Objectives: Coronavirus disease 2019 (COVID-19) vaccination is reportedly efficient in people with HIV (PWH) but vaccine trials included participants with normal CD4 þ Tcell counts. We analyzed seroconversion rates and antibody titers following two-dose vaccination in PWH with impaired CD4 þ T-cell counts. Methods:We collected retrospective postvaccination SARS-COV-2 serology results available in a university hospital for PWH vaccinated between March and September, 2021 who were tested for antispike antibodies from 8 to 150 days following dose 2. Antibody titers were compared in PWH with CD4 þ T-cell count less than 200 cells/ml, 200 < CD4 þ T-cell counts < 500 cells/ml and CD4 þ T-cell count greater than 500 cells/ml at vaccination.Results: One hundred and five PWH were included: n ¼ 54 in the CD4 þ T-cell count less than 500 cells/ml group (n ¼ 18 with CD4 þ <200 cells/ml, n ¼ 36 with 200 < CD4 þ < 500 cells/ml) and 51 in the CD4 þ T-cell count greater than 500 cells/ml group. They received two doses of BNT162b2 (75%), mRNA-1273 (8.5%), or ChAdOx1 nCoV-19 (16.5%). The median time from vaccine dose 2 to serology was consistent across all groups (73 days, interquartile range [29-97], P ¼ 0.14). Seroconversion rates were 100% in the CD4 þ T-cell count greater than 500 cells/ml group but 89% in participants with CD4 þ T-cell counts less than 500 cells/ml (22 and 5.5% seronegative in the CD4 þ T-cell counts <200 cells/ml and 200 < CD4 þ < 500 cells/ml groups, respectively). Median antibody titers were 623.8 BAU/ml [262.2-2288] in the CD4 þ greater than 500 cells/ml group versus 334.3 BAU/ml [69.9-933.9] in the CD4 þ less than 500 cells/ml group (P ¼ 0.003). They were lowest in the CD4 þ less than 200 cells/ml group: 247.9 BAU/ml [5.88-434.9] (P ¼ 0.0017) with only 44% achieving antibody titers above the putative protection threshold of 260 BAU/ml. Conclusion:PWH with CD4 þ T-cell counts less than 500 cells/ml and notably less than 200 cells/ml had significantly lower seroconversion rates and antispike antibody titers compared with PWH with CD4 þ T-cell counts greater than 500 cells/ml, warranting the consideration of targeted vaccine strategies in this fragile population.

Objective To assess safety and efficacy of TNF-α antagonists and tocilizumab in patients with Takayasu arteritis (TAK). Methods and Results Two-hundred nine patients with TAK [median age of 29 years [7–62], and 186 (89%) females] were included. They received either TNF-α antagonists [n = 132 (63%) with 172 lines; infliximab (n = 109), adalimumab (n = 45), golimumab (n = 8), certolizumab (n = 6) and etanercept (n = 5)], or tocilizumab [n = 77 (37%) with 121 lines; intravenous and subcutaneous in 95 and 26 cases, respectively]. A complete response at 6 months was evidenced in 101/152 (66%) on TNF-α antagonists and 75/107 (70%) on tocilizumab, respectively. Age ≥ 30 years [OR = 2.09 [1.09; 3.99]] was associated with complete response, whereas vascular signs [0.26 [0.1; 0.65]], baseline prednisone ≥ 20 mg/day [0.51 [0.28; 0.93]] were negatively associated with the complete response to TNF-α antagonists or tocilizumab. During a median follow-up of 36 months, 103 relapses were noted. Supra-aortic branches and thoracic aorta involvements [HR 2.44 (1.06; 5.65) and 3.66 (1.18; 11.4), respectively], and systemic signs at baseline [HR 2.01 (1.30; 3.11)] were significantly associated with relapse. The cumulative incidence of treatment discontinuation and relapse were similar in TNFα antagonists and tocilizumab. Fifty-eight (20%) adverse effects occurred on biological-targeted therapies of whom 37 (21%) and 21 (17%), (p= 0.4) on TNF-α antagonists and tocilizumab, respectively. Conclusion This large multicentre study shows high efficacy of biological-targeted treatments in refractory TAK. Efficacy, relapse and drug retention rate were equivalent with TNF-α antagonists and tocilizumab.

Objectives Systemic-onset juvenile idiopathic arthritis (SJIA) and adult-onset Still’s disease (AOSD) are the same sporadic systemic auto-inflammatory disease. Spondyloarthritis (SpA) is a group of inflammatory non-autoimmune disorders. We report the observations of eight patients with SJIA/AOSD who also presented features of SpA during their disease evolution and estimate the prevalence of SpA in SJIA/AOSD. Methods This was a retrospective national survey of the departments of paediatric and adult rheumatology and internal medicine. To be included, SJIA patients had to fulfil the ILAR criteria, AOSD patients the Yamaguchi or Fautrel criteria, and all patients the ASAS classification criteria for axial or peripheral SpA, ESSG criteria for spondyloarthropathy or CASPAR criteria for psoriatic arthritis. The data were collected with a standardized form. Results Eight patients (five adults) were identified in one paediatric and two adult departments. In all but one patient, SpA manifestations occurred several years after SJIA/AOSD onset (mean delay 6.2 ± 3.8 years). Two patients had peripheral and three axial SpA, and four later exhibited psoriatic arthritis and one SAPHO syndrome. The prevalence of SpA in an adult cohort of 76 patients with AOSD was 6.58% (95% CI [2.17–14.69]), greater than the prevalence of SpA in the French general population (0.3%, 95%CI [0.17–0.46]). The prevalence of SpA in an SJIA cohort of 30 patients was 10% (95%CI [2.11–26.53]), more than that reported in the general population of industrialized countries, estimated at 0.016% to 0.15%. Conclusion Whilst the temporal disassociation between SpA and AOSD in most cases might suggest a coincidental finding, our work raises the possibility of an SpA AOSD spectrum overlap that needs further study.