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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of COVID-19. Though many COVID-19 vaccines have been developed, most of them are delivered via intramuscular injection and thus confer relatively weak mucosal immunity against the natural infection. Virus-Like Particles (VLPs) are self-assembled nanostructures composed of key viral structural proteins, that mimic the wild-type virus structure but are non-infectious and non-replicating due to the lack of viral genetic material. In this study, we efficiently generated SARS-CoV-2 VLPs by co-expressing the four SARS-CoV-2 structural proteins, specifically the membrane (M), small envelope (E), spike (S) and nucleocapsid (N) proteins. We show that these proteins are essential and sufficient for the efficient formation and release of SARS-CoV-2 VLPs. Moreover, we used lentiviral vectors to generate human cell lines that stably produce VLPs. Because VLPs can bind to the virus natural receptors, hence leading to entry into cells and viral antigen presentation, this platform could be used to develop novel vaccine candidates that are delivered intranasally., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

As clinicians have gained experience in treating patients with the novel SARS-CoV-2 (COVID-19) virus, mortality rates for patients with acute COVID-19 infection have decreased. The Centers for Disease Control (CDC) has identified the African American population as having increased risk of COVID-19 associated mortality, however little is known about echocardiographic markers associated with increased mortality in this patient population. We aimed to compare the clinical and echocardiographic features of a predominantly African American patient cohort hospitalized with acute COVID-19 infection during the first (March-June 2020) and second (September-December 2020) waves of the COVID-19 pandemic, and to investigate which parameters are most strongly associated with composite all-cause mortality. We performed consecutive transthoracic echocardiograms (TTEs) on 105 patients admitted with acute COVID-19 infection during the first wave and 129 patients admitted during the second wave. TTE parameters including left ventricular ejection fraction (LVEF), left ventricular global longitudinal strain (LVGLS), right ventricular global longitudinal strain (RVGLS), right ventricular free-wall strain (RVFWS), and right ventricular basal diameter (RVBD) were compared between the two groups. Clinical and demographic characteristics including underlying co-morbidities, biomarkers, in-hospital treatment regimens, and outcomes were collected and analyzed. Univariable and multivariable analyses were performed to determine variables associated with all-cause mortality. There were no significant differences between the two waves in terms of age, gender, BMI, or race. Overall all-cause mortality was 35.2% for the first wave compared to 14.7% for the second wave (p < 0.001). Previous medical conditions were similar between the two waves with the exception of underlying lung disease (41.9% vs. 29.5%, p = 0.047). Echocardiographic parameters were significantly more abnormal in the first wave compared to the second: LVGLS (- 17.1 ± 5.0 vs. - 18.9 ± 4.8, p = 0.02), RVGLS (- 15.7 ± 5.9% vs. - 19.0 ± 5.9%, p < 0.001), RVFWS (- 19.5 ± 6.8% vs. - 23.2 ± 6.9%, p = 0.001), and RVBD (4.5 ± 0.8 vs. 3.9 ± 0.7 cm, p < 0.001). Stepwise multivariable logistic analysis showed mechanical ventilation, RVFWS, and RVGLS to be independently associated with mortality. In a predominantly African American patient population on the south side of Chicago, the clinical and echocardiographic features of patients hospitalized with acute COVID-19 infection demonstrated marked improvement from the first to the second wave of the pandemic, with a significant decrease in all-cause mortality. Possible explanations include implementation of evidence-based therapies, changes in echocardiographic practices, and behavioral changes in our patient population. Mechanical ventilation and right-sided strain-based markers were independently associated with mortality., (© 2021. The Author(s), under exclusive licence to Springer Nature B.V.)

Background: Long period of SARS-CoV-2 infection has been associated with psychiatric and cognitive disorders in adolescents and children. SARS-CoV-2 remains dormant in the CNS leading to neurological complications. The wide expression of ACE2 in the brain raises concern for its involvement in SARS-CoV-2 infection. Though, the mechanistic insights about blood-brain barriers (BBB) crossing by SARS-CoV-2 and further brain infection are still not clear. Moreover, the mechanism behind dormant SARS-CoV-2 infections leading to chronic neurological disorders needs to be unveiled. There is an urgent need to find out the risk factor involved in COVID-19-associated neurological disease. Therefore, the role of immune-associated genes in the pathogenesis of COVID-19 associated neurological diseases is presented which could contribute to finding associated genetic risk factors., Method: The search utilizing multiple databases, specifically, EMBASE, PubMed (Medline), and Google Scholar was performed. Moreover, the literature survey on the involvement of COVID-19, neuropathogenesis, and its consequences was done., Description: Persistent inflammatory stimuli may promote the progression of neurodegenerative diseases. An increased expression level of cytokine, chemokine, and decreased expression level of immune cells has been associated with the COVID-19 patient. Cytokine storm was observed in severe COVID-19 patients. The nature of SARS-CoV-2 infection can be neuroinflammatory. Genes of immune response could be associated with neurodegenerative diseases., Conclusion: The present review will provide a useful framework and help in understanding COVID-19-associated neuropathogenesis. Experimental studies on immune-associated genes in COVID-19 patients with neurological manifestations could be helpful to establish its neuropathogenesis., (Copyright © 2021 Elsevier Ltd. All rights reserved.)