ArticleBMC geriatrics2026
Immune-inflammatory mediators of frailty and long COVID in older adults: a prospective cohort study.
Article in BMC geriatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo clarify the impact of COVID-19 infection on older frail patients, explore the immunological and inflammatory mechanisms (via peripheral blood CD8+ T lymphocytes and C-reactive protein [CRP]) underlying the interaction between frailty and Long COVID syndrome (LCS), identify relevant biomarkers, and validate the efficacy of antiviral combined with immune modulation therapy for improving long-term outcomes in frail patients with LCS.
methodsA single-center prospective cohort study was conducted on older patients (≥ 60 years) hospitalized for COVID-19 at the Second Affiliated Hospital of Soochow University between December 2022 and October 2023. Frailty was assessed using the Clinical Frailty Scale (CFS) at admission and 6-month follow-up, with evaluations by two geriatricians. Primary outcomes were all-cause mortality (in-hospital and post-discharge) and LCS incidence (per WHO definition: persistent symptoms ≥ 2 months post-infection, Post-acute Sequelae of SARS-CoV-2 Infection [PASC] score ≥ 12). Secondary outcomes included frailty progression, length of hospital stay (LOS), oxygen therapy duration, post-discharge care needs, and readmission rate. Peripheral blood CD8 + T lymphocyte counts, CRP, interleukin-6 (IL-6), ferritin, and routine blood tests were measured within 24 h of admission and 48 h pre-discharge. Scores for Sequential Organ Failure Assessment (SOFA), Nutritional Risk Screening 2002 (NRS2002), and Age-Adjusted Charlson Comorbidity Index (ACCI) were calculated. Univariate/multivariate logistic regression and mediation analysis (Bootstrap, 500 iterations) were performed.
resultsOf 145 enrolled patients, 115 completed 6-month follow-up (mean age 77.2 ± 6.8 years; 60 frail [CFS ≥ 5], 55 non-frail [CFS < 5]). Compared with non-frail patients, frail patients had higher in-hospital mortality (12.0% vs 1.4%, P = 0.01), LCS incidence (26.7% vs 10.9%, P = 0.004), longer LOS (P = 0.004), longer oxygen therapy duration (11.3 ± 4.2 vs 7.6 ± 3.1 days, P = 0.005), greater post-discharge care needs (P = 0.004), and higher readmission rate (P = 0.01). Frail patients also had lower CD8 + T lymphocyte counts at admission (P = 0.006) and discharge (P = 0.03), and higher discharge CRP (P = 0.01). Discharge CD8+ T lymphocytes were protective against frailty (OR = 0.95, 95%CI:0.93–0.98, P = 0.01) and frailty progression (OR = 0.98, 95%CI:0.96–0.99, P = 0.02), while discharge CRP was a risk factor (frailty: OR = 1.05, 95%CI:1.01–1.11, P = 0.04; progression: OR = 1.05, 95%CI:1.01–1.10, P = 0.02). Mediation analysis showed CD8+ T lymphocytes (mediation proportion = 11.4%, P = 0.04) and CRP (12.8%, P = 0.02) mediated the frailty-LCS association. In frail patients, antiviral-immune modulation therapy reduced LCS incidence (17.5% vs 45.0%, P = 0.03) and increased CD8+ T lymphocyte elevation (P = 0.02) vs. no therapy, with no significant benefits in non-frail patients (P > 0.05).
conclusionFrailty is an independent risk factor for adverse outcomes (including LCS) in older COVID-19 survivors. Discharge of CD8 + T lymphocytes and CRP mediates the frailty-LCS association, and antiviral combined with immune modulation therapy may be a targeted intervention to improve prognosis in frail older patients with COVID-19.
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