Dr. Philip McMillan, John McMillan
As we navigate early 2025, a significant disconnect has emerged between public perception of COVID-19 and what surveillance data tells us about its continued impact. While many consider COVID-19 a resolved issue, clinicians are observing patterns that tell a different story. These patterns suggest we’re dealing with a virus that behaves unlike typical respiratory infections, with implications that extend far beyond the initial infection period.
Dr. Philip McMillan, a leading researcher in the field, suggests that the situation is analogous to a town nestled at the base of an active volcano, where local geologists have repeatedly assured residents that an eruption is unlikely. As seismic activity increases and steam vents appear, these early warning signs are downplayed. The scientists, having staked their professional reputations on the volcano’s stability, find themselves in a difficult position. Acknowledging the growing threat would mean admitting their initial assessments were wrong. So instead, they maintain their original stance and criticize anyone who dares to speak out, even as the evidence of impending eruption mounts. When the volcano finally erupts, they simply claim they couldn’t have predicted this outcome, despite the warning signs that were present all along.
Current Transmission Rates Paint a Concerning Picture
Current data supports these concerns. The ZOE Health study in the UK reports that over 97,000 people are COVID-positive or becoming positive, a number that would have seemed shocking in early pandemic days but now passes with little notice. CDC wastewater surveillance data reveals very high viral activity across northern states, painting a picture of widespread, ongoing transmission.
However, it’s not just the transmission rates that worry medical experts. New research published in Communications Medicine has uncovered a mechanism that might explain why some patients experience lasting effects after infection. At the heart of this mechanism is a protein called ACE2 (angiotensin-converting enzyme 2), which serves multiple vital functions in the body.
The ACE2 Connection: Understanding the Autoimmune Response
ACE2 normally helps regulate blood pressure, wound healing, and inflammation. It’s also, unfortunately, the entry point that COVID-19 uses to infect cells. The new research reveals that patients who experience severe COVID-19 develop antibodies that target their own ACE2 proteins, potentially disrupting these important regulatory functions.
“This is pretty serious stuff,” notes Dr. McMillan. “What happens is that there seems to be a delay of weeks or a month before people get sick. They experience one set of symptoms, and then a month later, they develop different symptoms.” This might explain why some patients develop seemingly unrelated symptoms weeks after their initial infection.
The research team found these self-targeting antibodies appear at higher levels in patients who experienced severe COVID-19. As lead author Eric S. Geanes and colleagues note, “These results demonstrate that SARS-CoV-2 infection can increase autoantibody levels to ACE2 and other immune factors. The levels of these autoantibodies are associated with COVID-19 disease severity.” These findings imply that the virus might trigger a cascade of immune responses that continue long after the initial infection clears.
What makes this particularly concerning is the widespread nature of current transmission. In a family gathering of ten people, statistically, one person is likely to be positive. “And if one person is positive,” Dr. McMillan points out, “there’s a pretty good chance another five or six will become positive within a week.”
The clinical implications extend beyond respiratory symptoms. Since ACE2 is present in multiple organ systems, including the brain stem, heart, and kidneys, autoimmune responses targeting this protein could affect various body systems. Doctors are observing unusual patterns: patients may experience double vision, dizziness, or ringing in the ears – symptoms that don’t fit typical viral infection patterns but might be explained by ACE2 autoimmunity.
Meanwhile, the virus continues to evolve. CDC data shows rapid shifts in dominant variants throughout 2024, suggesting we’re dealing with a moving target. This evolution, combined with the autoimmune findings, suggests we’re dealing with a more complex threat than initially understood and presents a complex challenge for clinicians trying to understand and treat long-term effects.
For the medical community, these findings underscore the need for a deeper understanding of how COVID-19 works, particularly its effects on the body’s immune system. Like the hypothetical geologists observing the volcano, researchers and clinicians are seeing warning signs that demand attention, even if they haven’t yet captured broader public awareness.
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