Long-term effects of SARS-CoV-2 infection on human brain and memory.
Qiulu DingHanJun ZhaoPublished in: Cell death discovery (2023)
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants have caused several waves of outbreaks. From the ancestral strain to Omicron variant, SARS-CoV-2 has evolved with the high transmissibility and increased immune escape against vaccines. Because of the multiple basic amino acids in the S1-S2 junction of spike protein, the widespread distribution of angiotensin-converting enzyme 2 (ACE2) receptor in human body and the high transmissibility, SARS-CoV-2 can infect multiple organs and has led to over 0.7 billion infectious cases. Studies showed that SARS-CoV-2 infection can cause more than 10% patients with the Long-COVID syndrome, including pathological changes in brains. This review mainly provides the molecular foundations for understanding the mechanism of SARS-CoV-2 invading human brain and the molecular basis of SARS-CoV-2 infection interfering with human brain and memory, which are associated with the immune dysfunction, syncytia-induced cell death, the persistence of SARS-CoV-2 infection, microclots and biopsychosocial aspects. We also discuss the strategies for reducing the Long-COVID syndrome. Further studies and analysis of shared researches will allow for further clarity regarding the long-term health consequences.
Keyphrases
- respiratory syndrome coronavirus
- sars cov
- angiotensin converting enzyme
- coronavirus disease
- cell death
- angiotensin ii
- amino acid
- working memory
- endothelial cells
- oxidative stress
- case report
- mental health
- case control
- high glucose
- diabetic rats
- risk assessment
- climate change
- cell proliferation
- induced pluripotent stem cells
- gene expression
- single molecule
- drug induced
- genome wide
- stress induced
- light emitting