This retrospective study was designed to explore whether neutrophil to lymphocyte ratio (NLR) is a prognostic factor in patients with coronavirus disease 2019 (COVID-19). A cohort of patients with COVID-19 admitted to the Tongren Hospital of Wuhan University from 11 January 2020 to 3 March 2020 was retrospectively analyzed. Patients with hematologic malignancy were excluded. The NLR was calculated by dividing the neutrophil count by the lymphocyte count. NLR values were measured at the time of admission. The primary outcome was all-cause in-hospital mortality. A multivariate logistic analysis was performed. A total of 1004 patients with COVID-19 were included in this study. The mortality rate was 4.0% (40 cases). The median age of nonsurvivors (68 years) was significantly older than survivors (62 years). Male sex was more predominant in nonsurvival group (27; 67.5%) than in the survival group (466; 48.3%). NLR value of nonsurvival group (median: 49.06; interquartile range [IQR]: 25.71-69.70) was higher than that of survival group (median: 4.11; IQR: 2.44-8.12; P < .001). In multivariate logistic regression analysis, after adjusting for confounding factors, NLR more than 11.75 was significantly correlated with all-cause in-hospital mortality (odds ratio = 44.351; 95% Xisheng Yan and Fen Li contributed equally to this work.

Corona Virus Disease 2019 (COVID-19) is caused by the novel coronavirus SARS-CoV-2. Emerging genetic and clinical evidence suggests similarities between COVID-19 patients and those with severe acute respiratory syndrome and Middle East respiratory syndrome. Hematological changes such as lymphopenia and thrombocytopenia are not rare in COVID-19 patients, and a smaller population of these patients had leukopenia. Thrombocytopenia was detected in 5-41.7% of the patients with COVID-19. Analyzing the dynamic decrease in platelet counts may be useful in the prognosis of patients with COVID-19. However, the mechanisms underlying the development of thrombocytopenia remain to be elucidated. This review summarizes the hematological changes in patients infected with SARS-CoV-2 and possible underlying mechanisms of thrombocytopenia development. Coronavirus types and their receptorsSix types of human CoVs have been identified till date: HCoV-NL63 and HCoV-229E are Alphacoronaviruses and HCoV-OC43, HCoVHKU1, SARS-CoV, and Middle East respiratory syndrome coronavirus (MERS-CoV) are Betacoronaviruses (Table I) [6-10]. SARS-CoV-2 is the seventh member of the RNA-containing enveloped CoV family. SARS-CoV-2 and SARS-CoV reside on different branches of the phylogenetic tree, but the genome of SARS-CoV-2 shares more than 85% homology with that of SARS-CoV [7]. HCoV-229E, OC43, NL63, and HKU1 cause mild respiratory diseases. The last two decades have seen fatal infections caused by SARS-CoV and MERS-CoV [8].CoVs use cell surface receptors to enter host cells [9]. SARS-CoV primarily binds to the angiotensin-converting enzyme 2 (ACE2) [10], whereas MERS-CoV interacts with dipeptidyl peptidase 4 (DPP4; also known as CD26; Table I). Similar to SARS-CoV, COVID-19 develops upon binding of SARS-CoV-2 viral particles to ACE2, but not to other CoV receptors, such as aminopeptidase N and DPP4 [7]. SARS-CoV has similar antigenic characteristics as human 12]. HCoV-229E enters monocytes and macrophages via CD13 and induces cell apoptosis [13]. In addition, Betacoronaviruses can utilize CEACAMla (CD66a) as receptors [4,14]. Clinical manifestations and treatment of COVID-19Patients with COVID-19 can be divided into four categories based on their clinical manifestations: light, common, severe, and critical. Guan et al. performed a retrospective study (n = 1099) demonstrated that COVID-19 is associated with a wide range of symptoms [1]. Fever

Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread around the world at an unprecedented rate. In the present study, 4 marine sulfated...