0:00
/
0:00
Transcript

Why Scientists Are Worried About the New Combo Vaccine Strategy

When technology moves faster than transparency, we must stop and ask: what are the risks we're being asked to accept?

On the horizon is a new combined mRNA flu and COVID vaccine. It is being hailed as a convenience—one jab, two protections. But for those of us who have been following the science with a critical lens, there is far more beneath the surface.

If this new combo shot fails, it is not just about efficacy—it is a potential financial disaster for Moderna. And that, rather than long-term safety, seems to be the pressure point. As always, I come to these discussions from an autoimmune paradigm. That lens has consistently guided me to accurate predictions, including our early work on autoimmunity to ACE2 in COVID-19, which has since been confirmed.

The question we now face is this: should we combine two vaccines when we do not fully understand the consequences of either, especially with regard to long-term immune tolerance?


Dengue as a Warning from the Past

Some viral diseases, like dengue, do not respond well to vaccination. Dengue is infamous for immune imprinting. An infection with one strain can prime the immune system to overreact when exposed to another, sometimes fatally, as seen in dengue hemorrhagic fever.

COVID-19 shares a dangerous similarity. Severe cases are driven by cytokine storms and immune overactivation. If the immune system is already dysregulated or misdirected, pushing it further could do harm. That is why I argue for extreme caution. Once autoimmunity is triggered, it does not fade—it persists.


Moderna’s Trial and the Mismatch of Immune Responses

The trial for the new combo vaccine, mRNA-1083, claims non-inferior immune responses compared to current flu and COVID vaccines. But if you follow the fine print, critical questions emerge. The data is not openly accessible. Why hide the findings if they support safety and efficacy?

In their study, they used XBB.1.5 as the COVID component. Yet prior research shows that after a bivalent booster, the strongest antibody response was not to the target variant but to the original Wuhan strain. That is classic immune imprinting.

In another study involving BA.2.87.1, the largest neutralization increase, 13.4-fold, was not to the intended strain, but to JN.1, a closely related but unintended variant. This is not just immune cross-reactivity, it is immune confusion. When the immune system keeps returning to outdated viral profiles, we fail to mount effective defenses.

Rudman Spergel AK, Wu I, Deng W, et al. Immunogenicity and Safety of Influenza and COVID-19 Multicomponent Vaccine in Adults ≥50 Years: A Randomized Clinical Trial. JAMA. Published online May 07, 2025. doi:10.1001/jama.2025.5646


The IgG4 Factor and a Game Changer in Immunology

Then there is IgG4, a subclass of antibodies not commonly seen in high quantities after vaccination. Yet repeated mRNA exposure appears to trigger a shift toward IgG4 production. This subclass does not trigger strong immune responses, it tells the immune system to stand down.

In some contexts, such as beekeepers developing tolerance to stings, IgG4 is useful. But in response to viral pathogens, it is deeply concerning. Autopsy studies have revealed viral dissemination in tissues long after vaccination, suggesting reduced clearance, possibly due to IgG4-driven suppression.

In one 2023 study, mRNA-vaccinated individuals with no prior infection showed up to 46 percent of their spike antibodies were IgG4. That is nearly half the response encouraging tolerance, not defense.


Long-Term Risks and Autoimmunity on the Horizon

We must ask what happens when you combine flu and COVID vaccines in this immunological environment. If the mRNA component drives IgG4 production, will it also suppress the immune response to the flu virus? What happens if flu-specific antibodies also start skewing toward IgG4?

The targets of spike-related autoimmunity—ACE2, Neuropilin-1, and CD147—are central to vascular, neurological, and immune functions. Autoantibodies to these proteins could lead to:

• Hypertension, kidney dysfunction, and pulmonary issues (ACE2)
• Neuropathy, dysautonomia, and chronic pain (Neuropilin-1)
• Vascular inflammation and immune suppression (CD147)

And because IgG4 can mute inflammation, these conditions may not manifest acutely but instead slowly, silently over years.


Three, Five, and Ten Years: The Autoimmune Timeline

Let us extrapolate:

One to three years
Elevated IgG4 levels. Increased reinfections. Reactivation of latent viruses like Epstein-Barr and shingles. Slight mortality increase, subtle but rising.

Three to five years
Dominant IgG4 profile. Suppressed vaccine responses. Rising cancer signals and chronic inflammatory disease. The immune system starts losing adaptability.

Five to ten years
Early-onset cancers. Poor responses to new infections. Resurgence of diseases like TB, measles, and enteric pathogens. All-cause mortality climbs.

This trajectory echoes the asbestos tragedy. Warnings in the 1950s. Ban delayed until 1999. By then, the damage was done.


A Final Thought

The push to combine flu and COVID mRNA vaccines, without long-term safety data and in the presence of immune imprinting and IgG4 dominance, feels rushed, opaque, and financially driven.

We must ask harder questions. Demand open data. Push for transparency. If you silence the skeptics today, you may regret not hearing them tomorrow.

For those who want to stay informed, I invite you to explore our ongoing immune monitoring projects and upcoming courses on how to recognize and mitigate long-term immune dysfunction. Stay vigilant. Ask questions. And never trade truth for convenience.

Vejon COVID-19 Review is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.

OSZAR »