When Health and Human Services Secretary Robert F. Kennedy Jr. terminated $500 million in federal funding for mRNA vaccine research last week, claiming he had “reviewed the science,” his press release linked to a 181-page document as justification.

I reviewed Kennedy’s “evidence.” It doesn’t support ending mRNA vaccine development. It makes the case for expanding it.

The document isn’t a government analysis or systematic review. It’s a bibliography assembled by outside authors that, according to its own title page, “originated with contributions to TOXIC SHOT: Facing the Dangers of the COVID ‘Vaccines’” with a foreword by Sen. Ron Johnson (R-Wisc.). The lead compiler is a dentist, not an immunologist, virologist, or vaccine expert.

NIH Director Jay Bhattacharya has suggested the funding was terminated due to lack of public trust in mRNA vaccines. But misrepresenting evidence to justify policy decisions is precisely what erodes public trust. If we want to restore confidence in public health, we need to start by accurately representing what the science actually says.

Here’s what Kennedy apparently missed: Most of the compiled papers are in vitro studies (laboratory experiments in test tubes or petri dishes) documenting effects of SARS-CoV-2 spike protein, not vaccination. These laboratory experiments, while limited in their clinical relevance and unable to establish causation, consistently show harmful effects from the spike protein produced during infection. The implicit message throughout: Infection produces spike protein that can cause harm, therefore vaccination, which produces controlled amounts of spike without the virus making copies of itself, makes sense.

Some of the papers included in the bibliography are even explicit about this. One examining neurological effects concludes “the benefits of COVID-19 vaccination far outweigh the risks of a neurological complication.” Another review in the packet directly compares infection with vaccination and concludes vaccination is “the more favorable option for protection.” Kennedy is literally citing evidence that contradicts his position.

The document’s methodology reveals how this happened. The authors of the compilation acknowledge that “most in vitro studies cited here used recombinant spike proteins or spike proteins in pseudoviral vectors,” not actual vaccines. They grabbed papers using any mention of spike protein, whether from infection or vaccination, and presented them as evidence against vaccines.

The apparent deception runs deeper. Multiple cited studies inject spike protein or mRNA intravenously into mice, inducing myocarditis, or even directly into brain tissue, routes obviously never used in human vaccination. (Vaccines are injected into shoulder muscle.) The packet includes studies with hippocampal injection of spike, brain infusion in mice, and injection into cerebrospinal fluid. While these experiments help identify theoretical hazards, they reveal nothing about the real-world risk from the intended intramuscular injection in humans.

When it isn’t misreading studies’ conclusions, the compilation uses them in an intellectually dishonest way. For instance, it misleads about how long spike protein stays in the body. It cites studies showing spike protein from SARS-CoV-2 infection lasting months, driven by the virus continuously making copies of itself, to suggest vaccine spike persists similarly.

But vaccine spike typically clears within two weeks because there’s no replicating virus. Those who assembled the document know this distinction but obscure it.

The safety distortions are egregious. The document highlights anaphylaxis rates as high as 1 in 2,280 doses from selective studies, while systematic CDC surveillance estimates 4.5 per million doses, 400 times lower. They emphasize myocarditis in young males, which peaked at about 100 per million among males ages 16-17 after the second dose, without mentioning that SARS-CoV-2 infection causes myocarditis at higher rates with worse outcomes, or that rates have since dropped to background levels.

Most damning is what’s absent. The compilation ignores the Danish nationwide study of approximately 1 million JN.1 booster recipients that found no increased risk for 29 specified conditions. It omits the Global Vaccine Data Network analysis of 99 million vaccinated across multiple countries finding no new or hidden safety signals. It excludes CDC data showing the unvaccinated had a 53-fold higher risk of death during Delta, demonstrating the critical importance of mRNA vaccination. The Commonwealth Fund estimates Covid vaccines prevented approximately 3.2 million U.S. deaths through 2022.

The papers themselves often contradict the compilation’s framing. Multiple studies state “we cannot infer any causality” from their findings. The document’s own sources describe challenges as surmountable, not fatal flaws. Yet Kennedy presents these tentative findings, which the authors themselves call preliminary, as definitive evidence requiring immediate action.

Beyond Covid vaccines, Kennedy’s decision undermines pandemic preparedness. The 22 terminated projects worth $500 million represent the expensive late-stage development that BARDA uniquely funds — Phase 3 trials, manufacturing scale-up, and strategic stockpiling that private companies can’t afford. Kennedy promises “safer, broader, whole-virus vaccines” as alternatives, apparently unaware these take six months minimum to update versus weeks for mRNA. When the next pandemic virus emerges, those extra months will translate directly into preventable deaths.

I’ve analyzed Covid vaccine safety data intensively since 2020. There are real discussions to have about rare side effects, risk communication, and policy trade-offs. But those require honest representation of evidence.

What Kennedy has done is different. Most papers in the compilation found infection-related harms, evidence that actually supports vaccination, yet he is wielding it against vaccines. He’s citing sources that explicitly support vaccination while claiming they oppose it.

This isn’t scientific disagreement. It’s either staggering incompetence or willful misrepresentation. When half-billion-dollar decisions affecting pandemic preparedness rest on such foundations, the scientific community must respond clearly: Kennedy is using evidence that refutes his own position to justify dismantling tools we’ll desperately need when the next pandemic arrives.

Jake Scott, M.D., is an infectious disease physician and clinical associate professor at Stanford University School of Medicine.

Around 5–10% of people with COVID infections go on to experience long COVID, with symptoms lasting three months or more.

Researchers have proposed several biological mechanisms to explain long COVID. However, in a perspective article published in the latest Medical Journal of Australia, we argue that much, if not all, long COVID appears to be driven by the virus itself persisting in the body.

Since relatively early in the pandemic, there has been a recognition that in some people, SARS-CoV-2 – or at least remnants of the virus – could stay in various tissues and organs for extended periods. This theory is known as “viral persistence”.

While the long-term presence of residual viral fragments in some people’s bodies is now well established, what remains less certain is whether live virus itself, not just old bits of virus, is lingering – and if so, whether this is what causes long COVID. This distinction is crucial because live virus can be targeted by specific antiviral approaches in ways that “dead” viral fragments cannot.

Viral persistence has two significant implications:

1. when it occurs in some highly immunocompromised people, it is thought to be the source of new and substantially different-looking variants, such as JN.1

2. it has the potential to continue to cause symptoms in many people in the wider population long beyond the acute illness. In other words, long COVID could be caused by a long infection.

What does the research say?

While there remains no single study that confirms that persistent virus is the cause of long COVID, collectively several recent key papers make a compelling case.

In February, a study in Nature found a high number of people with mild COVID symptoms had extended periods of shedding the genetic material of the virus, so-called viral RNA, from their respiratory tract. Those with persistent shedding of this viral RNA – which almost certainly represents the presence of live virus – were at higher risk of long COVID.

Other key papers detected replicating viral RNA and proteins in blood fluid of patients years after their initial infection, a sign that the virus is likely replicating for long periods in some hidden reservoirs in the body, perhaps including blood cells.

Another study detected viral RNA in ten different tissue sites and blood samples 1–4 months after acute infection. This study found the risk of long COVID (measured four months following infection) was higher in those with persistently positive viral RNA.

The same study also gave clues about where in the body the persisting virus resides. The gastrointestinal tract is one site of considerable interest as a long-term viral hideout.

Earlier this week, further evidence of persistent virus increasing likelihood of long COVID has been published as part of the RECOVER initiative, a collaborative research project that aims to address the impacts of long COVID.

However, formal proof that virus capable of replicating can last for years in the body remains elusive. This is because isolating the live virus from reservoirs inside the body where the virus “hides” is technically challenging.

In its absence, we and other scientists argue the cumulative evidence is now sufficiently compelling to galvanise action.

What needs to happen next?

The obvious response to this is to fast-track trials of known antivirals for prevention and cure of long COVID.

This should include more left-field therapies such as the diabetes drug metformin. This has possible dual benefits in the context of long COVID:

• its antiviral properties, which have demonstrated surprising efficacy against long COVID

• as a potential therapeutic in treating impairments related to fatigue.

However, another major thrust should be the development of new drugs and the establishment of clinical trial platforms for rapid testing.

Science has uncovered exciting therapeutic options. But translating these into forms usable in the clinic is a large hurdle that requires support and investment from governments.

Demystify and preventing long COVID

The notion of “long infection” as a contributor or even the driver of long COVID is a powerful message. It could help demystify the condition in the eyes of the wider community and increase awareness among the general public as well as medical professionals.

It should help raise awareness in the community of the importance of reducing rates of re-infection. It is not just your first infection, but each subsequent COVID infection carries a risk of long COVID.

Long COVID is common and isn’t restricted to those at high risk of severe acute disease but affects all age groups. In one study, the highest impact was in those aged 30 to 49 years.

So, for now, we all need to reduce our exposure to the virus with the tools available, a combination of:

• clean indoor air approaches. In its simplest form, this means being conscious of the importance of well-ventilated indoor spaces, opening the windows and improving airflow as COVID spreads through air. More sophisticated ways of ensuring indoor air is safe involve monitoring quality and filtering air in spaces that cannot be easily naturally ventilated

• using high-quality masks (that are well-fitting and don’t let air in easily, such as N95-type masks) in settings where you don’t have confidence of the quality of the indoor air and/or that are crowded

• testing, so you know when you’re positive. Then, if you’re eligible, you can get treatment. And you can be vigilant about protecting those around you with masks, staying at home where possible, and ventilating spaces

• staying up to date with COVID booster doses. Vaccines reduce long COVID and other post-COVID complications.

Hopefully one day there will be better treatments and even a cure for long COVID. But in the meantime, increased awareness of the biomedical basis of long COVID should prompt clinicians to take patients more seriously as they attempt to access the treatments and services that already exist.

Read more: The latest COVID booster will soon be available. Should I get one? Am I eligible?