Studies have found increased rates of dysosmia in patients with Novel Coronavirus disease 2019 (COVID-19). However, the mechanism that causes olfactory loss is unknown. The primary objective of this study was to explore local proinflammatory cytokine levels in the olfactory epithelium in patients with COVID-19. Biopsies of the olfactory epithelium were taken from patients with confirmed COVID-19 as well as uninfected controls. Levels of tumor necrosis factor α (TNF-α) and interleukin-1-beta (IL-1β) were assessed using ELISA and compared between groups. Average TNF-α levels were significantly increased in the olfactory epithelium of the COVID-19 group compared to the control group (P < 0.05). However, no differences in IL-1β were seen between groups. Elevated levels of the proinflammatory cytokine TNF-α were seen in the olfactory epithelium in patients with COVID-19. This suggests that direct inflammation of the olfactory epithelium could play a role in the acute olfactory loss described in many patients with COVID-19.

Background and objectives With the increase in the number of COVID-19 infections, the global health apparatus is facing insufficient resources. The main objective of the current study is to provide additional data regarding the clinical characteristics of the patients diagnosed with COVID-19, and in particular to analyze the factors associated with disease severity, lack of improvement, and mortality. Methods 102 studies were included in the present meta-analysis, all of which were published before September 24, 2020. The studies were found by searching a number of databases, including Scopus, MEDLINE, Web of Science, and Embase. We performed a thorough search from early February until September 24. The selected papers were evaluated and analyzed using Stata software application version 14. Results Ultimately, 102 papers were selected for this meta- analysis, covering 121,437 infected patients. The mean age of the patients was 58.42 years. The results indicate a prevalence of 79.26% for fever (95% CI: 74.98–83.26; I2 = 97.35%), 60.70% for cough (95% CI: 56.91–64.43; I2 = 94.98%), 33.21% for fatigue or myalgia (95% CI: 28.86–37.70; I2 = 96.12%), 31.30% for dyspnea (95% CI: 26.14–36.69; I2 = 97.67%), and 10.65% for diarrhea (95% CI: 8.26–13.27; I2 = 94.20%). The prevalence for the most common comorbidities was 28.30% for hypertension (95% CI: 23.66–33.18; I2 = 99.58%), 14.29% for diabetes (95% CI: 11.88–16.87; I2 = 99.10%), 12.30% for cardiovascular diseases (95% CI: 9.59–15.27; I2 = 99.33%), and 5.19% for chronic kidney disease (95% CI: 3.95–6.58; I2 = 96.42%). Conclusions We evaluated the prevalence of some of the most important comorbidities in COVID-19 patients, indicating that some underlying disorders, including hypertension, diabetes, cardiovascular diseases, and chronic kidney disease, can be considered as risk factors for patients with COVID-19 infection. Furthermore, the results show that an elderly male with underlying diseases is more likely to have severe COVID-19.

The recent coronavirus disease of 2019 (COVID-19) pandemic has adversely affected people worldwide. A growing body of literature suggests the neurological complications and manifestations in response to COVID-19 infection. Herein, we explored the inflammatory and immune responses in the post-mortem cerebral cortex of patients with severe COVID-19. The participants comprised three patients diagnosed with severe COVID-19 from March 26, 2020, to April 17, 2020, and three control patients. Our findings demonstrated a surge in the number of reactive astrocytes and activated microglia, as well as low levels of glutathione along with the upregulation of inflammation- and immune-related genes IL1B, IL6, IFITM, MX1, and OAS2 in the COVID-19 group. Overall, the data imply that oxidative stress may invoke a glial-mediated neuroinflammation, which ultimately leads to neuronal cell death in the cerebral cortex of COVID-19 patients.

The coronavirus disease 2019 (COVID-19) is a novel coronavirus infection that has rapidly spread worldwide, causing a pandemic. The main objective of this meta-analysis was to evaluate the prevalence of the most common symptoms and complications of COVID-19. All relevant studies on the clinical complications of COVID-19 have been identified by searching two web databases (i.e., PubMed and Scopus). Afterward, the relevant data were extracted from the selected studies, and then analyzed by the STATA (Version 14) random-effects model. The 30 studies selected for our meta-analysis covered 6,389 infected patients. The prevalence rates of the most common symptoms were as follows:

<b><i>Background:</i></b> Recently, it has been shown that coronavirus disease 2019 (COVID-19), which has caused a pandemic since December 2019, can be accompanied by some neurological disorders. This study aimed to assess the prevalence of the most common neurological symptoms and comorbidities and systematically review the literature regarding the most prevalent neurological complications of COVID-19 infection. <b><i>Methods:</i></b> All relevant studies had been collected from PubMed, Scopus, Embase, and Web of Science databases. All extracted data were analyzed using Stata version 11.2. The <i>I</i>² index was applied, and a random-effects model or a fixed-effects model was used for pooled estimation to assess the heterogeneity of studies. Furthermore, Egger and Beeg’s tests were used to evaluate the publication bias. <b><i>Results:</i></b> Fifty-seven studies (26 observational and 31 case reports) were included (including 6,597 COVID-19 patients). The most prevalent general symptoms were fever, cough, and dyspnea with 84.6% (95% CI: 75.3–92.1; <i>I</i>² = 98.7%), 61.3% (95% CI: 55.3–67.0; <i>I</i>² = 94.6%), and 34.2% (95% CI: 25.6–43.4; <i>I</i>² = 97.7%), respectively. Neurological symptoms observed among COVID-19 patients were fatigue, gustatory dysfunction, anorexia, olfactory dysfunction, headache, dizziness, and nausea with 42.9% (95% CI: 36.7–49.3; <i>I</i>² = 92.8%), 35.4% (95% CI: 11.2–64.4; <i>I</i>² = 99.2%), 28.9% (95% CI: 19.9–38.8; <i>I</i>² = 96.3%), 25.3% (95% CI: 1.6–63.4; <i>I</i>² = 99.6%), 10.1% (95% CI: 2.7–21.0; <i>I</i>² = 99.1%), 6.7% (95% CI: 3.7–10.5; <i>I</i>² = 87.5%), and 5.9% (95% CI: 3.1–9.5; <i>I</i>² = 94.5%). The most prevalent neurological comorbidity in COVID-19 was cerebrovascular disease with 4.3% (95% CI: 2.7–6.3; <i>I</i>² = 78.7%). <b><i>Conclusion:</i></b> The most prevalent neurological manifestations of COVID-19 include fatigue, gustatory dysfunction, anorexia, olfactory dysfunction, headache, dizziness, and nausea. Cerebrovascular disorders can either act as a risk factor for poorer prognosis in COVID-19 patients or occur as a critical complication in these patients. Guillain-Barre syndrome, encephalitis, and meningitis have also been reported as complications of COVID-19.

Currently, the COVID-19 pandemic is an international challenge, largely due to lack of effective therapies. Pharmacotherapy has not yet been able to find a definitive treatment for COVID-19. Since SARS-CoV-2 affects several organs, treatment strategies that target the virus in a wider range are expected to be ultimately more successful. To this end, a two-step treatment strategy has been presented. In the first phase of the disease, when the patient is newly infected with the virus and the cytokine storm has not yet been developed, a chimeric peptide is used to inhibit virus entry into the host cell cytosol (by inhibiting endosomal pH acidification) and viral replication. After the virus entry and decrease of angiotensin converting enzyme 2 (ACE2) level, some people are unable to properly compensate for the ACE2 pathway and progress toward the cytokine storm. In the beginning of the cytokine storm, sACE2 protein is very effective in regulating the immune system toward the anti-inflammatory pathway, including M2 macrophages. Hence, the genes of 8P9R chimeric peptide and sACE2 would be inserted in an episomal vector with a separate promoter for each gene: the chimeric peptide gene promoter is a CMV promoter, while the sACE2 gene promoter is a NF-κB-sensitive promoter. The NF-κB-sensitive promoter induces the expression of sACE2 gene soon after elevation of NF-κB which is the main transcription factor of inflammatory genes. Thus, as the expression of inflammatory cytokines increases, the expression of sACE2 increases simultaneously. In this condition, sACE2 can prevent the cytokine storm by inhibiting the pro-inflammatory pathways. To deliver the designed vector to the target cells, mesenchymal stem cell-derived (MSC-derived) exosome-liposome hybrids are used. Herein, the strategy can be considered as a personalized clinical therapy for COVID-19, that can prevent morbidity and mortality in the future.

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Recent investigations of COVID-19 have largely focused on the effects of this novel virus on the vital organs in order to efficiently assist individuals who have recovered from the disease. In the present study we used hippocampal tissue samples extracted from people who died after COVID-19. Utilizing histological techniques to analyze glial and neuronal cells we illuminated a massive degeneration of neuronal cells and changes in glial cells morphology in hippocampal samples. The results showed that in hippocampus of the studied brains there were morphological changes in pyramidal cells, an increase in apoptosis, a drop in neurogenesis, and change in spatial distribution of neurons in the pyramidal and granular layer. It was also demonstrated that COVID-19 alter the morphological characteristics and distribution of astrocyte and microglia cells. While the exact mechanism(s) by which the virus causes neuronal loss and morphology in the central nervous system (CNS) remains to be determined, it is necessary to monitor the effect of SARS-CoV-2 infection on CNS compartments like the hippocampus in future investigations. As a result of what happened in the hippocampus secondary to COVID-19, memory impairment may be a long-term neurological complication which can be a predisposing factor for neurodegenerative disorders through neuroinflammation and oxidative stress mechanisms.