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Since December 2019, humankind has been experiencing a ravaging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak, the second coronavirus pandemic in a decade after the Middle East respiratory syndrome coronavirus (MERS-CoV) disease in 2012. Infection with SARS-CoV-2 results in Coronavirus disease 2019 (COVID-19), which is responsible for over 3.1 million deaths worldwide. With the emergence of a second and a third wave of infection across the globe, and the rising record of multiple reinfections and relapses, SARS-CoV-2 infection shows no sign of abating. In addition, it is now evident that SARS-CoV-2 infection presents with neurological symptoms that include early hyposmia, ischemic stroke, meningitis, delirium and falls, even after viral clearance. This may suggest chronic or permanent changes to the neurons, glial cells, and/or brain vasculature in response to SARS-CoV-2 infection or COVID-19. Within the central nervous system (CNS), microglia act as the central housekeepers against altered homeostatic states, including during viral neurotropic infections. In this review, we highlight microglial responses to viral neuroinfections, especially those with a similar genetic composition and route of entry as SARS-CoV-2. As the primary sensor of viral infection in the CNS, we describe the pathogenic and neuroinvasive mechanisms of RNA viruses and SARS-CoV-2 vis-à-vis the microglial means of viral recognition. Responses of microglia which may culminate in viral clearance or immunopathology are also covered. Lastly, we further discuss the implication of SARS-CoV-2 CNS invasion on microglial plasticity and associated long-term neurodegeneration. As such, this review provides insight into some of the mechanisms by which microglia could contribute to the pathophysiology of post-COVID-19 neurological sequelae and disorders, including Parkinson’s disease, which could be pervasive in the coming years given the growing numbers of infected and re-infected individuals globally.

The findings from this investigation provide persuasive scientific support for the traditional use of G. kola seed in the treatment of diabetes and its associated complications.

The role of oxidative stress in the pathogenesis of alcoholic diseases in the liver is well documented. Kolaviron (KV), a biflavonoid complex from Garcinia kola seeds, possesses a variety of biological activities, including antioxidant. Our aim was to investigate in vivo whether KV may attenuate oxidative stress in liver of Wistar albino rats following chronic ethanol administration. Thirty-six male Wistar albino rats were randomly divided into six groups. Toxicity was induced by administering 7.5% or 45% ethanol at 3 g/kg of body weight daily for 8 weeks. Rats were treated with KV at 200 mg/kg of body weight for the same duration. Treatment was by oral gavage. Integrity of liver was assessed by determining the levels of serum alanine and aspartate aminotransferases (ALT and AST, respectively) and alkaline phosphatase (ALP). The antioxidant status was monitored by determining the levels of hepatic superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), reduced glutathione (GSH), and malondialdehyde (MDA), the end product of lipid peroxidation (LPO). Experimentally, chronic ethanol administration led to hepatotoxicity as evidenced by the increase in levels of serum ALT, AST, and ALP. Ethanol also enhanced the formation of MDA in the liver. Specifically, MDA was elevated by 70% and 98% in animals treated with 7.5% and 45% ethanol, respectively. Levels of hepatic SOD, CAT, GST, and GSH were significantly (P < .05) reduced by ethanol treatment. Co-administration of KV during ethanol treatment inhibited hepatic LPO and ameliorated SOD and GST activities. These findings demonstrated that KV could have a beneficial effect by inhibiting the oxidative damage in liver of Wistar rats caused by chronic ethanol administration.

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Influenza A viruses (IAV) induce cytokine storm and host's intracellular redox imbalance to ensure continuous replication and survival, leading to severe immunopathology and death.