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Monocyte HLADR and Immune Dysregulation Index as Biomarkers for COVID-19 Severity and Mortality
Namrata Punit Awasthi1, Sridhar Mishra1, Vandana Tiwari2
1Department of Pathology, Dr. Ram Manohar Lohia Institute of Medical Sciences, Gomti Nagar, 226010 Lucknow, Uttar Pradesh India.
Insights
Immune dysregulation index (IDI) and monocyte HLA-DR (mHLA-DR) show promise in predicting COVID-19 severity and mortality. These markers, along with neutrophil CD64 (nCD64), aid in early risk assessment and patient management.
Area of Science:
- Immunology
- Infectious Diseases
- Critical Care Medicine
Background:
- COVID-19-associated immune dysregulation is a key driver of severe disease and mortality.
- Assessing immune markers like monocyte HLA-DR (mHLA-DR) and neutrophil CD64 (nCD64) is crucial for understanding disease progression.
Purpose of the Study:
- To evaluate the diagnostic and prognostic value of mHLA-DR, nCD64, and a novel Immune Dysregulation Index (IDI) in COVID-19 patients.
- To compare these immune markers with established clinical and laboratory parameters for predicting severity and mortality.
Main Methods:
- Flow cytometry was used to measure mHLA-DR, nCD64, and IDI in 100 COVID-19 patients and 30 healthy controls within 12 hours of admission.
- Clinical data, including C-reactive protein (CRP), Procalcitonin (PCT), Absolute Lymphocyte Count (ALC), Absolute Neutrophil Count (ANC), and Neutrophil to Lymphocyte Ratio (NLR), were recorded.
- Patients were followed until discharge or death to assess outcomes.
Main Results:
- Significant down-regulation of mHLA-DR and increasing IDI values were observed with increasing COVID-19 severity (mild vs. severe).
- IDI demonstrated high diagnostic accuracy (AUC 0.99) for differentiating between mild and severe COVID-19.
- mHLA-DR and IDI levels differed significantly between survivors and non-survivors, with specific thresholds associated with mortality risk.
Conclusions:
- mHLA-DR and IDI are valuable biomarkers for assessing COVID-19 severity and predicting mortality risk.
- The novel IDI shows particular promise for early risk stratification and patient management.
- Integrating these immune markers with NLR and ALC can enhance patient triaging, monitoring, and intervention strategies.
Abstract:
Immune dysregulation in COVID-19 is the major causal factor associated with disease progression and mortality. Role of monocyte HLA-DR (mHLA-DR), neutrophil CD64 (nCD64) and Immune dysregulation index (IDI) were studied in COVID-19 patients for assessing severity and outcome. Results were compared with other laboratory parameters. Antibody bound per cell for mHLA-DR, nCD64 and IDI were measured in 100 COVID-19 patients by flow cytometry within 12 h of hospital admission. Thirty healthy controls (HC) were included. Clinical and laboratory parameters like C - reactive protein (CRP), Procalcitonin (PCT), Absolute Lymphocyte count (ALC), Absolute Neutrophil count (ANC) and Neutrophil to Lymphocyte ratio (NLR) were recorded. Patients were followed up until recovery with discharge or death. Parameters from 54 mild (MCOV-19), 46 severe (SCOV-19) and 30 HC were analysed. mHLA-DR revealed significant and graded down regulation in MCOV-19 and SCOV-19 as compared to HC whereas IDI was lowest in HC with increasing values in MCOV-19 and SCOV-19. For diagnostic discrimination of MCOV-19 and SCOV-19, IDI revealed highest AUC (0.99). All three immune parameters revealed significant difference between survivors (n = 78) and non-survivors (n = 22). mHLA-DR < 7010 and IDI > 12 had significant association with mortality. Four best performing parameters to identify patients with SCOV-19 at higher risk of mortality were IDI, NLR, ALC and PCT. mHLA-DR and IDI, in addition to NLR and ALC at admission and during hospital stay can be utilized for patient triaging, monitoring, early intervention, and mortality prediction. IDI reported for the first time in this study, appears most promising. Immune monitoring of 'in hospital' cases may provide optimized treatment options.
Supplementary Information:
The online version contains supplementary material available at 10.1007/s12291-022-01087-z.
