Malgorzata Gasperowicz, a Calgary based developmental biologist, says that if immunity debt fully explained rising infection counts we’d expect to see a uniform rebound across all pathogens. But we don’t, she says.

For instance, a 2024 study of more than 4000 viral cases from Ontario, Canada,4 found higher rates of bacterial infections in people recovering from covid-19 than in those recovering from influenza or RSV—although study groups weren’t perfectly matched by age or clinical setting, limiting direct comparisons.

Jeimy says that many infants and toddlers admitted to hospital with rare infections since 20225 weren’t yet born when pandemic restrictions were in place, and they therefore couldn’t be experiencing immunity debt. They were, however, likely exposed to SARS-CoV-2.

Wolfgang Leitner, chief of the Innate Immunity Section at the US National Institute of Allergy and Infectious Diseases (NIAID), speculates that covid-19 may somehow impair the immune system’s “memory” of past infections, potentially making even healthy people more vulnerable to future pathogens. He wonders whether the virus leaves lasting scars on the immune system’s T cell defences. “But that’s just (my) hypothesis,” he emphasises in an email.

SARS-CoV-2 is linked to “an unusually high level of ‘indiscriminate’ killing of T cells,”6 says Leitner, adding that this observation is “reminiscent of” measles, which can cause immune amnesia by depleting memory B cells (a different type of immune cell), leaving people vulnerable to pathogens they were previously immune to.7

This concept of immune “reset” after infections isn’t new. A hallmark of this phenomenon is the reactivation of dormant viruses, which re-emerge while the immune system is in a weakened state. Reactivation of viruses, including Epstein-Barr virus (EBV) and varicella zoster virus (VZV), has been commonly observed after covid-19.

A 2023 study reported EBV reactivation in covid positive patients at more than double the rate seen in covid negative patients.8 As for VZV, a 2022 analysis of US insurance records found that people over 50 were 15% more likely to develop herpes zoster after a covid-19 diagnosis.9 Jeimy says, “There’s a pathophysiology that already exists for other viruses like EBV or measles. The plausibility is there. The precedent is there.”

Brazilian researchers found that covid-19 triggered a sharp rise in T cell exhaustion and cellular ageing.10 Although the comparator group was limited, the strongest effects were seen in CD8+ T cells, which suppress latent viruses such as EBV and VZV. These effects were seen even after mild infections.

Some researchers believe that these lingering immune effects, which are often subtle, may represent the sorts of immune system “scars” that Leitner describes.

Dawn Bowdish, Canada research chair in ageing and immunity at McMaster University in Ontario, says that clinical signs are visible. “For people who test positive for covid-19, there’s an uptick in antibiotic prescriptions,” she says. “Covid-19 does have this association, for sure.”

Akiko Iwasaki, director of the Yale Center for Infection and Immunity in Connecticut, USA, says that the clinical picture aligns with what she sees at the cellular level. Iwasaki says that even in patients not admitted to hospital, her lab sees clinically significant reductions in circulating T cells.

A 2025 study published in the Lancet11 tracked more than 830 000 US veterans and found that even non-admitted patients who tested positive for covid-19 had higher rates of bacterial, viral, and fungal infections in the year that followed. It also found that patients admitted to hospital with covid-19 were more likely to develop sepsis than those admitted with influenza.

A Cell study12 of people with “long” covid suggests that SARS-CoV-2 infection can reprogram bone marrow stem cells, imprinting epigenetic changes that persist for at least a year, skewing some immune cells towards a state of hypersensitivity and inflammation. The findings signal a possible novel mechanism for longer term immune changes not strictly limited to populations with long covid.

Finally, a 2024 study13 of long covid by researchers at the University of California, San Francisco, found viral RNA in gut tissue two years after infection. Using positron emission tomography (PET) imaging, the team found that T cell activity was clustered in places where SARS-CoV-2 RNA—a likely marker of viral persistence—was also present.

“There has definitely been a change in the character of the immune response since 2019,” says Tim Henrich, immunologist and senior author of the study. “It’s certainly impacting our immune health, and probably our overall health as well.”

Long covid remains a hot topic among the public and researchers and has certainly raised awareness of postviral disease. Yet there persists an awkwardness, even a hostility, when it comes to the idea of SARS-CoV-2 undermining immune health.

Ashish Jha, former White House covid-19 response coordinator under President Biden, has publicly rejected this hypothesis. “There’s a lot of bad information out there about how covid-19 damages the immune system. It really doesn’t,” he posted on X in early 2024.14 More than a year later, his view is unchanged.

Jha, an internal medicine physician by training, tells The BMJ, “Of course, some very small proportion of people who get covid will get immune dysfunction and long covid. Thankfully, that is increasingly rare among new infections.” He maintains that “a lot of people who don’t have much expertise” have overstated covid’s potential to cause immune disruption in the wider population.

“I have seen zero evidence to support that—and in fact, all the evidence we have suggests that is not true,” he says. “Except for the small proportion of people who might get some immune dysfunction—which happens with other viruses too—covid doesn’t damage the immune system.”

Others argue that it needn’t be as black and white as “covid does or does not damage the immune system.” Nor does it necessarily have the same effect in everyone.

Jeimy thinks that people who are unwilling to consider the possibility of immune damage are perhaps driven by a fear of what those answers might mean. “Nobody wants to be the one that says, ‘Yes, covid-19 causes disability’ [beyond long covid],” she says, alluding to the health and economic implications of such a conclusion.

Gasperowicz says that “the burden of proof has flipped: instead of showing that something is safe, we’re asked to prove harm.”

Henrich doesn’t see the hypothesis as controversial. “We’ve shown immune dysfunction post covid, including signs of exhaustion and inflammation in people without symptoms,”15 he says, adding that, at the population level, “we are probably living with more inflammation on a day-to-day basis than we were before.”

The difficulty is that these changes aren’t uniform. In some patients the impact of covid-19 is dramatic; in others it’s invisible. Iwasaki and her team have found persistent immune system changes in people who have recovered from covid-19, even without any symptoms.

“There are some subtle differences between healthy controls and convalescent controls,” she says, referring to people who have recovered from covid. “More subtle things might be happening in that population. And now the entire world is pretty much the convalescent control.”