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.

These results indicate that compounds affected HSV-1 mostly before adsorption and might interact with the viral envelope. Thymol exhibited a high selectivity index and seems to be a promising candidate for topical therapeutic application as antiviral agent for treatment of herpetic infections.

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.

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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.

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