Observational cohort study of the clinical outcomes associated with B.1.1.7/SGTF among hospitalized COVID-19 patients in Lebanon.

Background: The B.1.1.7 SARS-CoV-2 variant results in spike gene target failure (SGTF) in reverse transcription-quantitative polymerase chain reaction (RT-PCR) assays. Few studies have been published on the clinical impact of B.1.1.7/SGTF. Aims: To assess the incidence of B.1.1.7/SGTF and its associated clinical characteristics among hospitalized COVID-19 patients. Methods: This observational, single-centre, cohort study was conducted between December 2020 and February 2021 and included 387 hospitalized COVID-19 patients. The Kaplan-Meier method was used for survival analysis, and logistic regression to identify risk factors associated with B.1.1.7/SGTF. Results: By February 2021, B.1.1.7/SGTF (88%) dominated the SARS-CoV-2 PCR results in a Lebanese hospital. Of the 387 eligible COVID-19 patients confirmed by SARS-CoV-2 RT-PCR, 154 (40%) were non-SGTF and 233 (60%) were B.1.1.1.7/SGTF; this was associated with a higher mortality rate among female patients [22/51 (43%) vs 7/37 (19%); P = 0.0170]. Among patients in the B.1.1.7/SGTF group, most were aged ≥ 65 years [162/233 (70%) vs 74/154 (48%); P < 0.0001]. Independent predictors of B.1.1.7/SGTF infection were hypertension (OR = 0.415; CI: 0.242-0.711; P = 0.0010), age ≥ 65 years (OR = 0.379; CI: 0.231-0.622; P < 0.0001), smoking (OR = 1.698; CI: 1.023-2.819; P = 0.0410), and cardiovascular disease (OR = 3.812; CI: 2.215-6.389; P < 0.0001). Only non-SGTF patients experienced multi-organ failure [5/154 (4%) vs 0/233 (0%); P = 0.0096]. Conclusion: There was a clear difference between the clinical features associated with B.1.1.7/SGTF and non-SGTF lineages. Tracking viral evolution and its clinical impact is crucial for proper understanding and management of the COVID-19 pandemic.

Hemophagocytic Syndrome and COVID-19: A Comprehensive Review.

Hemophagocytic lymphohistiocytosis (HLH), a hyperinflammatory hyperferritinemic syndrome, is triggered by various etiologies and diseases and can lead to multiorgan dysfunction and death. There are two types of HLH: primary and secondary. Primary HLH (pHLH) is caused by a genetic mutation resulting in dysfunction in cytotoxic T lymphocytes (CTLs), natural killer (NK) cells, hyperactivated immune cells, and hypercytokinemia. In secondary HLH (sHLH), an underlying etiology is the cause of the disease. Infections, malignancy, and autoimmune diseases are well-known triggers for sHLH. Infectious triggers for sHLH are most frequently viruses, where different mechanisms, including dysregulated CTLs and NK cell activity and persistent immune system stimulation, have been reported. Similarly, in severe coronavirus disease 2019 (COVID-19) patients, a hyperinflammatory mechanism leading to hypercytokinemia and hyperferritinemia has been demonstrated. A similar dysfunction in CTLs and NK cells, persistent immune system stimulation with increased cytokines production, and severe end-organ damage have been reported. Therefore, a significant overlap is present between the clinical and laboratory features seen in COVID-19 and sHLH. However, SARS-CoV-2, similar to other viruses, can trigger sHLH. Hence, a diagnostic approach is needed in severe COVID-19 patients presenting with multiorgan failure, in whom sHLH should be considered.