ABSTRACT
Coronavirus 2019 (COVID-19) is an infectious respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that mainly affects the lungs. COVID-19 symptoms include the presence of fevers, dry coughs, fatigue, sore throat, headaches, diarrhea, and a loss of taste or smell. However, it is understood that SARS-CoV-2 is neurotoxic and neuro-invasive and could enter the central nervous system (CNS) via the hematogenous route or via the peripheral nerve route and causes encephalitis, encephalopathy, and acute disseminated encephalomyelitis (ADEM) in COVID-19 patients. This review discusses the possibility of SARS-CoV-2-mediated Multiple Sclerosis (MS) development in the future, comparable to the surge in Parkinson's disease cases following the Spanish Flu in 1918. Moreover, the SARS-CoV-2 infection is associated with a cytokine storm. This review highlights the impact of these modulated cytokines on glial cell interactions within the CNS and their role in potentially prompting MS development as a secondary disease by SARS-CoV-2. SARS-CoV-2 is neurotropic and could interfere with various functions of neurons leading to MS development. The influence of neuroinflammation, microglia phagocytotic capabilities, as well as hypoxia-mediated mitochondrial dysfunction and neurodegeneration, are mechanisms that may ultimately trigger MS development.
Subject(s)
COVID-19/complications , COVID-19/pathology , Central Nervous System/pathology , Multiple Sclerosis/pathology , Neurodegenerative Diseases/virology , Central Nervous System/virology , Cytokine Release Syndrome/pathology , Cytokines/blood , Cytokines/metabolism , History, 20th Century , Humans , Influenza Pandemic, 1918-1919/statistics & numerical data , Multiple Sclerosis/virology , Neurodegenerative Diseases/pathology , SARS-CoV-2/immunology , Post-Acute COVID-19 SyndromeABSTRACT
Background The current pandemic of the novel coronavirus disease (COVID-19) is a global health challenge. Pulmonary dysfunction is the main outcome of COVID-19 infection. In critically ill patients, however, liver complications have also been reported. Thus, we conducted a systematic review and meta-analysis to draw generalized conclusions regarding impaired liver biochemistry and its potential relationship with COVID-19 disease severity. Materials and Methods We searched the PubMed, Scopus, and Web of Science databases for all the related literature published up to June 20, 2020. The data were analyzed using R statistical software. A random-effects model was employed for pooling the data. The risk of bias and quality of included studies was assessed using the modified Newcastle-Ottawa Scale (NOS) for cohort studies. Results The present meta-analysis comprises 10 retrospective and two prospective studies (6,976 COVID-19 patients). The serum analysis revealed significantly higher levels of alanine aminotransferases and aspartate aminotransferases and significantly lower albumin levels. Moreover, insignificant increases in serum levels of total bilirubin were observed. Upon subgroup analysis of six studies (severe cases, n=131; non-severe cases, n=334) stratified on the basis of disease severity, we found that these abnormalities were relatively higher in severe cases of COVID-19 (albumin [weighted mean difference (WMD), 34.03 g/L; 95% CI, 27.42 to 40.63; p<0.0001; I2=96.83%); alanine transaminase (ALT) [WMD, 31.66 U/L; 95% CI, 25.07 to 38.25; p<0.0001; I2=55.64%]; aspartate aminotransferase (AST) [WMD, 41.79 U/L; 95% CI, 32.85 to 50.72; p<0.0001; I2=51.43%]; total bilirubin [WMD, 9.97 µmol/L; 95% CI, 8.46 to 11.48; p<0.0001; I2=98%]) than in non-severe cases. Conclusion Deranged liver enzymes serve as prognostic factors to assess the severity of COVID-19. Liver markers should, therefore, be observed and monitored continuously.