he epidemiology and clinical characterization of patients with coronavirus disease 2019 (COVID-19) has been reported. [1][2][3] As angiotensin-converting enzyme (ACE) 2 serves as the receptor for severe acute respiratory syndrome coronavirus 2 to gain entry into cells, 4 ACE2-expressing cells are susceptible to COVID-19 infection. 5 The use of ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) is common treatment in cardiovascular disorders, including hypertension, and data regarding the association of these drugs with ACE2 levels are conflicting. 6,7 However, to our knowledge, there are no clinical data indicating whether patients with hypertension who are taking ACEIs/ARBs have increased severity of illness or risk of mortality during COVID-19 infection and whether these patients should continue to use ACEIs/ARBs or switch to other antihypertensive drugs. MethodsPatients with COVID-19 admitted to the Central Hospital of Wuhan (Hubei Province, China) from January 15, 2020, to March 15, 2020, were included in this retrospective analysis. The study was approved by the institutional ethics board of the Central Hospital of Wuhan and the requirement for informed consent was IMPORTANCE Data are lacking whether patients with hypertension who are taking angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) have increased severity or risk of mortality during hospitalization for coronavirus disease 2019 .OBJECTIVE To investigate the association between ACEIs/ARBs and severity of illness and mortality in patients with hypertension hospitalized for COVID-19 infection.

In December 2019, a cluster of acute respiratory illness caused by a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) occurred in Wuhan, China. 1,2 Epidemiological and clinical characteristics, risk factors for mortality of patients infected with SARS-CoV-2, and risk factors in the susceptibility to SARS-CoV-2 included age and chronic disease have been reported. 3-6 However, the use of biological markers to predict the susceptibility to SARS-CoV-2 has not been well described. So far, only one study has reported that ABO blood groups were associated with the susceptibility to SARS-CoV-2Á 7 In the present study, after eliminating other confounding risk factors (including age, gender and comorbidities), we further investigated and confirmed the association of ABO blood groups and risk of SARS-CoV-2 pneumonia in patients from the Central Hospital of Wuhan, as well as two hospitals in Wuhan, China.Patients diagnosed with SARS-CoV-2 who died or were discharged between February 1 and March 25, 2020, were included in this retrospective cohort study. The study was approved by the Ethics Committee of the Central Hospital of Wuhan, and the need for informed consent was waived. 8 Epidemiological information, clinical data, underlying comorbidities, CT images of lungs, laboratory findings and clinical outcomes were extracted from electronic medical records. The blood group distribution data of the other two hospitals (Wuhan Jinyintan Hospital and Renmin Hospital of Wuhan University) and healthy controls in Wuhan came from the paper published online. 7 Data were expressed as percentages (%). We used chi-squared tests or Fisher's exact tests in order to compare the various groups.The ABO blood group in 265 patients infected with SARS-CoV-2 from the Central Hospital of Wuhan showed a distribution of 39Á3 %, 25Á3 %, 9Á8 % and 25Á7 % for A, B, AB and O, respectively (Table I). The proportion of blood group A in patients infected with SARS-CoV-2 was significantly higher than that in healthy controls (39Á3 % vs. 32Á3 %, P = 0Á017), 7 while the proportion of blood group O in patients infected with SARS-CoV-2 was significantly lower than that in healthy controls (25Á7 % vs. 33Á8 %, P < 0Á01).We next investigated whether age, gender and chronic disease influence the ABO blood group distribution (Table I).The results showed that, among blood group A (43Á6 % vs. 32Á2 % in controls, P < 0Á01) and blood group O (22Á2 % vs. 33Á8 % in controls, P < 0Á01), patients over 60 years of age were consistent with all the above patients. Similarly, we Conceived and designed the experiments:

a-Tocopheryl succinate (a-TOS) is a selective inducer of apoptosis in cancer cells, which involves the accumulation of reactive oxygen species (ROS). The molecular target of a-TOS has not been identified. Here, we show that a-TOS inhibits succinate dehydrogenase (SDH) activity of complex II (CII) by interacting with the proximal and distal ubiquinone (UbQ)-binding site (Q P and Q D , respectively). This is based on biochemical analyses and molecular modelling, revealing similar or stronger interaction energy of a-TOS compared to that of UbQ for the Q P and Q D sites, respectively. CybL-mutant cells with dysfunctional CII failed to accumulate ROS and underwent apoptosis in the presence of a-TOS. Similar resistance was observed when CybL was knocked down with siRNA. Reconstitution of functional CII rendered CybL-mutant cells susceptible to a-TOS. We propose that a-TOS displaces UbQ in CII causing electrons generated by SDH to recombine with molecular oxygen to yield ROS. Our data highlight CII, a known tumour suppressor, as a novel target for cancer therapy.

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