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Can monoclonal antibodies or antiviral drugs clear spike protein from someone with long COVID?
Executive Summary
Three small case reports and several hypothesis papers have suggested that monoclonal antibodies may rapidly relieve severe long COVID symptoms, leading to the claim that these therapies could clear persistent SARS‑CoV‑2 spike protein from tissue reservoirs; however, those reports did not measure spike levels, and broader clinical evidence that monoclonal antibodies or antiviral drugs reliably remove spike protein in long COVID patients is currently absent. Experimental reviews and proposed treatment protocols present plausible mechanisms and research plans, but randomized clinical trials with direct biomarker measurements are still needed to confirm whether these interventions clear spike protein and alter long‑term outcomes [1] [2] [3] [4] [5].
1. Dramatic case reports sparked the idea — but they don’t prove spike clearance.
Three published case histories describe patients with severe long COVID who experienced rapid, complete remission after receiving the casirivimab‑imdevimab monoclonal antibody cocktail; the authors interpreted these rapid recoveries as consistent with antibodies neutralizing residual viral components such as spike protein, yet none of the cases included pre‑ and post‑treatment measurements of spike antigen or viral RNA to demonstrate actual clearance from tissues or blood. These reports are clinically intriguing because the symptom resolution was fast and substantial, but they remain anecdotal and hypothesis‑generating rather than definitive evidence that monoclonal antibodies remove persistent spike protein or that antivirals accomplish the same effect [1] [2] [3].
2. Scientific plausibility exists — animal and in vitro work shows antibodies can neutralize spike, but translation to people is unproven.
Laboratory and animal studies show that monoclonal antibodies bind the SARS‑CoV‑2 spike protein, block ACE2 interaction, and in some models promote degradation or clearance of spike fragments; scoping reviews catalogue monoclonal antibodies among modalities able to neutralize or remove spike in experimental systems. Those preclinical data make the mechanism biologically plausible, but scoping reviews and experimental reports do not provide clinical evidence that these molecular events occur in human long COVID compartments such as gut, brain, or lymphoid tissues, nor do they establish the clinical significance of removing detectable spike fragments in those compartments [4] [6].
3. Antiviral drugs are conceptually useful but lack direct proof for spike elimination in long COVID.
Antiviral agents reduce viral replication, and in acute infection they lower viral load; this suggests a possible indirect route to reduce ongoing production of spike protein if active reservoirs are present. However, the literature assembled here shows that antivirals have not yet been demonstrated to clear residual spike protein in long COVID patients: most discussions frame antivirals as part of proposed protocols or as search terms in reviews rather than reporting clinical trials measuring spike antigen elimination. Consequently, antiviral efficacy against persistent spike remains a theoretical but unproven pathway needing targeted biomarker trials [4] [5].
4. Practical and regulatory complications weaken the immediate relevance of monoclonal antibody signals.
Monoclonal antibody formulations are strain‑specific; several early products, including casirivimab‑imdevimab, lost effectiveness against later Omicron subvariants, prompting regulatory withdrawals or revocations of emergency authorizations. That makes prior case signals less directly actionable today because many authorized monoclonals no longer neutralize circulating variants, and trials must use antibodies matched to current spike sequences. Proposed multiphase protocols that place monoclonal antibodies as the second step to neutralize tissue‑bound spike need updating to reflect variant escape and regulatory status, and they must be tested with appropriate biomarker endpoints to show actual spike clearance [3] [5].
5. The path forward: what evidence would change the claim from plausible to proven?
Definitive evidence requires randomized controlled trials or well‑designed prospective cohort studies that administer monoclonal antibodies or antivirals to long COVID patients and measure spike antigen and viral RNA in blood and relevant tissues before and after treatment, alongside standardized clinical outcome measures. Ongoing and planned trials (some referenced in hypothesis papers) aim to test these ideas, and proposed protocols combine fibrinolytics, antibody cocktails, and antivirals in staged approaches; these designs illustrate a research agenda but do not substitute for rigorous, biomarker‑driven trials. Until such trials report consistent spike reduction with concordant clinical benefit, the claim that monoclonal antibodies or antivirals can clear spike protein in long COVID remains an evidence‑based hypothesis rather than an established fact [1] [4] [5].