Coronavirus Disease 2019 (COVID-19) caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to considerable morbidity and mortality worldwide. The clinical manifestation of COVID-19 ranges from asymptomatic or mild infection to severe or critical illness, such as respiratory failure, multi-organ dysfunction or even death. Large-scale genetic association studies have indicated that genetic variations affecting SARS-CoV-2 receptors (angiotensin-converting enzymes, transmembrane serine protease-2) and immune components (Interferons, Interleukins, Toll-like receptors and Human leukocyte antigen) are critical host determinants related to the severity of COVID-19. Genetic background, such as 3p21.31 and 9q34.2 loci were also identified to influence outcomes of COVID-19. In this review, we aimed to summarize the current literature focusing on human genetic factors that may contribute to the observed diversified severity of COVID-19. Enhanced understanding of host genetic factors and viral interactions of SARS-CoV-2 could provide scientific bases for personalized preventive measures and precision medicine strategies.

This study aims to investigate the changes of serum erythropoietin (EPO) in premature infants with retinopathy of prematurity (ROP) after birth. The premature infants were divided into two groups, the first were infants with ROP, and the rest were infants without ROP. The peripheral blood of these infants after birth was collected, aiming to identify the correlation of serum EPO with ROP in the first 8 weeks after birth and before 38 weeks' postconceptual age. A total of 299 infants without ROP and 107 infants with ROP were recruited into our study. It was suggested that serum the EPO level in ROP group was significantly lower than it is in the group without ROP on the 28th day after birth. The median value of serum EPO in the group with and without ROP at day 28 of life were 0.44 mIU/mL and 0.62 mIU/mL, respectively ( = 0.017). These data indicated that there was no significant association between serum EPO and the clinical factors. Multivariate analysis identified only EPO serum level on the 28th day after birth and gestational age as independent predictors of ROP ( was 0.025 and 0.021, respectively). EPO serum level may serve as a surrogate marker for the development of ROP.

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<b><i>Background:</i></b> Accurate detection of cerebral oxygen saturation (rSO₂) may be useful for neonatal brain injury prevention, and the normal range of rSO₂ of neonates at high altitude remained unclear. <b><i>Objective:</i></b> To compare cerebral rSO₂ and cerebral fractional tissue oxygen extraction (cFTOE) at high-altitude and low-altitude areas in healthy neonates and neonates with underlying diseases. <b><i>Methods:</i></b> 515 neonates from low-altitude areas and 151 from Tibet were enrolled. These neonates were assigned into the normal group, hypoxic-ischemic encephalopathy (HIE) group, and other diseases group. Near-infrared spectroscopy was used to measure rSO₂ in neonates within 24 h after admission. The differences of rSO₂, pulse oxygen saturation (SpO₂), and cFTOE levels were compared between neonates from low- and high-altitude areas. <b><i>Results:</i></b> (1) The mean rSO₂ and cFTOE levels in normal neonates from Tibet were 55.0 ± 6.4% and 32.6 ± 8.5%, significantly lower than those from low-altitude areas (<i>p</i> &#x3c; 0.05). (2) At high altitude, neonates with HIE, pneumonia (<i>p</i> &#x3c; 0.05), anemia, and congenital heart disease (<i>p</i> &#x3c; 0.05) have higher cFTOE than healthy neonates. (3) Compared with HIE neonates from plain areas, neonates with HIE at higher altitude had lower cFTOE (<i>p</i> &#x3c; 0.05), while neonates with heart disease in plateau areas had higher cFTOE than those in plain areas (<i>p</i> &#x3c; 0.05). <b><i>Conclusions:</i></b> The rSO₂ and cFTOE levels in normal neonates from high-altitude areas are lower than neonates from the low-altitude areas. Lower cFTOE is possibly because of an increase in blood flow to the brain, and this may be adversely affected by disease states which may increase the risk of brain injury.

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