnow has publicly stated to drop his COVID hubris after having his heart harmed and has started advocating for avoiding reinfection.
thetyee.ca/Analysis/2022/…
/ Compared to non-infected controls, assessment of the cumulative risks of repeated infection showed that the risk and burden of all-cause mortality and the prespecified health outcomes increased in a graded fashion according to the number of infections.
/ Risks were lowest in people with 1 infection, increased in people with 2 infections, and highest in people with 3 or more infections.
/ Altogether, the findings show that reinfection adds non-trivial risks of all-cause mortality and adverse health outcomes in the acute and post-acute phase of the reinfection.
/ The findings highlight the consequences of reinfection and emphasize the importance of preventing reinfection SARS-CoV-2.

/
/ Chronic infections such as HIV or Epstein-Barr virus typically exhaust T cells. Already early on during the pandemic, there was evergrowing suspicion and, increasingly, evidence that also #SARSCoV2 leads to a non-neglibile fraction of chronic infections.
/ By now, there is a clear picture emerging that at least a fraction of #LongCovid patients suffer from persistent or chronic and persistent infection inflaming the immune system.
doherty.edu.au/news-events/se…
/ Another study reported that COVID infects and kills T cells contributing to immune dysfunction that favours viral persistence in the body. nature.com/articles/s4139…
/ Researchers commented:"infected T cells are not only compromised in their ability to control viral infection, but they can also transport viruses to other parts of the body through the bloodstream,causing the spread of infection, affecting various organs and parts of the body.”
/ @VirusesImmunity hypothesizes that #LongCOVID can be caused by persistent virus infection, viral remnants or an autoimmune reaction. A study on 99 patients revealed exhausted T cells that suggested the patients were fighting an active chronic infection.
/ The strength of T-cell exhaustion corresponded with the reactivation of Epstein-Barr virus in patients.
/ The drug company Merck now lists COVID as a major cause of lymphocytopenia: the destruction of white blood cells including T cells.
msdmanuals.com/professional/h…
/ If #SARSCoV2 infection causes immune dysregulation, one may expect a reactivation of other latent pathogens (shingles, EBV, etc.) and a greater vulnerability to other viral, bacterial or fungal infection?

This hypothesis was coined “the Leonardi Effect” by Dr. David Joffe.
/ In fact, since the pandemic, an increase of in severe respiratory illness requiring hospitalization in children caused by normally mild enterovirus was noted by the U.S. Centers for Disease Control and Prevention.
nytimes.com/2022/09/16/wel…
/ U.S. hospitals have also reported admitting children with an unusual array of two and even three respiratory infections — all at once.
washingtonpost.com/health/2022/06…
/ Monkeypox, a rodent virus nominally confined to Africa, has made an unusual pandemic dash around the world. Polio has resurged in New York and London. A Coxsackie virus erupted in India this year creating unusual tomato-sized rashes.
/ A severe hepatitis emerged and mysteriously affected the livers of more than 1,000 children, leading Chinese scientists to suspect Omicron infection might have increased the risk.
/ Non-viral infections have also been on the rise. The U.S. Centers for Disease Control reported a 15 per cent increase in antimicrobial resistance in hospitals in the first year of the pandemic.
/ Some researchers have speculated that a rash of fungal diseases that have plagued COVID patients may in part be due to depleted T cells. They are known to play a vital role in the adaptive immune response against fungal infections.
/ There has also been a rise in brain infections among children. A 2022 survey of 109 U.S. hospitals found a 236 per cent leap in bacterial brain infections since the beginning of the pandemic. Some were treatable with antibiotics while others required surgery.
/ Researchers speculated that bacteria in the mouth and nose might travel to the brain as COVID weakens the immune system.
/ Microbiologist Brendan Crabb, director of Melbourne’s Burnet Institute, told Bloomberg that #SARSCoV2 infection impairs the immune system in long COVID patients. bloomberg.com/news/newslette…
/ #SARSCoV2 infection leads to hyperinflammatory immune responses. It can be understood to be an accelerator of old age.
pubmed.ncbi.nlm.nih.gov/34943875/
/ In patients with severe disease, higher levels of proinflammatory cytokines are found in serum, including, e.g., IL-6, IL-2, IL-8.
pubmed.ncbi.nlm.nih.gov/34746804/
/ IL-6 is a reliable marker for biological aging.
pubmed.ncbi.nlm.nih.gov/17071038/
/ One of the immunological markers for #LongCovid is the augmented level of T cells producing IL6.
/ IL6 plays a role in long term neuropsychiatric conditions
ncbi.nlm.nih.gov/pmc/articles/P…
/ Thus, an infection with #SARSCoV2 is a potent age booster. It induces biological/immunological/cellular senescence. Telomer shortening is a biological age marker.
nature.com/articles/s4146…
/ Neurological forms of #LongCOVID involve T-cell dysfunction:
ncbi.nlm.nih.gov/labs/pmc/artic…
/
/ #SARSCoV2 first and foremost docks on to the ACE2 receptor.
/ The brain is heavily affected by #LongCovid
/ The cost of Neuro-#LongCovid
/ NEMO is cleaved in the brain
nature.com/articles/s4159…
/Long Covid may be nerve-wracking
institute.global/policy/hidden-…
/LC frequency
/Where does Parkinson come from?
/
/ #LongCovid is a vascular problem. It involves microclotting and inflammatory molecule abnormalities.
medrxiv.org/content/10.110…
/ Inflammation-type dysbiosis of the oral microbiome

pubmed.ncbi.nlm.nih.gov/34403368/
/ The risk of gut dysbiosis has been shown to increase during SARS-CoV-2 infection, as well as post-acute COVID sequelae (PASC), the latter of which is more commonly known as ‘Long COVID.
news-medical.net/news/20220927/…
/ T cell depletion characterizes severe disease (to complete the picture) regarding exhaustion of the immune system.
nature.com/articles/s4141…
/ The ORF8 protein play an important role in disrupting host epigenetic regulation via histone mimicry
/ One of the most groundbreaking studies on #LongCovid so far revealed that immune profiling yields a 94% match with self-reported LC in surveys. The data presented in this study shows that LC is physical. medrxiv.org/content/10.110…
/ LC participants have reduced central memory T cells, increased exhausted CD4 and CD8 T cells, increase IL-4/IL-6 double positive T cells, activated B cells, and dendritic B cells. The exhausted T cells suggest chronic antigens stimulating these T cells.
/ LC patients show herpes virus reacitivation (Eppstein-Barr EBV, Varicella coster VZV). LC patients show abnormally low cortisol levels. The latter appears to be one of the strongest physiological signs of LC.
/ Cortisol is a steroid hormone produced by adrenal and endocrine glands. Cortisol affects several aspects of the body and mainly helps regulate the body's response to stress. Having lower-than-normal cortisol levels (chronic hypocortisolism) is considered adrenal insufficiency.
/ There are two types of adrenal insufficiency: primary and secondary. The causes of adrenal insufficiency include an autoimmune reaction in which the immune system attacks healthy cells in the adrenal glands.
/ The following collection involves 300 papers on viral persistence, from February 2020 until June 2022: drive.google.com/file/d/1z4gS_K…
/ One can imagine #LongCovid to be a state of damaged immune system. For further reading, here is a link to a thread written about this study by one of the authors:
/ Several studies describing persisting immune efficiency post covid infection are collected here:
/ Contrary to a common misconception, data suggests that Omicron subvariants pose a significant risk for #LongCovid. medrxiv.org/content/10.110…
/ The risk of developing #LongCovid may increase with every (re)infection. This is what a study suggests based on 257,427 cohort participants with first SARS-CoV-2 infection and 38,926 participants who had SARS-CoV-2 reinfection (two or more infections).
/ 5,396,855 participants with no record of positive SARS-CoV-2 infection were in the control group. A legitimate concern is the shortcoming of the sampling bias (veterans may be comorbid).
/ Compared to patients after a 1st infection, those with reinfection exhibited an increased risk of all-cause mortality (Hazard Ratio (HR) 2.14; 95% confidence interval (CI): 1.97, 2.33)
/ And excess burden of all-cause mortality estimated at 23.8 (95% CI: 18.9, 29.2) per 1000 persons at 6 months. All burden estimates represent excess burden and are given per 1,000 persons at 6 months.
/ People with a reinfection also had an increased risk of hospitalization (HR 2.98 (2.83, 3.12); burden of 95.47 (89.17, 102.03)), and having at least one sequela of SARS-CoV-2 infection (HR 1.82 (1.78, 1.88); burden of 196.2 (186.57, 205.87)).
/ Compared to w.1st infection, those w.reinfection had increased risk of sequelae in the pulmonary (HR 2.49 (2.34, 2.65); burden 50.35 (45.64, 55.32)), and several extrapulmonary organ systems incl. cardiovascular disorders (HR 2.36 (2.23, 2.51); burden 49.83 (45.07, 54.86)),
/ coagulation and hematologic disorders (HR 2.22 (2.05, 2.41); burden 25.93 (22.51, 29.6)), , fatigue (HR 2.4 (2.22, 2.58); burden 33.39 (29.41, 37.65)), gastrointestinal disorders (HR 1.69 (1.58, 1.8); burden 27.45 (23.24, 31.93)),
/ kidney disorders (HR 1.70 (1.45, 2.46); burden 14.31 (10.69, 18.34)), mental health disorders (HR 1.97 (1.9, 2.04); burden 121.05 (113, 129.31)), diabetes (HR 1.62 (1.49, 1.76); burden 21.98 (17.56, 26.75)),
/ musculoskeletal disorders (HR 1.29 (1.2, 1.38); burden 12.97 (9.04, 17.17)), and neurologic disorders (HR 1.39 (1.32, 1.46); burden 36.02 (30.16, 42.12)).
/ Analyses of prespecified subgroups based on vaccination status prior to the reinfection (no vaccination, 1 shot, or 2 or more shots) showed that reinfection (compared to first infection) was associated with a higher risk of all-cause mortality,
/ hospitalization, at least one sequelae, and sequelae in the different organ systems in people with no prior vaccination, one vaccine shot, or two or more vaccine shots.
/ Compared to those with first infection, those with reinfection exhibited increased risk and excess burden of all-cause mortality, hospitalization, and at least one sequela in the acute phase and the post-acute phase of the reinfection.
/ / The risks and excess burdens of all-cause mortality, hospitalization, and at least on sequela during the post-acute phase gradually attenuated over time but remained evident even six months after reinfection.
/ Examination of sequelae by organ system suggested an increased risk and excess burden in all organ systems during the acute phase. The risks and burdens persisted in the post-acute phase of reinfection, and most were still evident at 6 months after reinfection.
/ How big is the cumulative risk per infection?
In the study, there was a graded association in that the risks of adverse health outcomes increased as the number of infections increased.
/ Compared to the non-infected control group, those who only had one infection had an increased risk of at least one sequela (HR 1.35 (1.4, 1.36); burden 84.13 (82.03, 86.24)).
/ The risk was higher in those who had two infections (HR 2.11 (2.07, 2.15); burden 234.58 (227.08, 241.92)) and highest in those with three or more infections (HR 3.00 (2.71, 3.31); burden 362.82 (326.37, 398.08)).
/ In pairwise comparison of those with two infections vs first infection, those with two infections had an increased risk of at least one sequela (HR 1.57 (1.53, 1.60); burden 150.36 (142.95, 157.79));
/ in pairwise comparison of those with three or more infections vs those with only two infections, those with three or more infections had a higher risk of at least one sequela (HR 1.42 (1.28, 1.57); burden 128.33 (91.88, 164.31)).
researchsquare.com/article/rs-174…
/ There may well be a limit of how many infections with SARS-CoV-2 an individual can survive.

medium.com/@socialcreatur…
/ Circulating anti-nuclear autoantibodies in COVID-19 survivors predict long-COVID symptoms

nbcnews.com/health/health-…
/ Senescence may be used to refer to biological ageing.

An infection with #SARSCoV2 appears to act on the human body like a potent senescence booster.
mdpi.com/2073-4409/10/1…
/ T-cells are named for the thymus where T-lymphocytes migrate from the bone marrow to mature. Its regression has been linked to the reduction in immunosurveillance and the rise of infectious disease and cancer incidence in the elderly.
/ Thymic involution sets the clock of the aging T-cell landscape.
sciencedirect.com/science/articl…
/ Virus infection and inflammation contribute to thymus involution, a phenomenon manifested as loss of thymus cellularity, increased stromal fibrosis and diminished naïve T-cell output.
/ Upon severe disease (COVID-19), AT2-Zellen infected by #SARSCoV2 exhibit senescence and proinflammatory phenotype. In vitro, #SARSCoV2 infection induces senescence and inflammation.
/ Infected cells can source #SARSCoV2 mutagenesis. #SARSCoV2 induced senescence is thus likely to be a key molecular mechanism promoting persistence and mutagenes.
pubmed.ncbi.nlm.nih.gov/35086840/
/ Human immune system perform at their peak when people are in their 30s, but decline when people enter their 50s. A paper this yerar confirmed that the age of 50 is indeed an inflection point for COVID deaths.
/ It posited that the loss or narrowing of T cell diversity in response to infections might explain why.
pnas.org/doi/10.1073/pn…
/ A suspicion is that #SARSCoV2 comprises a “superantigen” (SAg). These are a class of antigens that result in excessive activation of the immune system.
/ Specifically it causes non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release.
/ SAgs are produced by some pathogenic viruses and bacteria most likely as a defense mechanism against the immune system.
/ Compared to a normal antigen-induced T-cell response where 0.0001-0.001% of the body's T-cells are activated, these SAgs are capable of activating up to 20% of the body's T-cells.
/ The large number of activated T-cells generates a massive immune response which is not specific to any particular epitope on the SAg thus undermining one of the fundamental strengths of the adaptive immune system, that is, its ability to target antigens with high specificity.
/ More importantly, the large number of activated T-cells secrete large amounts of cytokines, the most important of which is Interferon gamma. This excess amount of IFN-gamma in turn activates the macrophages.
/ The activated macrophages, in turn, over-produce proinflammatory cytokines such as IL-1, IL-6 and TNF-alpha. TNF-alpha is particularly important as a part of the body's inflammatory response.
/ In normal circumstances it is released locally in low levels and helps the immune system defeat pathogens.
/ However, when it is systemically released in the blood and in high levels (due to mass T-cell activation resulting from the SAg binding), it can cause severe and life-threatening symptoms, including shock and multiple organ failure.
/ The potential superantigenic character of #SARSCoV2. pnas.org/doi/10.1073/pn…
/ More on the question of superantigenic effect of #SARSCoV2:
news-medical.net/news/20220329/…
/ Link to the mother thread

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More from @DyorsMathew

Mathew Dyors @dyorsmathew@mstdn.science Profile picture
Nov 11
1/ 🧵How much would you trust Harvard as a source of information as opposed to your family and friends?

Well, today, Harvard Medical School published an article as a part of its continuing coverage of COVID-19.

I would like to cite a few sentences.
2/ "Currently, published medical literature suggests that #LongCovid occurs in 5 to 80 percent of patients following an infection. The U.S. Centers for Disease Control and Prevention suggests that nearly one in five American adults who have had COVID-19 now have long COVID.
3/ A conservative estimate from the Brookings Institution suggests that #LongCovid may be keeping as many as 4 million Americans out of work.

#LongCOVID, considered a silent pandemic by many, is running parallel to the COVID-19 pandemic.
Read 10 tweets
Mathew Dyors @dyorsmathew@mstdn.science Profile picture
Nov 9
/ 🧵I. The two false binaries (“the double binary fallacy”) upon which public health responses to #SARSCoV2 mostly have been based on so far

This thread is part 1 of 7 of the mother thread #FreshStart2PublicDebate.
/ This subthread conjectures that public health responses have been relying on an overly simplistic understanding of immunity and of health, respectively.
/ Arguing black and white is of course almost always wrong. Health is not black and white. Immunity is not black and white.

However, people often argue that they have "had COVID-19" and seem to be done with the topic.
Read 10 tweets
Mathew Dyors @dyorsmathew@mstdn.science Profile picture
Nov 9
/ 🧵A call for a fresh start to a public debate amidst an unfolding public health disaster

We need to discuss the future of public health.
/ A global public health disaster has been and still is haunting us. At best, learning from it will allow us to understand more about how to deal with the unfolding climate disaster.
/ This “mother thread” comprising seven subthreads is aimed at multiplicators who are invited to write their own story. Moreover, it is aimed at everyone for discussing, criticizing, supporting it, and for retweeting in order to facilitate a #FreshStart2PublicDebate.
Read 17 tweets
Mathew Dyors @dyorsmathew@mstdn.science Profile picture
Nov 9
/ 🧵III. Why is immunity not “binary” (immune vs not immune against a pathogen)?

This thread is part 3 of 7 of the mother thread #FreshStart2PublicDebate.
/ Our immune system has two arms: the innate immune system and the adaptive immune system. The innate immune system is the first line of defense. It sends out the alarm that something is wrong. It generally recognizes patterns in cells that help sort self from pathogens.
/ For example, when an innate immune cell comes into contact with a bacteria cell, it identifies it as not self because bacteria have a cell wall structure that’s not found in human cells.
Read 46 tweets
Mathew Dyors @dyorsmathew@mstdn.science Profile picture
Oct 14
1/ 🧵 on China’s oral vaccine

#ConvideciaAir

by CanSino Inc.

that received an emergency authorization in China.
2/ Booster vaccination with Convidecia Air (Ad5-nCoV) induced a superior T-cell response and neutralizing antibody responses compared to those induced by the homologous inactivated vaccine booster or heterologous recombinant protein vaccine booster.
3/ At day 7 after booster vaccination, intramuscular Ad5-nCoV induced an obvious IgG antibody response, but no IgG antibody response was found in the aerosolized Ad5-nCoV group, indicating that aerosolized Ad5-nCoV stimulated a slower systemic immune response .
Read 14 tweets
Mathew Dyors @dyorsmathew@mstdn.science Profile picture
Oct 14
1/ 🧵Jetzt beginnt eine neue Welle.

Dass @Karl_Lauterbach am 8. Oktober 2022 nicht wusste, dass im November eine Welle (BQ1.1, XBB, ...) Deutschland treffen wird, darf man wohl getrost als unmöglich erachten.

2/ Es am 8.10 als eine zunehmende Unwahrscheinlichkeit zu bezeichnen, dass BA.5 die einzige Variante in der Zeit bis zum nächsten Sommer bleibt, war nicht ein scherzhafter Euphemismus.
3/ Damit bleiben zwei Optionen:

Es war
a) eine absichtliche Verzerrung der Realität; oder
b) die Frucht einer Selbsttäuschung.
Read 17 tweets

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