tetano
Editor, Senior Moderator
Hum Vaccin Immunother
. 2025 Dec;21(1):2494934.
doi: 10.1080/21645515.2025.2494934. Epub 2025 May 13. Detection of S1 spike protein in CD16+ monocytes up to 245 days in SARS-CoV-2-negative post-COVID-19 vaccine syndrome (PCVS) individuals
Bruce K Patterson[SUP] 1 [/SUP], Ram Yogendra[SUP] 2 [/SUP], Edgar B Francisco[SUP] 1 [/SUP], Jose Guevara-Coto[SUP] 3 [/SUP], Emily Long[SUP] 1 [/SUP], Amruta Pise[SUP] 1 [/SUP], Eric Osgood[SUP] 4 [/SUP], John Bream[SUP] 5 [/SUP], Mark Kreimer[SUP] 6 [/SUP], Devon Jeffers[SUP] 7 [/SUP], Christopher Beaty[SUP] 1 [/SUP], Richard Vander Heide[SUP] 8 [/SUP], Rodrigo A Mora-Rodríguez[SUP] 3 [/SUP]
Affiliations
Despite over 13 billion SARS-CoV-2 vaccine doses administered globally, persistent post-vaccination symptoms, termed post-COVID-19 vaccine syndrome (PCVS), resemble post-acute sequelae of COVID-19 (PASC). Symptoms like cardiac, vascular, and neurological issues often emerge shortly after vaccination and persist for months to years, mirroring PASC. We previously showed the S1 subunit of the SARS-CoV-2 spike protein persists in CD16+ monocytes after infection, potentially driving PASC. Approved vaccines (Pfizer, Moderna, Janssen, AstraZeneca) deliver synthetic S1 to elicit immunity, suggesting a shared mechanism. We hypothesized that vaccine-derived S1 persistence in CD16+ monocytes sustains inflammation akin to PASC, contributing to PCVS. We studied 50 individuals with PCVS symptoms lasting over 30 days post-vaccination and 26 asymptomatic controls, using (1) machine learning-based immune profiling to compare cytokine signatures with PASC, (2) flow cytometry to detect S1 in CD16+ monocytes, and (3) LC-MS to confirm S1 across vaccine types. We correlated S1 persistence with symptom duration and inflammation. Prior infection was excluded via clinical history, anti-nucleocapsid antibody tests, and T-detect assays, though definitive tests are lacking. Preliminary findings suggest S1 persistence in CD16+ monocytes and an associated inflammatory profile may contribute to PCVS. Further studies are needed to confirm causality and prevalence.
Keywords: CCR5; COVID-19; PASC; SARS CoV-2 S1 protein; fractalkine; non-classical monocytes.
. 2025 Dec;21(1):2494934.
doi: 10.1080/21645515.2025.2494934. Epub 2025 May 13. Detection of S1 spike protein in CD16+ monocytes up to 245 days in SARS-CoV-2-negative post-COVID-19 vaccine syndrome (PCVS) individuals
Bruce K Patterson[SUP] 1 [/SUP], Ram Yogendra[SUP] 2 [/SUP], Edgar B Francisco[SUP] 1 [/SUP], Jose Guevara-Coto[SUP] 3 [/SUP], Emily Long[SUP] 1 [/SUP], Amruta Pise[SUP] 1 [/SUP], Eric Osgood[SUP] 4 [/SUP], John Bream[SUP] 5 [/SUP], Mark Kreimer[SUP] 6 [/SUP], Devon Jeffers[SUP] 7 [/SUP], Christopher Beaty[SUP] 1 [/SUP], Richard Vander Heide[SUP] 8 [/SUP], Rodrigo A Mora-Rodríguez[SUP] 3 [/SUP]
Affiliations
- PMID: 40358138
- PMCID: PMC12077440
- DOI: 10.1080/21645515.2025.2494934
Despite over 13 billion SARS-CoV-2 vaccine doses administered globally, persistent post-vaccination symptoms, termed post-COVID-19 vaccine syndrome (PCVS), resemble post-acute sequelae of COVID-19 (PASC). Symptoms like cardiac, vascular, and neurological issues often emerge shortly after vaccination and persist for months to years, mirroring PASC. We previously showed the S1 subunit of the SARS-CoV-2 spike protein persists in CD16+ monocytes after infection, potentially driving PASC. Approved vaccines (Pfizer, Moderna, Janssen, AstraZeneca) deliver synthetic S1 to elicit immunity, suggesting a shared mechanism. We hypothesized that vaccine-derived S1 persistence in CD16+ monocytes sustains inflammation akin to PASC, contributing to PCVS. We studied 50 individuals with PCVS symptoms lasting over 30 days post-vaccination and 26 asymptomatic controls, using (1) machine learning-based immune profiling to compare cytokine signatures with PASC, (2) flow cytometry to detect S1 in CD16+ monocytes, and (3) LC-MS to confirm S1 across vaccine types. We correlated S1 persistence with symptom duration and inflammation. Prior infection was excluded via clinical history, anti-nucleocapsid antibody tests, and T-detect assays, though definitive tests are lacking. Preliminary findings suggest S1 persistence in CD16+ monocytes and an associated inflammatory profile may contribute to PCVS. Further studies are needed to confirm causality and prevalence.
Keywords: CCR5; COVID-19; PASC; SARS CoV-2 S1 protein; fractalkine; non-classical monocytes.