Beyond the lungs: SARS-CoV-2 reveals multiple organ effects

In a recent review published in discovery of cell death In the journal, researchers unraveled the mechanisms underlying the effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on the brain and memory.

They also identified long-term coronavirus disease (COVID) risk factors and discussed ways to prevent post-coronavirus disease (COVID-19) conditions.

study: Long-term effects of SARS-CoV-2 infection on the human brain and memory. Image credit: Justlight/Shutterstock.com

Background

Several waves of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have occurred. SARS-CoV-2 evolved from the ancestral Wuhan-Hu-1 strain to the Omicron variant with excellent transmissibility and immunological evasion.

Prolonged exposure to COVID-19 can lead to persistent symptoms such as fatigue, frequent headaches, shortness of breath, impaired motor function, and poor concentration and memory.

Long-term exposure to the new coronavirus can cause pathological changes in the brain and impair human memory.

About reviews

In this review, the researchers present a mechanism by which SARS-CoV-2 infects the brain and affects memory. They also discussed long-term COVID-19 risk factors and prevention strategies.

SARS-CoV-2 infects the human brain and affects human memory, facilitated by host receptors.

Long-term COVID-19 patients can develop latent cognitive impairment, with dementia following acute COVID-19 treatment being a major risk factor. SARS-CoV-2 infects the nasal cavity and can directly infect the olfactory bulb of the brain via the olfactory nerve.

On the other hand, SARS-CoV-2 infection in the respiratory tract, where viral titers are high, can lead to virus entry into circulation and spread to other organs with the help of angiotensin-converting enzyme 2 (ACE2), resulting in considerable It can cause pathological changes. Production by different types of cells.

SARS-CoV-2 can also infect the eye and travel to the occipital brain via the optic nerve. SARS-CoV-2 disrupts the tight connection between the blood-brain barrier (BBB) ​​and intracellular cargo, potentially allowing it to invade various organs.

Sustained SARS-CoV-2 replication and interaction of the SARS-CoV-2 spike protein with the host ACE2 receptor triggers the development of syncytia and increases the synthesis of cytokines and autoantibodies, thereby leading to long-term May affect brain function and memory.

ACE2 is a key receptor for SARS-CoV-2 to invade the host and is expressed in various tissues including lung, liver, heart, kidney, brain and intestine. Cluster of differentiation (CD147), tyrosine protein kinase receptor UFO (ALX), neuropilin 1 (NRP1), and C-type lectins are potential SARS-CoV-2 receptors expressed on various cell types.

Structural studies revealed reduced dimensions in the parahippocampal gyrus, orbitofrontal region and olfactory cortex of the brain. Cytokines such as interleukin-1 (IL-1) and IL-6, and tumor necrosis factor alpha (TNF) through Toll-like receptor (TLR) signaling and microglial activation induced by SARS-CoV-2 increased production of May adversely affect memory and cognition.

Risk factors and prevention for post-COVID-19 conditions

Infection with SARS-CoV-2 causes immune impairment and can lead to cell death, which is directly responsible for long-term effects on body tissues. SARS-CoV-2 can stimulate the immune system, release cytokines and cause cell lysis.

Dysregulation of cytokine production can lead to cytokine storms, leading to severe illness that exacerbates the symptoms of COVID-19.

Fusion of the SARS-CoV-2 spike protein with host cells can cause hyperimmune responses, cell death, and prolonged symptoms after recovery from SARS-CoV-2.

Autoantibodies against type I interferon (IFN) may increase the likelihood of developing severe SARS-CoV-2 infection, cause acquired immunodeficiency, and prolong COVID-19 symptoms. Microcoagulation can trigger the formation of autoantibodies in affected organs, which may affect recovery from COVID-19.

The persistence of COVID-19 can unrestrainedly stimulate host immune system responses and SARS-CoV-2 protein expression. Spike proteins alone can cause behavioral and neuroinflammatory changes. COVID-19 symptoms are associated with emotional stress in certain individuals, which may be related to the biological and psychosocial effects of the disease.

Biopsychosocial variables may increase fear of COVID-19 and influence long-term COVID-19 recovery.

SARS-CoV-2 vaccination can effectively reduce symptoms, but SARS-CoV-2 infection cannot be avoided. Non-pharmaceutical measures such as mask use and social isolation have reduced transmission of SARS-CoV-2.

However, new drugs that can limit the spread of the virus are urgently needed to limit viral transmission and thus reduce the number of protracted COVID-19 cases.

Cytokine inhibitors given in the early stages of COVID-19 may help prevent later episodes of depression. Cognitive restorative treatments may help COVID-19 patients with cognitive impairment.

Additionally, optimal health can prevent SARS-CoV-2 infection. Regular physical activity, a regular sleep schedule, and a balanced diet (especially rich in vegetables, vitamins, magnesium, and zinc) are all important factors for overall health.

Conclusion

Overall, the review results suggest that the potential for brain injury associated with novel coronavirus disease (COVID-19), including direct SARS-CoV-2 infection, immune dysfunction, and persistent SARS-CoV-2 clarified the route

Prevention strategies such as vaccination, antiviral therapy, masks, exercise, regular sleep and a balanced diet are important to reduce the risk of cognitive impairment due to COVID-19.

Long-term effects such as memory loss can significantly reduce children’s self-confidence and learning efficiency, especially during early developmental stages. Further research is needed to improve our understanding of the long-term novel coronavirus pathophysiology.