Nyarko Joseph Asuam, Dogbe Patience Mawuena, Ativi Lawrencia Ami Emefa, Wutsika Jennifer, Agyenim Emmanuel Boateng, Awere-Duodu Aaron, Botaeng Anthony Twumasi, Ntim Nana Afia Asante
National Influenza Centre, Noguchi Memorial Institute for Medical Research, Accra, Ghana.
Department of Environmental Science, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.
Yale J Biol Med. 2024 Dec 19;97(4):431-445. doi: 10.59249/DQJH2274. eCollection 2024 Dec.
The Coronavirus Disease 2019 (COVID-19) pandemic, driven by the novel coronavirus and its variants, has caused over 518 million infections and 6.25 million deaths globally, leading to a significant health crisis. Beyond its primary respiratory impact, Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has been implicated in various extra-pulmonary complications. Research studies reveal that the virus affects multiple organs, including the kidneys, liver, pancreas, and central nervous system (CNS), largely due to the widespread expression of Angiotensin Converting Enzyme-2 (ACE-2) receptors. Clinical evidence shows that the virus can induce diabetes by disrupting pancreatic and liver functions as well as cause acute kidney injury. Additionally, neurological complications, including cognitive impairments and neuroinflammation, have been observed in a significant number of COVID-19 patients. This review discusses the mechanisms linking SARS-CoV-2 to acute kidney injury, Type 1 and Type 2 Diabetes Mellitus (T1DM and T2DM), emphasizing its effects on pancreatic beta cells, insulin resistance, and the regulation of gluconeogenesis. We also explore how SARS-CoV-2 induces neurological complications, detailing the intricate pathways of neuro-invasion and the potential to trigger conditions such as Alzheimer's disease (AD). By elucidating the metabolic and neurological manifestations of COVID-19 and the underlying pathogenic mechanisms, this review underscores the imperative for continued research and the development of effective therapeutic interventions to mitigate the long-term and short-term impacts of SARS-CoV-2 infection.
由新型冠状病毒及其变种引发的2019冠状病毒病（COVID-19）大流行已在全球造成超过5.18亿人感染和625万人死亡，导致了严重的健康危机。除了对呼吸系统的主要影响外，严重急性呼吸综合征冠状病毒2（SARS-CoV-2）还与各种肺外并发症有关。研究表明，该病毒会影响多个器官，包括肾脏、肝脏、胰腺和中枢神经系统（CNS），这在很大程度上是由于血管紧张素转换酶2（ACE-2）受体的广泛表达。临床证据表明，该病毒可通过破坏胰腺和肝脏功能诱发糖尿病，并导致急性肾损伤。此外，在大量COVID-19患者中观察到了包括认知障碍和神经炎症在内的神经并发症。本综述讨论了将SARS-CoV-2与急性肾损伤、1型和2型糖尿病（T1DM和T2DM）联系起来的机制，强调了其对胰腺β细胞、胰岛素抵抗和糖异生调节的影响。我们还探讨了SARS-CoV-2如何诱发神经并发症，详细阐述了神经侵袭的复杂途径以及引发阿尔茨海默病（AD）等疾病的可能性。通过阐明COVID-19的代谢和神经表现以及潜在的致病机制，本综述强调了持续研究和开发有效治疗干预措施以减轻SARS-CoV-2感染的长期和短期影响的紧迫性。
