Researchers identify viral suspects that could be fueling long COVID

A 17-expert review in eLife, including Rutgers researchers, argues that reactivation or co-infection with other pathogens—most notably Epstein-Barr virus (latent in roughly 95% of adults) and latent tuberculosis—may help explain some cases of long COVID, a syndrome affecting up to 400 million people worldwide; one early study found markers of recent EBV activity in about two-thirds of long COVID patients. The authors cite biological plausibility, rising rates of other infections in many countries and the idea that acute SARS‑CoV‑2 illness can impair immune control, and suggest that if co-infections are contributing drivers, existing antivirals, antibiotics and diagnostics could be repurposed and tested in clinical trials. However, they emphasize the hypothesis remains unproven—causation is not established—and call for large epidemiologic and animal-model studies before clinical or market conclusions can be drawn.

Analysis

A 17-expert review published in eLife and led in part by Rutgers researchers posits that reactivation or co-infection with other pathogens may contribute to long COVID; the condition is estimated to affect up to 400 million people worldwide and manifests with breathlessness, fatigue and cognitive impairment. The authors highlight Epstein-Barr virus (EBV) as a leading suspect — roughly 95% of adults carry latent EBV and an early study reported markers of recent EBV activity in about two‑thirds of long COVID patients — and flag latent tuberculosis (carried by roughly one‑quarter of the global population) as another plausible contributor because COVID can impair immune cells that contain TB. The paper cites broader epidemiologic signals — 44 countries reporting tenfold increases in at least 13 infectious diseases versus pre‑pandemic baselines — and advances the "immunity theft" hypothesis that acute SARS‑CoV‑2 illness can increase susceptibility to other infections; it also notes that existing antivirals, antibiotics and diagnostics could in principle be repurposed and tested in trials. The authors are explicit that the hypothesis remains unproven: correlation has not been shown to equal causation, reliable animal models are lacking, and the review calls for large epidemiologic and controlled clinical studies before clinical or commercial conclusions can be drawn.

Key Decisions for Investors

• Monitor registries and trial readouts testing antivirals, antibiotics or targeted therapies for EBV/TB reactivation in long COVID and only increase exposure after positive causal or Phase II/III results are reported
• Watch diagnostics and clinical‑lab companies developing validated assays for EBV reactivation and latent TB screening as potential early beneficiaries of increased testing demand once regulatory or reimbursement signals emerge
• Maintain a cautious posture on speculative long COVID therapeutics and favor selective, size‑limited positions or hedges until large epidemiologic studies and randomized trials establish causality and treatment efficacy