Infections with Other Diseases Could Cause Long Covid: New Research

Long COVID has few obvious links to other infectious diseases like tuberculosis. Yet, new research suggests hidden infections may activate alongside COVID-19. Viruses like Epstein-Barr could re-emerge as COVID-19 stresses immunity. This compound effect may explain fatigue, brain fog, and other Long COVID symptoms.

The study’s findings suggest coinfections may contribute to Long COVID development. These infections may exist before or emerge during COVID-19 infection. Their interaction with the immune system could drive persistent symptoms. This connection offers a new framework for understanding Long COVID mechanisms.

The study was published in eLife and led by 17 researchers. Many researchers involved were affiliated with Rutgers Health.

How are TB and EBV Linked to Long COVID?

Epstein-Barr virus (EBV) may be a major contributor to Long COVID symptoms. EBV causes mononucleosis and remains dormant in most adults. About 95 percent of adults carry latent EBV. It usually causes no symptoms or immune stress.

However, COVID-19 can weaken the immune system’s regulation of latent EBV infections. This disruption allows EBV to reactivate during or after COVID-19 illness.

Early studies found EBV markers in two-thirds of Long COVID patients. More severe symptoms correlated with higher EBV antibody levels.

Follow-up studies strengthened the EBV and Long COVID connection. Researchers linked EBV persistence to fatigue and cognitive impairment. These findings suggest viral reactivation may worsen Long COVID symptoms. EBV remains one of the strongest suspected contributors.

Tuberculosis (TB) may also play a role in Long COVID. About 25 percent of the global population has latent TB. COVID-19 infection may reduce immune activity that normally suppresses TB activity. This dampening effect could increase the risk of TB reactivation. TB may also worsen COVID-19 illness in some cases.

Why Might Coinfections Cause Long COVID?

The timing of coinfection appears to significantly affect outcomes. Preexisting infections may suppress immunity before COVID-19 exposure. Post-COVID infections may accelerate tissue damage. Infections emerging after recovery may exploit immune dysregulation.

COVID-19 can leave lasting immune system imbalances. These changes may increase vulnerability to other diseases by creating opportunities for dormant infections to resurface.

The authors identified disease surges across 44 countries. At least 13 diseases increased during the COVID-19 pandemic. These increases closely aligned with COVID-19 waves.

These findings, among others, led the authors to propose a concept called “immunity theft.” Immunity theft suggests severe COVID-19 infection weakens broader immune defenses. This impairment may increase susceptibility to other infectious diseases.

If the link is confirmed, existing treatments could target these coinfections. Antivirals or antibiotics might help reduce Long COVID symptoms.

Why Might Coinfections Cause Long COVID?

Clinical trials would be needed to test the immunity theft approach. Researchers must determine whether treating coinfections improves outcomes. This strategy could offer new options for Long COVID care. However, evidence remains limited.

The study’s authors emphasize their findings are preliminary. The proposed mechanisms are biologically plausible but unproven. More research is needed to confirm these connections. Large studies are required to validate the hypothesis.

Animal testing is especially challenging for Long COVID research. Reliable animal models for Long COVID remain rare. This limits researchers’ ability to test disease mechanisms.

Despite this, the authors remain hopeful that this work opens new research pathways. While it offers no immediate treatment guidance, the findings are significant. This lead may eventually help millions affected by Long COVID.

Conclusion

New research suggests Long COVID may involve reactivated or overlapping infections. Viruses like Epstein-Barr and latent tuberculosis may worsen symptoms after COVID-19. While evidence remains preliminary, this pathway could guide future treatments and research.

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Logan Hamilton is a health and wellness freelance writer for hire. He’s passionate about crafting crystal-clear, captivating, and credible content that elevates brands and establishes trust. When not writing, Logan can be found hiking, sticking his nose in bizarre books, or playing drums in a local rock band. Find him at loganjameshamilton.com.