Microvascular remodeling and endothelial dysfunction across the post-COVID-19 spectrum: a prospective observational case-control study

Abstract:

Background: Post-viral diseases, including post-COVID-19 syndrome (PCS) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), cause substantial long-term morbidity. Persistent cardiovascular (CV) risk after acute infection highlights the need for accessible tools to quantify microvascular health.

Methods: The “All Eyes on PCS” is a prospective observational study assessing the microcirculation using retinal vessel analysis (RVA). Both dynamic and static parameters (DVA and SVA) were compared across never SARS-CoV-2 infected individuals (NI, n = 96), SARS-CoV-2 recovered individuals (n = 102), and PCS patients (n = 102), including a subgroup fulfilling ME/CFS criteria (n = 62). Analyses were complemented by propensity score-based weighting and multivariable adjustment. Associations with symptom severity and circulating biomarkers of endothelial dysfunction and inflammation were examined.

Results: PCS patients showed reduced venular flicker-induced dilation compared with recovered individuals (3.7% ± 2.2 vs. 4.8% ± 3.0, p = 0.006) and narrower retinal arterioles (CRAE) compared with both recovered (178.3 ± 15.5 μm vs. 186.1 ± 15.7 μm, p = 0.001) and NI individuals (184.4 ± 14.3 μm, p = 0.009). Arteriolar-to-venular ratio (AVR) was lower in PCS compared with NI (0.83 ± 0.06 vs. 0.87 ± 0.06, p < 0.001) and recovered participants (0.86 ± 0.07, p = 0.034). Findings remained largely consistent after age and sex balancing and adjustment for CV risk factors, although the association for AVR was attenuated. PCS patients fulfilling ME/CFS criteria showed the most pronounced retinal microvascular alterations, and a combined model discriminated ME/CFS patients with good accuracy (AUC = 0.79). Higher symptom burden was associated with lower AVR (r = – 0.21, p = 0.037), particularly for neurocognitive symptoms. IL-6, ICAM-1, and VCAM-1 were elevated in PCS and ME/CFS, and lower AVR was associated with inflammatory and iron-related markers (all adjusted p < 0.01).

Conclusions: PCS is associated with persistent endothelial dysfunction, most pronounced in ME/CFS patients and linked to symptom severity and ongoing inflammation. These findings support the potential use of RVA as a non-invasive tool for assessing and monitoring endothelial health in post-viral syndromes, with implications for cardiovascular risk stratification.

Trial registration: The All Eyes on PCS Study has previously been registered at ClinicalTrials.gov (NCT05635552).

Source: Wallraven T, Günthner R, Lethen I, Ribeiro A, Lech M, Oertel FC, Reeß LG, Haller B, Streese L, Hanssen H, Basta-Wunderle M, Schmaderer C. Microvascular remodeling and endothelial dysfunction across the post-COVID-19 spectrum: a prospective observational case-control study. BMC Med. 2026 Aug 19;24(1):456. doi: 10.1186/s12916-026-05144-9. PMID: 42625188. https://link.springer.com/article/10.1186/s12916-026-05144-9 (Full text)

Subclinical neurovascular and immune correlates of post-COVID-19 syndrome detected by retinal imaging

Abstract:

Background: Post-COVID-19 Syndrome (PCS) encompasses a range of persistent symptoms, including cognitive and autonomic disturbances, potentially linked to microvascular or neuroinflammatory mechanisms. Retinal imaging provides a non-invasive window into the central nervous system and vascular integrity. This study aimed to assess retinal structural and microvascular alterations in PCS patients and explore their relationship with symptom severity.

Methods: In this monocentric, cross-sectional, exploratory study, we performed Optical Coherence Tomography (OCT) and OCT Angiography (OCTA) in patients with PCS and a group of COVID-19 recovered individuals. Multiple circulating biomarkers reflecting endothelial dysfunction and chronic inflammation were measured. Associations with validated symptom scores (PCS Score, C19-YRS, PHQ-9, GAD-7) were evaluated.

Results: After adjusting for age and gender, no significant differences were observed in OCTA-derived vessel density (VD) or foveolar avascular zone (FAZ) between PCS patients and COVID-19-recovered controls. However, PCS patients exhibited significant thinning of the peripapillary retinal nerve fibre layer (pRNFL), ganglion cell inner plexiform layer (GCIP), and total macular volume (TMV). Lower values of these structural parameters were consistently observed in patients with higher symptom severity. Vascular parameters (VD and FAZ) were not related to clinical scores. Higher MCP-1 levels, a chemokine associated with chronic inflammation, were linked to lower inner nuclear layer and GCIP thickness.

Conclusion: Structural retinal alterations in PCS were associated with symptom burden and may reflect underlying neuroinflammatory or neurodegenerative processes. OCT parameters could serve as potential non-invasive biomarkers, warranting further investigation in longitudinal, multicenter studies.

Source: Wunderle M, Wicklein R, Ribeiro A, Carbajo-Lozoya J, Wöhnl A, Negele J, Kesseler V, Wild A, Niedermayer S, Lethen I, Lech M, Menten MJ, Kreitner L, Schmaderer C, Wallraven T. Subclinical neurovascular and immune correlates of post-COVID-19 syndrome detected by retinal imaging. Brain Behav Immun Health. 2026 Jul 25;56:101315. doi: 10.1016/j.bbih.2026.101315. PMID: 42571220; PMCID: PMC13451791. https://pmc.ncbi.nlm.nih.gov/articles/PMC13451791/ (Full text)

Recovery trajectories and predictors of symptom resolution in post-COVID-19 condition: a population-based cohort study

Abstract:

Background: SARS-CoV-2 infection can lead to persistent symptoms, known as Post-COVID-19 Condition (PCC). Previous studies on PCC prognosis mainly looked at severe cases in rehabilitation settings and without knowledge about pre-infection symptom levels. Uncertainty remains about recovery trajectory in the general population, its predictors, and whether recovery differs by symptom.

Methods: We analysed data from Lifelines, a prospective population-based observational cohort. Adults completed 31 COVID-19 questionnaires between March 2020 and October 2022 providing longitudinal symptom data to assess PCC status, and recovery. PCC was defined as at least one moderately severe symptom, among 12 identified as PCC-specific, that worsened 90-150 days after infection. Cox-proportional hazard models estimated recovery, defined as symptom decline to an individual’s pre-infection baseline, adjusted for symptoms present at PCC diagnosis, age, sex, BMI, smoking, hospitalization, vaccination, and comorbidities.

Findings: We analysed time series of 809 cases (mean age 55.0; [SD 11.0]; 590 [73%] female; mean follow up 368 days; [SD 200]). Symptom decline to pre-infection baseline or below was observed in 558 participants; the Kaplan-Meier 24-month symptom decline estimate was 92%. Greater symptom burden was associated with a lower likelihood of recovery (HR per additional symptom 0.69, 95% CI 0.63-0.76), whereas younger age had a higher likelihood of recovery compared with middle adulthood (HR 1.52, 95% CI 1.06-2.18). Median time to symptom decline was 226 days (IQR 182-372), with most improvement within the first 235 days before slowing and plateauing.

Interpretation: Most individuals with PCC recover, but older adults and those with multiple symptoms are at higher risk of prolonged illness, underscoring the need for ongoing support.

Source: Brunet JL, van Ockenburg SL, Leyli-Abadi M, Lunter G, Rosmalen JGM. Recovery trajectories and predictors of symptom resolution in post-COVID-19 condition: a population-based cohort study. Lancet Reg Health Eur. 2026 Aug 8;69:101802. doi: 10.1016/j.lanepe.2026.101802. PMID: 42604070; PMCID: PMC13476563. https://pmc.ncbi.nlm.nih.gov/articles/PMC13476563/ (Full text)

Haptoglobin Phenotypes Stratify Post-Exertional Cognitive Dysfunction Associated with Altered Cerebral Oxygenation and Metabolic Signatures in Long COVID

Abstract:

Long COVID (LC) is a heterogeneous post-infectious syndrome characterized by persistent symptoms, yet the biological basis underlying its interindividual variability remains poorly understood. Given the clinical overlap between LC and myalgic encephalomyelitis (ME), and prior demonstration that haptoglobin (Hp) phenotypes modulate symptom severity in ME, we investigated whether Hp phenotypes similarly stratify post-exertional cognitive dysfunction in LC.
In this longitudinal observational study, 44 individuals with LC and 20 short-course COVID controls, who recovered rapidly from SARS-CoV-2 infection without persistent symptoms or sequelae, underwent Hp phenotyping alongside metabolomic and physiological profiling before and after a standardized 90 min passive post-exertional challenge. Hp phenotypes identified clinically distinct LC subgroups.
Compared with Hp1-1 individuals, Hp2 allele carriers exhibited greater fatigue, poorer physical function, and more severe post-exertional symptoms. Immediately following the challenge, Hp2-2 participants with LC showed significant cognitive decline, whereas Hp1-1 individuals demonstrated cognitive resilience and more favorable longitudinal cognitive trajectories.
This differential susceptibility was accompanied by higher post-exertional cerebral fractional tissue oxygen extraction in the right hemisphere in Hp1-1 individuals and by distinct metabolic signatures, with Hp2 allele carriers exhibiting lower post-exertional plasma concentrations of citric acid, isethionate, and glucosamine. Lower metabolite levels were associated with poorer cognitive performance.
These findings support Hp phenotypes as promising candidate biomarkers for biological stratification in Long COVID, pending validation in larger independent cohorts.

Source: Moezzi A, Elremaly W, Leveau C, Franco A, Nepotchatykh O, Armstrong CW, Moreau A. Haptoglobin Phenotypes Stratify Post-Exertional Cognitive Dysfunction Associated with Altered Cerebral Oxygenation and Metabolic Signatures in Long COVID. International Journal of Molecular Sciences. 2026; 27(15):7000. https://doi.org/10.3390/ijms27157000 https://www.mdpi.com/1422-0067/27/15/7000 (Full text)

Peripheral blood cytokines during early and post-acute stages of SARS-CoV-2 infection are associated with disease severity and long-term symptoms

Abstract:

Background: U.S. Veterans experience a high burden of COVID-19; characterizing immune responses associated with COVID-19 outcomes could help improve treatment. Changes in peripheral blood cytokines over time may predict both acute outcomes and long COVID symptoms.

Methods: Cytokine concentrations were quantified from peripheral blood collected 0-7 days (early) and 14-42 days (post-acute) after enrollment from SARS-CoV-2 positive participants in the EPIC3 study, a prospective, longitudinal cohort following U.S. Veterans. Responses were correlated with Veterans Affairs Severity Index for COVID-19 criteria and chronic symptoms with the modified Medical Research Council Dyspnea scale, Patient-Reported Outcomes Measurement Information System (PROMIS) Cognitive function, and PROMIS Fatigue scores 3 months after enrollment (60-135 days). Trends in cytokine concentration with COVID-19 severity were assessed. Odds of COVID-19 severity and long-term symptoms were estimated with logistic regression adjusted for sex, age, and morbidity. Longitudinal changes in cytokine concentration were examined for participants sampled during both time periods, by severity and long-term symptom group.

Results: Early HGF, IL-18, IL-1RA, IP-10, and VEGF-A and post-acute MIP-1α and VEGF-A concentrations trended positively with increasing COVID-19 severity (q-values < 0.05, Jonckheere-Terpstra trend test). Increases in EGF, MIP-1β, and RANTES concentration and decreases in MIP-1α concentration over time were associated with mild rather than moderate or severe disease. Increases in MIP-1β and RANTES concentration and decreases in Eotaxin concentration over time were associated with the absence of long-term symptoms.

Conclusions: Worse COVID-19 severity by 30 days was associated with higher early and post-acute period cytokine concentrations. Participants with long-term symptoms did not see resolution of cytokine responses over time.

Source: Mendall C, Li X, Pakanati V, Liu C, Wang T, Morelli D, Korpak A, Baraff A, Isaacs SN, Chang KM, Le E, Holodniy M, Sugimoto JD, Smith NL, Lee JS, Ross JM, Shah JA. Peripheral blood cytokines during early and post-acute stages of SARS-CoV-2 infection are associated with disease severity and long-term symptoms. Front Immunol. 2026 Jul 15;17:1870109. doi: 10.3389/fimmu.2026.1870109. PMID: 42528778; PMCID: PMC13415590. https://pmc.ncbi.nlm.nih.gov/articles/PMC13415590/ (Full text)

Altered TRPM3‐Dependent Cytosolic and Mitochondrial Calcium Influx in Natural Killer Cells of Post‐COVID‐19 Condition Patients

Abstract:

According to the World Health Organization (WHO), approximately 6% of COVID-19 cases develop serious long-term sequelae referred to as post-COVID-19 condition (PCC). Immunological disturbances such as persistent activation of immune cells and reduced cytotoxicity by natural killer (NK) cells are reported as key aspects in PCC.

Recently, electrophysiological studies by our group demonstrated impairment of transient receptor potential melastatin 3 (TRPM3) ion channels in NK cells from PCC patients. The significant reduction in TRPM3 channel function and reduced functional activity by NK cells warrants further investigation. Hence, using live cell calcium (Ca2+) imaging ex vivo, we examined the downstream impact of TRPM3 ion channel dysfunction on intracellular and mitochondrial Ca2+ mobilization in NK cells from N = 8 PCC patients, age and sex matched to N = 8 PCC healthy controls (HC).

Our findings provide new evidence of altered passive and TRPM3-mediated Ca2+ influx, significantly impacting cytoplasmic and mitochondrial Ca2+ mobilization in PCC. Passive cytosolic Ca2+ influx amplitude (p < 0.0001) was significantly reduced in PCC; however, passive mitochondrial Ca2+ mobilization (p < 0.0001) was significantly increased. Importantly, cytoplasmic and mitochondrial response rates (slope, p < 0.001) to pregnenolone sulphate stimulation were significantly reduced in PCC.

Consequently, TRPM3-dependent cytosolic (p < 0.001) and mitochondrial (p < 0.0005) Ca2+ mobilization were significantly reduced in PCC compared with HC. Altered ion channel Ca2+ signalling can severely impact both the immune system and bioenergetic processes, potentially leading to broader systemic dysregulations underpinning the pathomechanism of the PCC condition, and warrants further investigations.

Source: Magawa CT, Eaton-Fitch N, Muraki K, Marshall-Gradisnik S. Altered TRPM3-Dependent Cytosolic and Mitochondrial Calcium Influx in Natural Killer Cells of Post-COVID-19 Condition Patients. Eur J Immunol. 2026 Jul;56(7):e70240. doi: 10.1002/eji.70240. PMID: 42484498; PMCID: PMC13390657.  https://pmc.ncbi.nlm.nih.gov/articles/PMC13390657/ (Full text)

School Difficulties and Long COVID in Children and Adolescents

Abstract:

Objective: Pediatric Long COVID (LC) is an infection-associated chronic condition following SARS-CoV-2 infection. While research has begun to elucidate clinical phenotypes, functional impacts are not well described.

Methods: Cross-sectional data from the NIH-funded Researching COVID to Enhance Recovery (RECOVER) pediatric observational cohort were analyzed to assess associations in school-age children (6 to 11 years) and adolescents (12 to 17 years) between LC and caregiver-reported school-related functional outcomes. LC was defined using RECOVER age group-specific symptom-based LC research indices. The primary outcome was worsening of child grades. Secondary outcomes included difficulty paying attention, limited fun with friends, and having an Individualized Education Program (IEP). Using age-stratified analyses, children with and without LC were matched based on age, sex, and dates of infection and enrollment, to estimate risk ratios (RRs) between LC and each outcome.

Results: The cohort included 1976 children (406 school-age, 1570 adolescent). About 18% of school-age children and 29% of adolescents with LC had reported worsened grades, compared to 7% and 11% without LC, respectively [school-age: adjusted RR 2.18 (95% CI: 1.15-4.11); adolescent: adjusted RR 2.39 (95% CI: 1.86-3.06)]. In both age groups, children with LC were more likely to have difficulty paying attention, limited fun with friends, and IEPs.

Conclusions: LC in school-age children and adolescents was negatively associated with functional school-related outcomes, including academic performance, attention, and peer interactions. As LC affects a substantial proportion of U.S. children, these findings highlight the urgent need to develop, provide, and evaluate school-related services for children and adolescents with LC.

Source: Reeder HT, Kleinman LC, Stockwell MS, Thaweethai T, Pant DB, Rhee KE, Jernigan TL, Snowden JN, Salisbury AL, Kinser PA, Milner JD, Tantisira KG, Warburton D, Mohandas S, Wood JC, Fitzgerald ML, Carmilani M, Krishnamoorthy A, Foulkes AS, Gross RS; RECOVER-Pediatrics Consortium. School Difficulties and Long COVID in Children and Adolescents. Acad Pediatr. 2026 Jul;26(5):103314. doi: 10.1016/j.acap.2026.103314. Epub 2026 Apr 3. PMID: 41936816; PMCID: PMC13386493. https://pmc.ncbi.nlm.nih.gov/articles/PMC13386493/ (Full text)

Microstructural alterations in brain tissue of ME/CFS and long COVID using diffusion tensor imaging and diffusion kurtosis imaging

Abstract:

Introduction: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and long COVID have overlapping symptoms, such as profound fatigue, cognitive impairment, post-exertional malaise, pain and sleep disturbances that are debilitating and reduce quality of life. While Magnetic Resonance Imaging (MRI) techniques, specifically Diffusion Tensor Imaging (DTI) and Diffusion Kurtosis Imaging (DKI), have been used to investigate brain tissue microstructure in ME/CFS or long COVID, no study has yet combined these modalities to directly compare tissue microstructural differences between people living with ME/CFS and long COVID.

Methods: We recruited 37 ME/CFS participants (Age: 43.56 ± 12.5), 19 long COVID participants (Age: 47.92 ± 13.3), and 27 healthy controls (Age: 37.9 ± 10.4). Data were acquired using a 3 Tesla (3T) Prisma MRI scanner. DTI and DKI metrics were determined using MRtrix v3.0.7 and Designer V2.0 software, respectively. Voxel-based statistical analysis of cohort differences was performed using the Statistical Parametric Mapping (SPM12) toolbox in MATLAB. Correlation analysis was performed between DTI, DKI metrics and clinical measures such as duration of illness, fatigue severity, SF36 domains and WHODAS domains.

Results: Compared with healthy controls, individuals with ME/CFS showed microstructural alterations in the cingulum, supplementary motor areas, and parts of the corpus callosum (all p < 0.05). Long COVID participants demonstrated microstructural alterations in regions including the fusiform and precentral gyrus and in major white matter tracks (all p < 0.05). Direct comparisons between ME/CFS and long COVID revealed difference in the left corona radiata (p = 0.001).

Conclusion: This study identifies distinct tissue microstructural alterations in ME/CFS and long COVID and offers a vital insight into the neuropathological basis of shared symptoms in both conditions.

Source: Singh TB, Marshall-Gradisnik S, Barnden L, Eaton-Fitch N, Huynh TH, Inderyas M, Thapaliya K. Microstructural alterations in brain tissue of ME/CFS and long COVID using diffusion tensor imaging and diffusion kurtosis imaging. Front Med (Lausanne). 2026 Jul 17;13:1824498. doi: 10.3389/fmed.2026.1824498. PMID: 42539798; PMCID: PMC13424405. https://pmc.ncbi.nlm.nih.gov/articles/PMC13424405/ (Full text)

Risks of autoimmune and inflammatory post-acute COVID-19 conditions: a network cohort study in six European countries, the USA and Korea

Abstract:

Objectives: We aimed to assess the risk of incident autoimmune and inflammatory conditions during the post-acute period of COVID-19.

Design: Descriptive network cohort study.

Setting: Electronic health records from the UK and Dutch primary care, Norwegian linked health registry, hospital records of specialist centres in Spain, France and Korea and healthcare claims from Estonia and the USA.

Participants: We followed individuals between September 2020 and the latest available data from day 91 after a SARS-CoV-2 negative test (comparator) or a COVID-19 record (exposed patients, ie assessing patients during the post-acute phase). We further established a reinfection cohort (any further COVID-19 record among the exposed patients). We followed patients until an outcome, end of study period, death, day 365 or an infection (comparator only) or reinfection (exposed patients only).

Main outcome measures: We assessed postural orthostatic tachycardia syndrome (POTS) diagnoses/symptoms, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) diagnoses/symptoms, multi-inflammatory syndrome (MIS) and several autoimmune diseases (rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD) and type 1 diabetes mellitus (T1DM)). Meta-analysed crude incidence rate ratios (IRRs) of outcomes after COVID-19 versus negative testing and after reinfection versus a previous COVID-19 record yield the ratios of respective absolute risks of each assessed outcome. We performed subgroup analyses by age, sex and predominant variant periods.

Results: We included 2 521 812 individuals with a first COVID-19 record, 4 233 145 with a first negative test and 135 551 with a reinfection. Age and sex were largely comparable between exposure groups with a shorter follow-up for the reinfection cohorts. After COVID-19 compared with test-negative patients and equally after reinfection compared with previous COVID-19 patients, we did not observe increased rates for all outcomes and all subgroup analyses. Counts of MIS and JIA were too small for meta-analyses.

Conclusions: In our descriptive meta-analyses of crude IRRs among databases from various countries and settings, we did not observe increased rates of incident POTS, ME/CFS, RA, IBD, SLE and T1DM in COVID-19 versus test-negative or reinfection versus COVID-19 during the first 9 months of the post-acute phase of COVID-19 or reinfection (>90 days postinfection until month 12). Since causal interpretation cannot be made from this study, further causal research is warranted.

Source: Burkard TM, López-Güell K, Català M, Burn E, Delmestri A, Khalid S, Jödicke AM, Dedman D, Oyinlola J, Abellan A, Pérez-Crespo L, Mercadé-Besora N, Duarte-Salles T, Prieto-Alhambra D, Arinze J, Mosseveld M, Kolde R, Meléndez J, López-Blasco R, Martínez Á, Valdivieso B, Delseny D, Mercier G, Kim C, Kim JW, Kostka K, Ramírez-Anguita JM, Mayer MA, Trinh NTH, Nordeng H, Paredes R, Uusküla A, Nishimura A, Loste C, Mateu L, Xie J. Risks of autoimmune and inflammatory post-acute COVID-19 conditions: a network cohort study in six European countries, the USA and Korea. BMJ Public Health. 2026 Jul 24;4(3):e001686. doi: 10.1136/bmjph-2024-001686. PMID: 42516718; PMCID: PMC13404851. https://pmc.ncbi.nlm.nih.gov/articles/PMC13404851/ (Full text)

Inflammatory and neuroinjury blood biomarkers across COVID-19 severity groups in individuals with persistent neurological symptoms

Abstract:

Persistent neurological symptoms such as cognitive impairment, fatigue, and neuropsychiatric disturbances are increasingly reported in patients with long COVID, with chronic neuroinflammation and neuronal injury proposed as potential contributors. To characterize inflammatory and neuroinjury-related biomarker patterns, we conducted a case-control study including 325 participants recruited at King Chulalongkorn Memorial Hospital between January 2022 and December 2023, comprising 265 individuals with persistent neurological symptoms following COVID-19 infection and 60 asymptomatic COVID-19 participants who did not develop long COVID symptoms.

Blood samples were analysed for inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α, IFN-α, IL-4) using multiplex immunoassays, and for neuroinflammatory and neurodegenerative biomarkers, including neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), phosphorylated tau181, and beta-amyloid peptides (Aβ40, Aβ42) using SIMOA and ELISA platforms. Among 265 participants with complete data (critical = 7, severe = 22, moderate = 79, mild = 157), patients with severe and critical COVID-19 exhibited significantly higher concentrations of IL-6, IL-1β, TNF-α, and IL-8, together with elevated NfL, GFAP, and phosphorylated tau181 levels, and reduced Aβ42/40 ratios.

Strong positive correlations between neurodegenerative biomarkers and pro-inflammatory cytokines were observed in critically ill patients, whereas these associations were weak or absent in mild and moderate cases. Older age was also associated with greater disease severity and increased risk of persistent neurological complications.

These findings indicate that individuals with persistent neurological symptoms following COVID-19, particularly those with a history of severe or critical disease, exhibited higher inflammatory and neuroinjury-related biomarker levels, while blood-based biomarkers such as NfL, GFAP, and phosphorylated tau181 may serve as minimally invasive tools for characterizing neurological involvement and identifying patients at risk of long-term neurological sequelae.

Source: Ruchisrisarod C, Kaewpom T, Wanthong P, Luechaipanit W, Bunprakob S, Ampoot W, Yomrat S, Hemachudha P, Supharatpariyakorn T, Thanapornsangsuth P, Tammachote R, Saraya AW. Inflammatory and neuroinjury blood biomarkers across COVID-19 severity groups in individuals with persistent neurological symptoms. Int J Immunopathol Pharmacol. 2026 Jan-Dec;40:3946320261465568. doi: 10.1177/03946320261465568. Epub 2026 Jul 16. PMID: 42460883; PMCID: PMC13376473. https://pmc.ncbi.nlm.nih.gov/articles/PMC13376473/ (Full text)