Abstract
BackgroundSevere acute respiratory syndrome coronavirus 2 is a recently discovered pathogen responsible of coronavirus disease 2019 (COVID-19). The immunological changes associated with this infection are largely unknown.MethodsWe evaluated the peripheral blood mononuclear cells profile of 63 patients with COVID-19 at diagnosis. We also assessed the presence of association with inflammatory biomarkers and the 28-day mortality.ResultsLymphocytopenia was present in 51 of 63 (80.9%) patients, with a median value of 720 lymphocytes/µl (IQR 520-1,135). This reduction was mirrored also on CD8+ (128 cells/µl, IQR 55-215), natural killer (67 cells/µl, IQR 35–158) and natural killer T (31 cells/µl, IQR 11–78) cells. Monocytes were preserved in total number but displayed among them a subpopulation with a higher forward and side scatter properties, composed mainly of cells with a reduced expression of both CD14 and HLA-DR. Patients who died in the 28 days from admission (N=10, 15.9%), when compared to those who did not, displayed lower mean values of CD3+ (337.4 cells/µl vs 585.9 cells/µl; p=0.028) and CD4+ cells (232.2 cells/µl vs 381.1 cells/µl; p=0.042) and an higher percentage of CD8+/CD38+/HLA-DR+ lymphocytes (13.5% vs 7.6%; p=0.026).DiscussionThe early phases of COVID-19 are characterized by lymphocytopenia, predominance of Th2-like lymphocytes and monocytes with altered immune profile, which include atypical mononuclear cells.
Highlights
The early phases of COVID-19 are characterized by lymphocytopenia, predominance of Th2-like lymphocytes and monocytes with altered immune profile, which include atypical mononuclear cells
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new beta coronavirus identified in China in December 2019 which is responsible of coronavirus disease 2019 (COVID-19) [1]
Zheng and colleagues demonstrated an upregulation of the inhibitory receptor NKG2A expression on natural killer cells (NK) and cytotoxic lymphocytes (CTLs) in COVID-19 patients with a compromised degranulation capacity and a reduced production of interferon gamma (IFN-g), IL-2, granzyme B and tumor necrosis factor a (TNF-a) [7]
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new beta coronavirus identified in China in December 2019 which is responsible of coronavirus disease 2019 (COVID-19) [1]. Given the novelty of this virus, how the immune system deals with it is largely unknown. Preliminary studies from China highlighted a reduction of lymphocytes count, of CD4+ T and CD8+ T cells, an increase of the neutrophils-tolymphocytes ratio (NLR), a concomitant decrease in interferon gamma (IFN-g) production and an association with elevated inflammatory markers [3,4,5]. Preliminary unpublished reports described the presence of peripheral blood monocytes with morphologic and phenotypic changes displaying macrophage markers. Severe acute respiratory syndrome coronavirus 2 is a recently discovered pathogen responsible of coronavirus disease 2019 (COVID-19). The immunological changes associated with this infection are largely unknown
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