How to Deal With Vaccine Breakthrough Infection With SARS-CoV-2 Variants.

Novel Coronary Pneumonia is the most infectious disease with the highest number of morbidity and mortality in 100 years. Despite aggressive and effective COVID-19 prevention and control measures, countries have been unable to stop its outbreaks. With the widespread use of vaccines, the occurrence of COVID-19 has declined markedly. April 21, 2021, New York scholars reported Vaccine Breakthrough Infections with SARS-CoV-2 Variants, which immediately attracted widespread attention. In this mini-review, we focus on the characteristics of SARS-CoV-2 and its mutant strains and vaccine breakthrough infections. We have found that outbreaks of vaccine-breaking SARS-CoV-2 Delta infections in many countries are primarily the result of declining vaccine-generated antibody titers and relaxed outbreak management measures. For this reason, we believe that the main response to vaccine-breaking infections with the SARS-CoV-2 variant is to implement a rigorous outbreak defense policy and vaccine application. Only by intensifying the current vaccination intensity, gradually improving the vaccine and its application methods, and strengthening non-pharmaceutical measures such as travel restrictions, social distancing, masking and hand hygiene, can the COVID-19 outbreak be fully controlled at an early date.

The Long-Term Presence of SARS-CoV-2 on Cold-Chain Food Packaging Surfaces Indicates a New COVID-19 Winter Outbreak: A Mini Review.

Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is a highly infectious virus that is transmitted primarily through droplets or by coming in close contact with an infected person. In 2020, there was a global outbreak of COVID-19, resulting in an unprecedented global burden of disease, health care costs, and had a significant economic impact. Recently, SARS-CoV-2 was detected on the outer packaging of imported cold chain items in China and has led to virus transmission events, causing great concern. This paper analyses the factors of SARS-CoV-2 survival and transmission in different places and environments, especially the characteristics of low temperatures and object surfaces. It was found that SARS-CoV-2 could survive on surfaces of cold and moist objects in the cold chain for more than 3 weeks, potentially causing COVID-19 transmission. We believe that the low-temperature environment in winter may accelerate the spread of the outbreak and new outbreaks may occur. Overall, SARS-CoV-2 transmission that is susceptible to low winter temperatures is critical for predicting winter pandemics, allowing for the appropriate action to be taken in advance.

Attaching clinical significance to COVID-19-associated diarrhea.

The Corona Virus Disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), erupted in 2020 and created severe public health and socioeconomic challenges worldwide. A subset of patients, in addition to presenting with typical features such as fever, cough and dyspnea, was also afflicted with diarrhea. However, the clinical features and prognoses related to COVID-19-associated diarrhea have not attracted sufficient attention. This review of the medical literature examines the incidence, pathogenesis, clinical characteristics, fecal virus changes, prognoses and influencing factors of COVID-19-associated diarrhea. The reported incidence of diarrhea in patients with COVID-19 ranged from 2% to 49.5%. The main cause of diarrhea was found to be invasive by SARS-CoV-2 of ACE-2-expressing epithelial cells of the small intestine, causing local intestinal damage. This cellular invasion may be the key factor for the much longer duration of SARS-CoV-2 positivity observed for feces compared to pharyngeal swabs. The associated diarrhea in these patients upsets the balance of intestinal flora, resulting in more-severe disease intensity and worse prognosis. Clinicians should be vigilant to this kind of COVID-19-associated diarrhea, and design more effective prevention and treatment options for patients with positive fecal nucleic acid tests and intestinal microflora disorders.

Epidemiology and clinical characteristics of 43 COVID-19 patients in Weifang, China.

BACKGROUND: To investigate the epidemiology and clinical characteristics of patients infected with coronavirus disease 2019 (COVID-19) in Weifang, China. METHODS: The demographic data of 43 COVID-19 patients identified in Weifang were used to investigate whether they had traveled to epidemic areas and whether they had close contact with confirmed cases. On admission, patients' symptoms and results of laboratory tests and imaging were analyzed. RESULTS: Among the 43 COVID-19 patients. including 9 third generation infected cases, 16 (37.2%) were imported, who infected the rest. Most cases were middle-aged with approximate sex ratio. A "super spreader", Mr. Zhang made it necessary to quarantine 69 medical personnel. Mr. Zhang directly infected six individuals who, in turn, infected another six individuals. Another patient, Mr. Wang, spread the infection to his five family members at a family gathering. Subsequently, the daughter infected her husband. The most common COVID-19 symptoms were fever, weakness, dry cough, and cough sputum. In most patients, white blood cell counts were not elevated and lymphocyte counts were decreased. Elevated C-reactive protein and serum amyloid A protein (SAA) levels were commonly observed. There was no death among the patients or infection among the medical staff. CONCLUSIONS: The infection by the COVID-19 in Weifang was mostly the result of close contact with imported cases. These circumstances underscore the need to comprehensively strengthen the management for patients to prevent and control the spread of the virus.

MicroRNA­133b aggravates atherosclerosis by activating the Notch signaling pathway.

The aim of the present study was to investigate the effect of miR­133b on atherosclerosis (AS). A mouse model of AS (AS group) was established, and serum levels of total cholesterol, triglyceride, high­density lipoprotein cholesterol and low­density lipoprotein (LDL) cholesterol were detected. The thoracic aorta tissues were subjected to hematoxylin and eosin staining for pathological examination. Mice were intravenously injected with microRNA (miR)­133b mimics (the miR­133b mimic + AS group) and miR­133b mimics negative control (the miR­133b NC + AS group). Normal mice were named the Sham group. Vascular reconstruction parameters, the Collagen/Vascular Area Ratio (CA/CVA) and serum inflammatory factors of mice in each group were detected. mRNA expression was measured by reverse transcription­quantitative PCR and protein expression was determined by western blot analysis. An in vitro model of AS was induced in vascular smooth muscle cells (VSMCs) using oxidized (ox)­LDL. CCK­8 and wound healing assays were used to detect cell proliferation and migration. Compared with the Sham group, mice of the AS group, the AS + miR­133b NC group and the AS + miR­133b mimic group had higher intima thickness (IT), tumor necrosis factor (TNF)­α and monocyte chemoattractant protein (MCP)­1 levels, as well as increased Notch1 and Jagged1 expression; and they had lower medial thickness (MT), CA/CVA ratio and Notch3 expression (all P<0.05). In addition, miR­133b mimic promoted the proliferation and migration, upregulated Notch1 and Jagged1, and downregulated Notch3 in ox­LDL­induced VSMCs. Taken together, miR­133b aggravates AS by activating the Notch signaling pathway, which could serve as a potential target for the treatment of AS.

Association of serum hepcidin levels with the presence and severity of obstructive sleep apnea syndrome.

BACKGROUND: Inflammation is thought to be involved in the pathogenesis of obstructive sleep apnea syndrome (OSAS). Hepcidin, a 25-kD peptide hormone produced by the liver, modulates acute inflammatory responses. This study aimed to determine the association of serum levels of hepcidin with the presence and severity of OSAS. MATERIAL/METHODS: We enrolled 184 patients with OSAS and 110 healthy subjects. Serum levels of hepcidin were evaluated using enzyme-linked immunosorbent assay (ELISA) method. RESULTS: OSAS patients had significantly higher serum hepcidin levels compared with healthy controls. Multivariable logistic regression analysis indicated that serum hepcidin levels were an independent determinant of the presence of OSAS (OR 1.224, 95% CI 1.159-1.292; P<0.001). Serum hepcidin levels were significantly elevated in severe OSAS patients compared with mild and moderate OSAS patients. Spearman correlation analysis revealed that serum hepcidin levels were correlated with the severity of OSAS. In addition, serum levels of hepcidin were correlated with apnea-hypopnea index (AHI) in patients with OSAS. CONCLUSIONS: Elevated serum hepcidin levels are associated with the presence and severity of OSAS.