SARS-CoV-2 antibody vaccine response in Inflammatory Bowel Disease patients with positive anti-nucleocapsid serology or history of COVID-19 infection

Abstract

Background: Previous history of COVID-19 infection is a natural booster of the vaccine response in the general population. The response to COVID-19 vaccines is lessened in Inflammatory Bowel Disease patients on selected class of immunosuppressive treatments. Aims: The study was to assess anti-SARS-CoV-2 spike-specific IgG antibody response in Inflammatory Bowel Disease patients with a history of COVID-19 infection. Patients and methods: This single-center prospective study involved 504 Inflammatory Bowel Disease patients. Demographic data and clinical data were gathered through questionnaires and patient charts. Anti-SARS-CoV-2 spike-specific and antinucleocapsid antibody levels were measured at T1, T2 (after the 2-dose series), and T3 or T4 (booster vaccine). Results: This study included 504 Inflammatory Bowel Disease patients, and 234 completed one year follow-up with blood tests. Positive anti-nucleocapsid serology or history of COVID-19 infection was significantly associated with increased median anti- SARS-CoV-2 spike-specific IgG titers after the 2-dose series (1930 BAU/mL vs. 521 BAU/mL p < 0.0001) and the booster vaccine (4390 BAU/mL vs. 2160 BAU/mL, p = 0.0156). Multivariate analysis showed that higher anti-SARS-CoV-2 spike-specific IgG levels were independently associated with anti-nucleocapsid antibodies at T2 (OR=2.23, p < 0.0001) and T3 (OR=1.72, p = 0.00011). Immunosuppressive treatments did not impact the antibody response or levels in patients with a history of COVID-19 infection or positive anti-nucleocapsid serology. Conclusions: In Inflammatory Bowel Disease, prior COVID-19 infection or positive anti-nucleocapsid serology leads to increased anti-SARS-CoV-2 spike-specific IgG levels after vaccination, regardless of immunosuppressive treatments. This emphasizes the significance of accounting for previous infection in vaccination approaches.