Does COVID‐19 really impact on the oxy‐hemoglobin dissociation curve?

Costa, Flávia Zimmerle da Nóbrega; Mauad, Vitor Augusto Queiroz; Borducchi, Davimar Miranda Maciel

doi:10.1002/jha2.126

Cited by 6 publications

(3 citation statements)

References 8 publications

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“…The S protein of the virus was detected in tissue sections, accompanied by tissue damage and cell death ( 39 ). COVID-19 patients often have hypoxemia and tissue hypoxia, and the oxygenated hemoglobin saturation of the brain tissue is also significantly reduced ( 48 ). This can lead to energy metabolism disorders and cell apoptosis in key brain areas such as the hippocampus, damaging neuronal structure and function ( 49 ).…”

Section: Potential Mechanisms Underlying Post-covid Cognitive Impairmentmentioning

confidence: 99%

Cognitive impairment after long COVID-19: current evidence and perspectives

Li,

Zhang,

Zhang

et al. 2023

Front. Neurol.

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COVID-19, caused by the SARS-CoV-2 virus, is a respiratory infectious disease. While most patients recover after treatment, there is growing evidence that COVID-19 may result in cognitive impairment. Recent studies reveal that some individuals experience cognitive deficits, such as diminished memory and attention, as well as sleep disturbances, suggesting that COVID-19 could have long-term effects on cognitive function. Research indicates that COVID-19 may contribute to cognitive decline by damaging crucial brain regions, including the hippocampus and anterior cingulate cortex. Additionally, studies have identified active neuroinflammation, mitochondrial dysfunction, and microglial activation in COVID-19 patients, implying that these factors may be potential mechanisms leading to cognitive impairment. Given these findings, the possibility of cognitive impairment following COVID-19 treatment warrants careful consideration. Large-scale follow-up studies are needed to investigate the impact of COVID-19 on cognitive function and offer evidence to support clinical treatment and rehabilitation practices. In-depth neuropathological and biological studies can elucidate precise mechanisms and provide a theoretical basis for prevention, treatment, and intervention research. Considering the risks of the long-term effects of COVID-19 and the possibility of reinfection, it is imperative to integrate basic and clinical research data to optimize the preservation of patients' cognitive function and quality of life. This integration will also offer valuable insights for responding to similar public health events in the future. This perspective article synthesizes clinical and basic evidence of cognitive impairment following COVID-19, discussing potential mechanisms and outlining future research directions.

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Section: Potential Mechanisms Underlying Post-covid Cognitive Impairmentmentioning

confidence: 99%

Cognitive impairment after long COVID-19: current evidence and perspectives

Li,

Zhang,

Zhang

et al. 2023

Front. Neurol.

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show abstract

“…al 2020 suggested that new coronavirus has ability to act on the hemoglobin beta chain and has potential to code proteins, this causes oxygen transport capacity of hemoglobin to be lowered contributing to hypoxia thus worsening the condition. 10 In hemoglobin considering the structure of heme, is a combination of porphyrin with iron, porphyrin is ring like organic compound to which iron is attached. This iron atom attaches with oxygen reversibly and delivers oxygen.…”

Section: Discussionmentioning

confidence: 99%

Corona virus lowers hemoglobin more in severe infection than mild COVID-19 infection.

Chaudhry¹,

Rasheed

Shakir³

et al. 2021

TPMJ

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Objectives: To study the effect of corona virus on blood hemoglobin and the changes this virus causes on hemoglobin in COVID-19 infected patients. Study Design: Observational study. Settings: Rawal institute of Health Sciences and Pakistan Institute of Medical Sciences, Islamabad. Period: Feb 2021 to April 2021. Material & Methods: Total 100 adult patients were included all were suffering from corona virus infection. COVID-19 infected patients belonging to both genders with no other cause of anemia were selected and all adult patients in which anemia was due to diseases other than corona infection were excluded. The blood samples of COVID-19 infected patients was taken in 5cc syringe and was send to the laboratory of Rawal Institute Of Health Sciences Islamabad for hemoglobin estimation. Blood heamoglobin (Hb) at the time of admission was recorded. Changes in their blood Hb was noted. Statistical Analysis: Data was be entered into SPSS version 23, normality of data was checked. For non-normally distributed data kruskal wallis and Mann whitney U test was applied and for normally distributed data Anova and post hoc was used. Spearsman correlation was used to correlate non distributed data and Pearson’s correlation was used for normally distributed data. Results: 100 adult patients were divided in two groups. Group I with mild symptoms of corona virus and group II with severe symptoms of corona virus. Patients with mild corona symptoms their blood hemoglobin level was 12.2 g/dl and those with severe corona symptoms their blood hemoglobin level was 10.0 g/dl. Conclusion: It was observed that patients suffering from severe disease of corona COVID-19 had reduced hemoglobin levels than those suffering from milder form of disease, thus confirming that corona virus effects the hemoglobin level and reduces its serum value causing anemia leading to complication of disease.

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“…Numerous studies have revealed that some COVID-19 patients do experience significant hemolysis problems. There is a need for a more rational method of evaluating the hemoglobin affinity argument, particularly at the microcirculation level (112). Microscopic spectrophotometry analysis revealed a significant shift in a single COVID-19 patient's red blood cell (113).…”

Section: The Oxygen Dissociation Curve Was Insufficiently Interpretablementioning

confidence: 99%

COVID-19: Invades Erythrocytes through Plasmodium Falciparum Antigen and Complement-Like System

Liu

2021

Preprint

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Malaria symptoms are very similar to those of COVID-19, and infections can be symptomatic or asymptomatic. Common immunodominant epitopes are shared by the SARS-CoV-2 proteins and the Plasmodium falciparum antigen. Through bioinformatics methods such as domain search, this study discovered that the S, ORF3a proteins contained Plasmodium antigens rich in tryptophan and threonine. ORF3a, ORF8, S, and N and others also had more extended autotransporter domains. The Plasmodium antigen of S protein contained a C1q domain capable of binding to the complement receptor 1 on the red blood cell membrane. ORF3a contained the Plasmodium antigen EBA-175 domain, which was capable of binding to glycophorin A on the red blood cell membrane. S and ORF3a were bound to band 4.1 to anchor on the erythrocyte membrane skeleton, respectively. The Membrane attack complex component of the S protein formed fusion pores on the red blood cell membrane. Then it injected viral genetic material into the mature red blood cell. ORF3a used a thiol-activated cytolysin domain to create hemolytic pores in the red blood cell membrane. The coagulation factor calcium ions were involved in the red blood cell invasion process. The invasion would have no discernible hemolysis or hypoxia reactions. According to the Plasmodium antigen type for SARS-COV-2, the blood cells of people with blood types A and Knops were susceptible to attack by SARS-COV-2 virus proteins.

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Does COVID‐19 really impact on the oxy‐hemoglobin dissociation curve?

Cited by 6 publications

References 8 publications

Cognitive impairment after long COVID-19: current evidence and perspectives

Cognitive impairment after long COVID-19: current evidence and perspectives

Corona virus lowers hemoglobin more in severe infection than mild COVID-19 infection.

COVID-19: Invades Erythrocytes through Plasmodium Falciparum Antigen and Complement-Like System

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