By late 2022, I was pointing out that many people, after even mild infections, appeared to have reductions in plasmacytoid dendritic cells and other immune changes without reporting symptoms that would fit the conventional definition of Long COVID. These were not dramatic claims; they were mechanistic observations grounded in emerging data. However, the implications were stark. I had numerous media appearances discussing that immune harm was occurring. This was discussed in The Tyee by Andrew Nikiforuk.
https://thetyee.ca/Analysis/2022/11/07/COVID-Reinfections-And-Immunity/

In April 2023,

http://FactCheck.org

published a piece that characterized concerns about lasting immune effects from mild infections as exaggerated. They quoted Professor Danny Altmann, who stated there was “no phenotype” resembling immunodeficiency, only “nuanced differences” that did not translate to real-world consequences. The article framed early warnings as misinformation, implying that those raising them were overstating risks. This was not neutral correction; it was authoritative closure of debate. The message was clear: mild infection left no meaningful immune scar outside severe disease or formally diagnosed Long COVID. Discussion effectively ended there for many. https://factcheck.org/2023/04/scicheck-posts-exaggerate-lab-findings-about-covid-19s-impact-on-immune-system/

Where did factcheck find the authority to promise that no such immune harm was occurring? Did they truly seek to understand what the consequences of broad t cell activation, differentiation, and death would manifest in? The dismissal was reckless and arrogant. And now proven wrong.

The personal cost for telling the truth when people were actually concerned about covid was immediate and lasting. I was tagged in threads alongside senior immunologists who dismissed the ideas outright, accused (implicitly or explicitly) of fearmongering or misinterpreting preliminary data. These characterizations spread quickly on social media, embedding themselves in timelines and memories. People lied about me. Zeynep and Jeremy Kamil said that I had paid for my own PhD, when it was actually paid directly by the National Cancer Institute for my discovery of a linked mechanism of T cell death and differentiation. Years later, a search of my name still surfaces echoes of those accusations, unaccompanied by context or correction. Professional relationships cooled; invitations to collaborate quietly dried up. I lost a fellowship offer at the National Cancer Institute as Tom Misteli, the head of NCI research, wrote how, "I needed to learn what I can and can not say." The energy spent defending basic mechanistic possibilities was energy not spent on research or clinical work. It was isolating, and it was unnecessary.

This manifested into something remarkably shocking and completely unprecedented in scientific literature. My two greatest and most eminent antithetical-fans teamed up and published an article mocking my twitter handle, saying that mild breakthrough infections correlated with 'fit and happy' t cells. https://onlinelibrary.wiley.com/doi/10.1111/imcb.12654
It was shared across social media with an interpretation to mock my claim that T cells were harmed. People that mocked me cheered, like the Harvard professor Mark Davis, along with zeynep saying that it was a good rebuttal to 'looney twitter-only claims.' On Indie Sage, Christina Pagel did not disagree with the scientific content but expressed disappointment at the devolution of my interlocutors, that she was not a fan of shaming and mocking no matter how outlandish my claims were. She was wrong on both counts. Their mockery is now a testament to their ignorance and the devolution. This is not something they can retract, only deny publicly.

When it occurred I reached out to the editor and he asked me if I would like to reply about the scientific content. I wanted to, but, on advice of a friend who was mortified at the conduct of the individuals and the journal itself, asked for an investigation of bullying from professors. The journal concluded the investigation saying that only my followers would know that I was the one being referenced, so were under no fault or obligation to amend the title. They retracted the offer for my response. (I included this saga and the emails to Nick and the BMJ. They chose not to include it.)

I continued to watch the literature. The signals did not vanish: persistent T-cell alterations, exhausted phenotypes, subtle shifts in innate compartments. These were not the province of fringe voices; they appeared in mainstream journals, yet the narrative remained that mild infection was immunologically inconsequential for most. The possibility that repeated or even single mild infections could erode immune resilience was treated as speculative at best, irresponsible at worst. I paid a price for insisting otherwise, not in fame or notoriety, but in the quieter currency of reputation and peace of mind.

Now, in early 2026, the conversation has shifted. A recent Daily Mail article discusses widespread reports of people “getting sicker more often,” with doctors noting struggling immune defences against routine bugs. The piece quotes Danny Altmann again, this time describing the hypothesis of lasting immune harm from mild COVID as “reasonable.”

The idea is presented as fresh and worthy of consideration. There is no mention of the earlier certainty that no such phenotype existed, no acknowledgement that some of us were attacked for articulating precisely this possibility years ago.

The system lacks both memory and foresight.

The absence of reckoning is striking. Those who confidently declared “no phenotype” now entertain the same hypothesis without reference to prior denial. No correction, no apology, no credit to those who endured the backlash. This is not personal grievance alone; it reflects a broader pattern in science where consensus resists challenge until the evidence becomes overwhelming, then absorbs the insight as if it were always obvious. History is replete with such examples (Semmelweis, Warren and Marshall), yet we seem incapable of learning the lesson.

The societal toll compounds the individual one. Delayed acceptance meant delayed mitigation: fewer precautions against reinfection, less urgency in studying immune reconstitution, slower recognition that population-level immune dysregulation might follow waves of mild cases. Excess respiratory illness, rising cancer concerns, unexplained reactivations. These are not abstract. They represent preventable burden born of a refusal to countenance uncomfortable possibilities when they were first raised.

Vindication, when it arrives quietly and without acknowledgement, is a hollow reward. The smears linger longer than the evidence ever did. Yet the deeper failure is not personal. It is the persistent hubris that treats early, mechanistic warnings as threats rather than contributions. Until we cultivate the humility to listen when the data are still emerging, rather than demanding certainty before engagement, we will pay this price again in the next crisis. I hope the record shows that some of us tried to warn you, not for credit, but because the immune system deserved better stewardship than it received.

I am glad I can look upon this period knowing that I did my very best, was ruthless, about conveying what seemed so clear to me, in very unambiguous terms. What is happening was more important than my professional standing as a fragile, early-career immunologist, because I was placed in a niche position as a specialist in T cell aging and death.

I hope I helped you. Thank you for your support.

AJ

1. immunocompromised individuals

2. Long Covid sufferers

3. parents protecting vulnerable kids

4. anyone still acknowledging that airborne viruses like SARS Cov 2, RSV, and flu are disruptions at best and serious threats at worst.

This is part of a persistent pattern. These figures, embedded in left-leaning elite media circles, have spent years pushing narratives that downplay ongoing Covid harms often through ridicule, selective science, and utilitarian trade-offs that dismiss the vulnerable. Stewart, once a fierce advocate for 9/11 first responders exposed to toxic air, now platforms and participates in dismissing precautions against a virus that causes comparable long-term damage: immune dysregulation, vascular injury, viral persistence. The hypocrisy is stark.

Let’s enumerate some of the interconnected threads here, because the connections run deep and reveal a machine at work.

1. Ridicule as the primary tool. The exchange uses humor to stigmatize caution, implying masking is now irrational. This echoes broader media tactics: frame ongoing precautions as eccentric or fear-driven, while ignoring evidence that repeated Covid infections amass cumulative harm via autoimmunity, cardiovascular events, neurological issues, and T cell exhaustion. Ridicule enforces conformity; it pressures people to abandon protections rather than engage with the science showing Covid isn’t “just a cold.”

2. Utilitarian dismissal of vulnerable lives. Emily Oster, the economist who became a pandemic parenting influencer, repeatedly downplayed risks to children, arguing schools weren’t major spreaders, that unvaccinated kids posed risks comparable to vaccinated elders, and that severe outcomes were rare. She ignored the transmission chain whereby kids spread to teachers, families, communities, and with disproportionate impact on lower-income workers in high-contact jobs. Yet Oster’s reach extended into elite Democratic circles. Michelle Obama included her on the “Kitchen Cabinet” for her nutrition imperative, the former First Lady’s child wellness initiative, promoting healthy food while downplaying infectious risks to kids.

3. Selective, inaccurate science platformed without challenge. Zeynep Tufekci, the NYT columnist and sociologist, appeared on Stewart’s podcast in earlier episodes discussing Covid with a “nuanced” lens that critics say consistently minimized Long Covid and immune impacts. Claims that Covid doesn’t meaningfully harm the immune system fly against studies showing persistent antigen, T cell exhaustion, T cell loss, and increased autoimmune risk after infection. With Stewart hosting her and Favreau echoing similar lines elsewhere reveals a feedback loop where left-media outlets cite those willing to overextend their competence and expertise toward minimization, manufacturing consent for endless circulation.

4. Ashish Jha, Dean at Brown (where Oster was) who led the Biden-era response to Covid, repeatedly downplayed immune harm. In 2024, he tweeted there’s “a lot of bad information” about COVID damaging the immune system, rejecting evidence of lasting dysregulation. His efforts helped normalize endless infections and falsely assuage valid concerns of rising immune dysfunction in the population, as noted in the BMJ and recently, eLife.

These aren’t coincidences. Drawing from traditions of elite consensus-building, this network of cable satire (Stewart), podcast insiders (Favreau), op-ed pages (Tufekci), parenting influencers tied to Obama-world (Oster) filters information to prioritize aggregate “normalcy” over individual harm. Economic pressures, political optics, industry lobbies all align to downplay testing and precautions and treat Covid as ordinary despite its exceptional properties (persistent antigen, neuroinvasion, immune reprogramming unlike seasonal coronaviruses).

The brutality is in the deception. Vulnerable people face mockery or isolation for basic self-protection, while evidence of excess deaths, overwhelmed Long covid clinics with no treatments, and immune harm gets sidelined. Let me remind you; these people laugh believing they are untouchable, but recent studies have found T cell loss of about 10 percent in normal people at least for 22 months, and over 80 percent loss of T cells in cardiac patients. The claims Long Covid is rare were wrong, because in my opinion, this constitutes long covid and will assert itself more strongly in the future as reinfections accumulate and compensation decompensates. We’re told it’s over and that caution is outdated even as the virus continues to whittle away.

This machine depends on public acquiescence. Rejecting the ridicule, demanding accurate science, and protecting the vulnerable without mockery is the path forward.

Take care,

AJ

Read more

There would be much to discuss if we expected sincerity and coherence in the modern world. From here, I do not recall ever seeing such chaos, incoherence, cynicism, and exploitation in my lifetime. We have the prospect of Covid vaccines being pulled from the market, the half-decade late admission of covid’s immune harm, and the silence of advocates who have been satiated with awards and institutes, but no answers. While I am pleased to see admissions of the oncogenic potential of sars cov 2, I admit I was surprised it was only conceded when there was a cure to market and to conservative media. Nevertheless, we approach a garishness and bathos exemplified by the president selling Trumpcoin on the front lawn, a full professor pronouncing their h-index, and the Pharisees lending money in the temple.

If you were in attendance at the Long Covid discussion in the spring, you may have heard me recommend to hunker down for the next 8 years. I reiterate that. Sadly, there will be no rescue from intellectual or moral superiors to follow. Where are they? Where are the adults, or champions? We are descending into highly polarized tribalism, the decay of complex systems, and a flaming pageant that I suspect is to distract us from the mess behind the curtain. Imagine Prometheus had torn down the mountain with the flame of knowledge in hand, arriving to a body of people whose minds have been anesthetized with 10 second videos confirming every bias they have chosen to keep. We are in decay. At least there will be award ceremonies, hor d'oeuvres, and honorariums. To those “leaders” complicit and thriving, congratulations on the world you have brought us to.

Nevertheless, we know how covid harms the immune system to the extent to have predicted the immune harm, to the surprise of everyone who believed it was like the common cold or influenza. I’d like to draw your attention to a denialist here:

Marc uses gish gallop in order to obfuscate the immune harm from covid

1) The phenotypes from infection, broad activation and high differentiation status show there is nonspecific T cell activation. This paper shows T cell exhaustion from sars cov 2 to other pathogens https://insight.jci.org/articles/view/146701…

2) There are papers showing primed T cell apoptosis from sars cov 2, and the infection of T cells by sars cov 2 https://nature.com/articles/s41418-022-00936-x… The cd8 response is dulled after infection https://nih.gov/news-events/news-releases/sars-cov-2-infection-weakens-immune-cell-response-vaccination…

3) Mechanism includes infection of T cells and broad activation 4) Epidemiologic evidence is a lagging marker, and a basic scientist would more likely been able to project this, like I had. Nevertheless, bad advice from scientists like Marc facilitated and even encouraged infection and antigenic immune escape, so now we can see the immune response to other pathogens is harmed. https://thelancet.com/journals/laninf/article/PIIS1473-3099(24)00831-4/abstract?dgcid=raven_jbs_aip_email…

People who had covid were more likely to be infected with other pathogens subsequently. The T cell damage was evident from the broad activation and differentiation. The problem is, he can claim that those people had exhaustion without Covid being the cause and that they were predisposed to getting Covid because of a pre-existing exhaustion. This is like the people that ask for experiments where HIV was introduced and then subsequently they get AIDS.

Essentially he is just a denialist. He’s also asking for the mechanism, which is not necessary to prove that Covid actually has the effect. Many people research the mechanism behind gravity, we don’t need to prove how it works in order to prove gravity exists. People are still even arguing over the mechanism of HIV’s harm to CD4 T cells but because they actually don’t know and it’s not 100% certain that it’s simply from dividing in the T cell. It could also be from chronically activating it with a superantigen.

Finally, asking for infection controls is code for asking for studies in which people were intentionally infected rather than matched because he’s trying to claim there is confounding. The recent study that was published in the Lancet shows an increase in risk for other infections and for hospitalization by those other infections after Covid. When you ask this guy who argued that people should count on this being like any other cold, he’s going to be the second to last to admit that harms the immune system.

Take care,

AJ

One striking example of this need is the recent discovery that Lyme disease, caused by the bacterium Borrelia burgdorferi, can persist in the uterus for over a year, leading to vaginal and uterine complications. This finding underscores how pathogens may interact differently with female reproductive tissues, potentially due to hormonal influences or immune responses unique to women. The female reproductive tract is an immunologically complex environment, balancing tolerance (e.g., for pregnancy) with defense against infection. Persistent Lyme in the uterus suggests that women may harbor chronic infections in ways that men do not, contributing to under-recognized symptoms like pelvic pain, abnormal bleeding, or infertility. Without dedicated research funding, these sex-specific manifestations remain poorly understood, leaving women vulnerable to misdiagnosis and ineffective care.

Similarly, the phenomenon of long COVID highlights how immune system differences between sexes can disproportionately burden women. Studies indicate that women are more likely to develop long COVID, experiencing persistent symptoms such as fatigue, brain fog, and autoimmune-like conditions. This disparity may stem from women’s more robust immune responses, driven by genetic factors and hormonal influences like estrogen, which enhance immune activity but may also predispose to immune dysregulation. In contrast, men often experience more severe acute COVID-19, while women bear the brunt of chronic sequelae. This pattern suggests that women’s immune systems handle pathogens differently over time, necessitating research into sex-specific mechanisms and therapies.

The implications of these examples extend beyond individual diseases to the broader framework of public health. Women’s health issues, particularly those tied to chronic or misunderstood conditions like Lyme disease and long COVID, impose significant societal costs—lost productivity, increased healthcare utilization, and diminished quality of life. Yet, funding for women’s health research remains a fraction of what is allocated to more generalized (and often male-centric) studies. By investing in specialized research, we can uncover the molecular and immunological underpinnings of these disparities, paving the way for precision medicine tailored to women. This approach not only benefits patients but also strengthens public health systems by addressing a historically neglected population.

In conclusion, the distinct biology of women’s bodies demands a paradigm shift in medical research funding. Discoveries like the persistence of Lyme in the uterus and the disproportionate impact of long COVID on women reveal the urgent need to prioritize sex-specific studies. As an immunologist and public health advocate, I see this as a moral and scientific imperative: we cannot achieve equitable healthcare without understanding how diseases uniquely affect half the population. By channeling resources into women’s health research, we can illuminate these differences, improve clinical outcomes, and honor the complexity of the female immune system. The time for action is now—women’s lives depend on it.

Yours,

AJ

I will address the claim of no harm to t cells here: The claim that "COVID does not harm T cells" can be directly challenged by evidence from several studies. These papers collectively demonstrate that SARS-CoV-2 infection, including its long-term manifestation as long COVID, induces specific and persistent damage to T cell populations and functionality in ways that distinguish it from typical viral effects.

First, a Nature Immunology study from January 2022 "Immunological dysfunction persists for 8 months following initial mild-to-moderate SARS-CoV-2 infection" shows that COVID-19 leads to a prolonged reduction in naive T cells (both CD4+ and CD8+) in individuals with long COVID, persisting up to eight months post-infection. Naive T cells are essential for initiating adaptive immune responses to new threats, and their depletion compromises the immune system’s ability to respond effectively over time. This sustained loss is accompanied by elevated interferon levels (IFN-β and IFN-λ1), suggesting a chronic inflammatory state that disrupts T cell homeostasis. Such a long-term impact on the naive T cell pool is not a standard feature of recovery from other acute viral infections like influenza, directly contradicting the assertion that COVID-19 does not harm T cells. The paper states it was unique to covid and compares it to other viral infections. This effect may not completely persist, however, what it represents is sloughing of the T cells.

Second, the Immunity study "Robust T cell responses to the Pfizer/BioNTech vaccine compared to infection and evidence of attenuated CD8+ T cell responses due to COVID-19" provides evidence of specific harm to CD8+ T cells, the cytotoxic T cells critical for killing virus-infected cells. The study found that unvaccinated individuals with prior SARS-CoV-2 infection exhibited significantly reduced levels of spike-specific CD8+ T cells compared to vaccinated individuals without prior infection. Even after vaccination, those with a history of COVID-19 showed weaker and less functional CD8+ T cell responses, a phenomenon likened to the immune damage seen in chronic viral infections like hepatitis C or HIV. This attenuation indicates that SARS-CoV-2 inflicts a lasting impairment on CD8+ T cell effector function, undermining the claim that T cells remain unharmed by COVID-19.

Thirdly, there is a paper in JCI insight showing T cell exhaustion to other infections following a covid infection. It is often overlooked by naysayers. https://insight.jci.org/articles/view/146701…

Finally, a Nature Immunology study from January 2024 "Long COVID manifests with T cell dysregulation, inflammation and an uncoordinated adaptive immune response to SARS-CoV-2" reveals further harm through T cell dysregulation in long COVID patients. The research identified increased frequencies of exhausted SARS-CoV-2-specific CD8+ T cells, alongside CD4+ T cells primed for inflammation, and a lack of coordination between T and B cell responses. T cell exhaustion—where T cells lose their ability to effectively respond to antigens—is a hallmark of immune dysfunction and was notably absent in individuals who fully recovered from COVID-19 without long-term symptoms. This chronic exhaustion and misalignment of the adaptive immune response highlight a specific deleterious effect of SARS-CoV-2 on T cells, refuting the idea that COVID-19 leaves them unscathed.

Together, these studies demonstrate that COVID-19 harms T cells in multiple ways: it depletes naive T cells, impairs CD8+ T cell functionality, and drives chronic exhaustion and dysregulation, particularly in long COVID. These effects persist beyond the acute phase of infection and differ from the transient T cell changes seen with many other viruses contrary to the claim that "COVID does not harm T cells."

The recent hypothesis is a kind of apologism for infection, but nevertheless, deserves analysis. A recent study allows for such an analysis in a correlative way. The study split children between frequently infected and less frequently infected. Also, and this is important, individuals that were immunocompromized were excluded from the study. This is important because it is expected that immunocompromized people will not gain immunity from infections to the extent that immune replete people would.

What is interesting is that the study found that individuals with less frequent infections in childhood also had less frequent infections in adolescence. Individuals with frequent infections in childhood had more moderate and severe infections than the other children in adolescence but also infections decreased compared to when they were younger.

We can say this corresponds with a facet of knowledge of immunity: In childhood we are frequently infected with bugs and this decreases with age and experience. However, it challenges the notion that each infection caught earlier staves off later infection in equal measure and reduces the severity. Instead, those with frequent infections continued the trend. What does it mean? That there is not a dominant effect of the number of infections conferring an immunity benefit. If there were, and if the effect were dominant, then we would have seen that individuals with frequent infections early in life would have fewer infections later.

It also means that severity of infections is not a function of novelty, but rather intrinsic from the immune system. There remain two hypotheses of why infections were more frequently severe later in life in the people frequently infected in childhood

1. That despite removing immunocompromised individuals from the cohort, there is some kind of immune problem these individuals had to begin with

   or

2. Frequent infections predispose to severe disease by virtue of aging or dysregulating the immune system

We will address this topic later, but my hypothesis is frequent or sustained immune activation can lead to decompensatory or poor responses later on.

Yours,

AJ

Let’s enumerate the people that seemingly believe both cov 2 is ‘mild,’ a ‘cold,’ and an engineered bioweapon. A general group of people would include Trump followers. Nevermind that Dear Leader actually took the virus seriously and said it was much worse than the flu.

Our dear X leader, Elon, also believes Fauci should be prosecuted, probably for his advocacy role in gain of function research, which may have begotten sars cov 2. Yet, Elon downplays covid and believes it is overly hyped.

Before I mention another individual who fancies themselves a leader, I am noticing a pattern here. People that consider themselves patriarchal leaders have a tendency to downplay what they publicly believe to be a bioweapon. Perhaps in America’s evolution from the Angloshpere the “stiff upper lip” became misconstrued into outright denial. Maybe that explains it.

Indeed, there are individuals who fervently posit that covid was created in a lab, like Zeynep Tufekci but also attest that “kids aren’t superspreaders”, “We need to go for herd immunity,” and that kids must be back in the classroom, even better so inhaling covid to build their immunity.

Every one of these individuals undermines their own arguments because they are beholden to the special interests of billionaire donors, shareholders, or that their own companies face profit losses. For example, Elon stood to lose productivity from the reaction to Covid. Others received big monies from people with special interests and endowed chairs. The true position of privilege is to be able to hold a belief that you are not employed to hold and to have beliefs that are consistent with one another. Such congruent belief systems are developed through living an examined life. Examined by yourself, silly.

Of course, this is murky with moral relativism. For example, I would view it as a moral and intellectual failing for me to catch covid and give it to someone else. I have yet to catch covid. I am simply capable of avoiding it, but I do not hold others to this standard. As a counter example, Professor Balloux probably sees it as a moral failing for “healthy children” to NOT be exposed to covid “sooner,” to achieve what he refers to as “endemicity.”

Let me make my position clear. Based upon publicly available information, sars cov 2 is enough of an anomaly and is sufficiently harmful physiologically to warrant avoidance and to be considered man-made. Woe to the obfuscators who hold discongruent beliefs; for reality will assert itself in the form of Long Covid or FOIA.

Faithfully Yours,

Dr. Anthony J. Leonardi, M.B.B.S., Ph.D.

Assuringly, states and the federal government have moved to contain the threat of viruses and a new pandemic by banning masks and ensuring the sale of raw milk. Such measures will contain the virus in the population rather than allow it to disappear. If only we contained the threat of BSE in the same manner by putting downer cows in bonemeal. (Maybe I should stop writing lest they get ideas.)

There is an interesting parallel to this event and BSE as both pathogens are cattle-borne. An interesting remnant to the BSE scare in England is that 1 in 2000 tonsils from the UK have the prions that cause vCJD. During the crisis, some people demonstrated stubborn resolve and protested by doubling down on beef-eating. Similarly, some Americans have begun to drink raw milk.

I can’t tell if it’s a race to the bottom with standards, or that we like feasting on viruses and swimming in sewage to prove our own vigour. It seems we cut corners on safety in order to make nutrition more affordable. If it ends up sparking another pandemic, however, we will all bear the cost. I guess that’s what is meant by privatizing gains and nationalizing losses.

In my opinion, bird flu is now endemic in cattle. Meaning, there are even more opportunities for it to cross into humans. Furthermore, the virus is poorly adapted to human receptors, and can refine. It may refine to facilitate human to human spread and see its lethality rise as a consequence of better adaptation. Unfortunately, because of what we are willing to accept as far as the risk of viruses goes, it is quite possible that there will be a human H5N1 pandemic. I recommend, as I have always done, preparation. This entails a stock of N95, a plan with family and friends, and a safe harbour.

Godspeed,

AJ

“But let’s be clear,” wrote a prominent Right-wing podcast host.

“I will not mask… I will not social distance… I will not vaxx.”

https://twitter.com/Liz_Wheeler/status/1776289478526537763

“They want bird flu to be the new Covid.”

“To your point, this new “deadly” H1N1 report of a farmer catching it from a cow caused conjunctivitis (pink eye.)”

https://twitter.com/MdBreathe/status/1775574070521721020

People have taken their appreciation of risk from SARS Cov 2 and directly transferred them over to bird flu. This is disappointing, because I would have hoped we would unite over bird flu as an intolerable and dangerous pathogen for our current way of life. However, this is not the case. It seems people are truly stratified by the way they would handle plagues.

Let me make my position clear: I think the cow farming industry should adopt new safety measures to curb bird flu introduction into dairy cows and cattle. I think this should also be done for pig farming as an anticipatory measure. While we enjoy low cost dairy and pork, times have changed; we have a newly endemic, highly pathogenic avian influenza knocking on our door. Costs should be handled by the consumer and the federal government in order to keep the work viable for farmers.

Additionally, this virus is not a walk in the park. “Since 2003, there have been 868 cases of human infection with H5N1 reported, of which 457 were fatal—a 53 percent case fatality rate.”

We don’t know how that figure will change as the virus gets better at infecting human tissues from training on other mammals.

I sought to draw from the wisdom of the crowd to see when people expected H5N1 to be able to infect between humans.

Time will tell.

In the meantime, stay safe, and consider getting a summer piece of land out in the countryside.

Best,

AJ

Let’s begin with Long Covid day:

Impressively callous, this story to downplay and even dissolve LC as an entity was held until Long Covid day. Without a doubt, this was done for maximum disruptive impact.

Then, Vinay Prasad jumped on the train.

What these aforementioned parties rely on includes the nebulousness of symptom reporting, questionnaires, and amorphously set parameters. There is a basic science truth that supersedes all of this:

Simply, Long Covid reporting individuals are enriched for persistent antigen/virus. Additionally, the virus is present many months out in the gastro and lymphatics of people, while influenza is not. There is a field of research called virology that can further explain this. So when people try to paint Long Covid with the same brush they paint flu with, all one must do is ask, What is the virus doing there? Where is the flu virus in this picture?

So, my friends, the best thing to say to refute the denialists, is to simply ask what the long term consequences of chronic sars cov 2 in the gut and brain?

Take care,

AJ

But not Francois Balloux, one of the individuals who has argued that covid induced lymphocytopenia is similar to that of a common cold (it’s not). In 2022 he claimed “TB incidence may represent the best bellweather for covid-induced post-infection immune damage…” “Latent TB turns into active disease in immunocompromised people.”

Dear reader, the best indicator for the immune harm following covid were the phenotypes of the cells of the immune system. If you understood those, you would understand how fighting this infection taxes the system.

If you look back to 2020, you can see I directly warn the control of intracellular pathogens can be compromised from such phenotypes. And what do we see? EBV reads going up, TB reactivating, mycoplasma pneumoniae rising.

What’s very interesting is how these infections are not going to stop. I have argued that sars cov 2 can harm the immune systems of a population to the extent for something that is normally an R value of .98 could theoretically be pushed into R- 1.01, and then you have spread of infection that wouldn’t have existed without covid’s help.

Take care,

AJ

The mainstream academic community has maintained that there in nothing unique about SARS cov 2 from the common cold coronaviruses. The most recent edict of it’s non-remarkability came here.

Firstly, when Phetsoupanh published his paper in 2022 he compared the changes to the immune system that occurred after sars cov 2 with the changes to the immune system from other common viral infections. He clearly states the changes following sars cov 2 were unique. Therefore, there is a unique immunomodulation.

Now, some argue this immunomodulation and harm is a function of the virus’ novelty rather than anything intrinsic. Namely, Professor Ralph Baric delivered this hypothesis (not as a hypothesis, unfortunately) in a lecture at the beginning of the pandemic.

Some pundits, journalists, and bean-counters, are unfortunately only as informed or correct as the people they speak to. Shortly after Baric’s hypothesis was presented as fact, people argued Novelty was the cause of Severity: the end of the pandemic. This piece left no room for hypothesis or for the possibility there was an intrinsic component of the virus that could create severe illness. Rather, it was the novelty that caused severe illness. Such a proclamation left no chance for reinfections to be severe in any form. Thus, the pandemic was over.

Now, there are historical examples of why this is not the case with many viruses. Dengue can cause more severe disease on reinfection. Ebola also can reinfect and is lethal when it does. Both of these viruses have an important commonality: it is their immunomodulation which creates the severe disease. T cells are killed en masse in ebolavirus infection, yet the virus itself does not infect them. The power is in immunomodulation.

A new piece of information enters the fray. SARS Cov 2 forms immunomodulatory complexes which cause overreaction and harm. And when the T cells die in ebola, they dump inflammation-causing interferons as a departing gift. Here, we have an intrinsic piece of the virus that is absolutely not going away with reinfection. The only thing that could change would be the host’s susceptibility or the code in the virus itself. The issue of an intrinsic factor creating severity persists much as the inflammation persists when viewed via modified PET several years following infection.

So, it seems each infection with sars cov 2 is unlike that of a common cold coronavirus. I hope you, dear reader, are not among those who thought it was.

Take care,

AJ

When working with bacteria, fungi, parasites, and viruses, there are protections in place in order to prevent infection from those pathogens. The protections are in place to protect two parties: the individuals doing the work and society at large. As such, there are pathogens that carry differing levels of risk to the individuals doing the work and society at large. Here are a few examples:

HIV research represents a moderate risk to the individual doing the work and a low risk to society at large, due to the inefficient means of its spread AND the ability for us to treat those who have lab accidents to avoid community spread. Additionally, the risk of infection is low as the virus must be introduced to only a few sites to make infection. It is BSL 2/3.

Yersinia Pestis (plague) research carries a high risk to the person and a high risk to society at large, it is lethal and spreads easily. It is BSL 3 as it is airborne and deadly.

Adenovirus research carries a low risk to the individual, and a low risk to society at large. For this reason it is used often for gene therapies and methods in genetic engineering. It is generally BSL 2, and often is modified to not be able to replicate.

Ebola research carries a severe risk to the person and a severe risk to society at large. If it escapes from a lab it has the potential to create a pandemic. It is BSL-4.

SARS coronaviruses are regarded as a severe threat to human health and did not circulate in humans other than briefly before, and were contained. They have high pandemic potential and a high threat to life. They were BSL-3 in the united states, but due to their high potential to uncontrollably integrate themselves in the human and animal populations, should have been BSL-4.

Lab accidents happen as humans are not infallible. What matters are layers of protection. These include redundancies, both systematic and on the level of personal protective equipment for the person doing the research. The higher the BSL level, the higher these redundancies and personal protection levels. If there is a pathogen not in circulation in humans and that has the potential to kill and maim, why should it not be at the highest level? This question is not rhetorical; it is not at the highest level due to financial parsimony and the cost barrier of entry to performing such research. We have treated biosafety with the lowest levels of safety acceptable due to financial parsimony and institutional laxity. Think of the Titan, the ship chartered and constructed by billionaires who scoffed at safety protocols and mechanisms, and became victims of their own hubris. They were intelligent people but became intoxicated by their own perception of control, authority, and power. The difference is, they are not taking the rest of society down on their ship. The higher the intelligence, the higher the ability to self-delude and rationalize.

It is easy to speak now from the position of hindsight, but indeed numerous advocates and scientists have argued before 2019 that SARS coronavirus research has had the potential to ignite the very epidemic it seeks to prevent. There is a scientist named Richard Ebright who has argued the enhancement of SARS coronaviruses and sars-like viruses carries little benefit to society at large. Indeed, the shining example of such a benefit faced poor results on clinical trial and were inferior to treatments made for SARS Cov 2 that were based on hypothesis-driven science.

Societal threats should be treated as never-events, not something simply reduced to an “acceptable level.” Unfortunately this creates a barrier of entry to research that some people will chafe at. But aren’t the innocent people worth constructing that barrier for? If sars cov 2 was found in a cave, cultured in a lab, and escaped in a city, wouldn’t you be bitter about the years of life expectancy the average person has lost?

We will discuss this all in a discussion on Twitter at 6 pm EST. https://twitter.com/i/spaces/1BRJjPakQWpKw?s=20

Enjoy.

AJ

The justifications and assurances still are being made. We have governments and virologists making attempts to redefine Herd Immunity into the sorry situation we have now, in order to falsely convey a mastery of which they have no control- “we finally have met herd immunity” and falsely reassure. We also have slipshod state-funded research greased through propaganda channels that “proves” no increased risk of infection with other pathogens.

Quite a lot of denial has been employed by these parties in order to reconcile how deranged immune phenotypes will not and do not increase risk for any other infections to the extent it even makes propagandists blush if they are forced to acknowledge it, such as in the excerpt below.

To get to the meat of the matter, here are the infections found to happen more likely after covid:

1. RSV https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10582888/

   Authors at Case Western Reserve University School of Medicine, a serious institution with a history of 16 Nobel laureates found about a 1.4x risk of rsv infection among youths after covid infection.

They concluded it had to do with harm from Covid on the immune system. A claim I had been slandered for.

2. Strep Throat https://www.bmj.com/content/380/bmj-2022-072529

   Authors in the BMJ found a 1.27x increased risk of strep infection after covid.

They did not attempt conclusions as to why or how this was observed.

3. Fungal Infections https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10310397/

   Authors at the CDC claimed, “COVID-19 infection is a substantial risk factor for certain fungal infections, particularly those caused by invasive molds, likely because of COVID-19–related immune system dysregulation and immunosuppressive therapies, such as corticosteroids or other immunomodulatory medications.”

In fact, fungal hospitalizations nationwide went up, which they attributed to Covid.

Bonus: Herpes Zoster Reactivation is increased after Covid https://onlinelibrary.wiley.com/doi/10.1002/jmv.28745

Authors found a 1.59x increased risk of herpes reactivation an a 2.8x increased risk of disseminated Herpes zoster with complications.

I could include the many instances of individuals saying none of this was possible, but here we have it. I do expect the list to grow.

All the best,

AJ

There is a huge lobby for normalization of SARS Cov 2. Entire industries depend on the public’s return to normal consumer and working behaviors. As such, the rationalizations and reassurances to the public that SARS Cov 2 is a normal seasonal Coronavirus are relentless. These are constructed like homilies and catch-phrases, such as “we must learn to live with it,” and, “it’s endemic,” with the implication of its endemicity referring to the abandonment of efforts which acknowledge its existence, such as testing.

It is a complete misconception that introduction of a virus to the immune system makes subsequent infections like a common cold, and that virulence is due to novelty. If nerves, organs, and immune systems could speak, they would tell a tale of exceptional inflammation, aging, and death, which we must turn to science to hear. Professor Fuhrer would be taken aback to find there are efforts to examine specific mechanisms which tell another tale than his own.

Here, I will give you, the reader, clear enumerations where SARS Cov 2 is unlike a common cold.

1. SARS Cov 2 triggers a unique, long-lived inflammatory overreaction unseen in Sepsis and influenza. https://genomemedicine.biomedcentral.com/articles/10.1186/s13073-023-01227-x

It caused cells of the immune system to react in a way to create further inflammation and activation of the immune system for an extended amount of time. For technical facets of this, please see the paper.

2. SARS Cov 2 sends T cells into the brain while lethal influenza does not.

   

3. SARS Cov 2 directly causes autoimmunity by reprogramming a special type of T cell called the T regulatory cell, which has never been observed before. https://www.frontiersin.org/articles/10.3389/fimmu.2020.589380/full

4. The human genetic line has not propagated any sarbecovirus elements therefore never has faced Sarbecovirus infection to the extent to evolutionarily adapt, except in the unlikely theoretical possibility of extremely negative selection (meaning infected humans did not create progeny.)

There are more exceptional facets but these are simple and digestible. There is also more to write about but I must make a confession. The status quo has morphed in such a way as to browbeat scientists into disavowing a harsh reality in order to acquiesce to corporate and business interests. As we see the average life expectancy decline, we have been left intellectually out in the cold. The truth tellers have been assaulted and crushed, and the individuals that comprise the public, in denial, will put off the realization of a below 70s life expectancy until each one approaches retirement in piecemeal, just as all the grains of sand in an hourglass do not fall at once.

Enjoy,

AJ

To write about it, we must first run a google search to retrieve the piece.

Above, we have the result of a brief google search, which tells a narrative in of itself. July 17th it has been proclaimed that we have achieved a Covid milestone of some sort of relative normalcy in deaths by the virus. Additionally, we can see “normalcy” was proclaimed to be achieved by Feb 2021, before Omicron killed more people than any other variant.

Beneath the ‘normalcy’ piece we have the “Scientific American’s” response to the normalcy claim in the NYT, that there is little normal considering the death toll. Finally, we have the “New York Magazine” telling us exactly who is positioned to make the most sense of the situation and interpret the goings-on for us, in a digestible, common-sense way.

Briefly, I must side-step this train of thought to address another. I absolutely do not understand the kind of people who look to another to synthesize a situation and report back. Surely, holding any body in this esteem would only serve to make the reader susceptible to propaganda and fanciful narratives. I cannot understand the national academy members I have heard of who entrust op-ed columnists to such a duty as well, and I have indeed heard of them. Personally, the only individual whose editorials I have looked forward to and have used to shape personal opinion from is Lewis H. Lapham and that was in high school when I was a teenager. It was on matters of culture and state rather than science. If you are such a person, outsourcing critical thought, you should be aware of your susceptibility to glib arguments and homilies. Has one who has outsourced their opinions abdicated critical thought beknown or unbeknown to themselves? Does it require an admission of insufficiency? I do not know. I have never outsourced my opinions. Now to return-

Alongside and within this opinion piece published in the New York Times in July 2023, were the comments of Dr. Ashish Jha, the director, in part, of the US covid response. According to him, it was a misconception that the immunocompromised were at increased risk from Covid. The article riffs off of his comments, concluding,

“Most immunocompromised people are at little additional risk from Covid — even people with serious conditions, such as multiple sclerosis or a history of many cancers.”

Given the formatting, this was delivered as a statement congruent to and supported by Dr. Jha’s, who again, was orchestrating the US response. Furthermore, this piece does not comment on whether it is a small increase in relative or absolute risk. This is a disservice to the reader and has the potential to misinform. Interestingly, a third US government party, the National Institutes of Health published their own comments about SARS Cov 2 infection treatment guidelines the same month:

“Some patients who are immunocompromised have prolonged, symptomatic COVID-19 with evidence of ongoing SARS-CoV-2 replication despite receiving a course of antiviral therapy.”

Now reader, we will dissect these two statements. Statement 1 from the NYT seems to only consider the risk of death from the virus. Statement 2 considers the risk of prolonged symptomatic infection. Are there fates worse than death? That is up for debate. What is certain though, is that the NYT piece is making a desperate effort in its attempt to convey normalcy, as it had done in February 2021.

Outside of the piece but on Twitter, the author delivers his thesis, the coup de grace that was too emotive, speculative, and homilist even for the pages of the NYT,

“…the virus has turned into an ordinary illness.”

The virus has not turned into an ordinary illness. Symptoms are familiar things, borne from the immune response and appreciated grossly, through amorphous metrics. (Think cough, chills, sore throat, trouble breathing, headache, fever.)

Pathophysiology however, what the virus is actually doing to the body, tells a different tale of effects that SARS Cov 2 is able to do that ordinary illnesses do not. For example, even extreme lethal cases of flu do not send T cells into the brain. SARS Cov 2 does.

Scientists examined T and B cell changes after infection with normal viruses versus covid. Only Covid, not the normal viruses, caused missing unactivated naive T and B cells, something I warned about in 2020.

So we see the thesis, that the illness itself has transitioned into normalcy, is a falsehood that serves to smooth over what is happening physiologically.

There is a further, more disturbing issue of what was normal in 2019 versus what is normal today. A recent study found little difference in chronic T cell activation between Long Covid patients and controls who recovered from covid. However, it found a difference in chronic T cell activation between people who had samples taken before SARS Cov 2 infected humans in 2019 and after 2020. Meaning our controls post pandemic are not only dwindling, but that infected are being subjected to chronic T cell activation issues on a population level. Meaning basically, all people living after 2020 are subject to chronic activation, whether you have “long covid” or not.

When it comes to buying the notion it is a normal illness, caveat emptor. Also, I would question the motives of these people singing siren songs.

https://twitter.com/fitterhappierAJ/status/1308051767981150208

Stay safe out there.

AJ