Understanding COVID-19: From Dysregulated Immunity to Vaccination Status Quo

Escobedo, Ruby; Singh, Dhiraj Kumar; Kaushal, Deepak

doi:10.3389/fimmu.2021.765349

Cited by 6 publications

(2 citation statements)

References 95 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, vaccinated individuals have been found to have lower viral loads compared to non-vaccinated individuals in subsequent episodes of infection, which may contribute to milder symptoms [ 49 ]. Furthermore, it has been reported that non-vaccinated individuals may have immune system dysregulation, leading to more severe symptoms of infection [ [50] , [51] , [52] ]. COVID-19 vaccination can help downregulate the immune response [ 51 ], potentially reducing cell damage and resulting in less severe symptoms, including respiratory symptoms and headaches.…”

Section: Discussionmentioning

confidence: 99%

Effects of vaccination on COVID-19 infection symptoms in multiple sclerosis patients

Sharifi,

Rezaeimanesh,

Moradi

et al. 2024

eNeurologicalSci

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Effects of vaccination on COVID-19 infection symptoms in multiple sclerosis patients

Sharifi,

Rezaeimanesh,

Moradi

et al. 2024

eNeurologicalSci

View full text Add to dashboard Cite

“…As of now, there are currently no variants of high consequence circulating in the United States, but there are four variants of concern in circulation: B.1.1.7 (Alpha), B.1.351 (Beta), B.1.617.2 (Delta), and P.1 (Gamma). Considering most vaccines are designed against the SARS-CoV-2 spike protein, mutations within this region are likely to result in less effective vaccinations ( Escobedo et al., 2021 ). However, a study focusing on the effectiveness of the AstraZeneca and Pfizer vaccines against the predominant variant (B.1.1.7) and the delta variant surging through India and the United Kingdom (B.1.617.2) showed small differences between both vaccines, suggesting that both vaccines may continue to protect against SARS-CoV-2 strains ( Lopez Bernal et al., 2021 ).…”

Section: Origin Of Sars-cov-2mentioning

confidence: 99%

Insights Into the Changing Landscape of Coronavirus Disease 2019

Escobedo

Kaushal

Singh

2022

Front. Cell. Infect. Microbiol.

Self Cite

View full text Add to dashboard Cite

Coronavirus disease 2019 (COVID-19) is a highly contagious, infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which emerged in late 2019 in Wuhan China. A year after the World Health Organization declared COVID-19 a global pandemic, over 215 million confirmed cases and approximately 5 million deaths have been reported worldwide. In this multidisciplinary review, we summarize important insights for COVID-19, ranging from its origin, pathology, epidemiology, to clinical manifestations and treatment. More importantly, we also highlight the foundational connection between genetics and the development of personalized medicine and how these aspects have an impact on disease treatment and management in the dynamic landscape of this pandemic.

show abstract

Could SARS-CoV-2 Spike Protein Be Responsible for Long-COVID Syndrome?

2022

Mol Neurobiol

111

View full text Add to dashboard Cite

SARS-CoV-2 infects cells via its spike protein binding to its surface receptor on target cells and results in acute symptoms involving especially the lungs known as COVID-19. However, increasing evidence indicates that many patients develop a chronic condition characterized by fatigue and neuropsychiatric symptoms, termed long-COVID. Most of the vaccines produced so far for COVID-19 direct mammalian cells via either mRNA or an adenovirus vector to express the spike protein, or administer recombinant spike protein, which is recognized by the immune system leading to the production of neutralizing antibodies. Recent publications provide new findings that may help decipher the pathogenesis of long-COVID. One paper reported perivascular inflammation in brains of deceased patients with COVID-19, while others showed that the spike protein could damage the endothelium in an animal model, that it could disrupt an in vitro model of the blood-brain barrier (BBB), and that it can cross the BBB resulting in perivascular inflammation. Moreover, the spike protein appears to share antigenic epitopes with human molecular chaperons resulting in autoimmunity and can activate toll-like receptors (TLRs), leading to release of inflammatory cytokines. Moreover, some antibodies produced against the spike protein may not be neutralizing, but may change its conformation rendering it more likely to bind to its receptor. As a result, one wonders whether the spike protein entering the brain or being expressed by brain cells could activate microglia, alone or together with inflammatory cytokines, since protective antibodies could not cross the BBB, leading to neuro-inflammation and contributing to long-COVID. Hence, there is urgent need to better understand the neurotoxic effects of the spike protein and to consider possible interventions to mitigate spike proteinrelated detrimental effects to the brain, possibly via use of small natural molecules, especially the flavonoids luteolin and quercetin. KeywordsACE2 • Antibodies • Blood-brain barrier • Brain • Coronavirus • Endothelial cells • Receptor • Spike protein

show abstract

Understanding COVID-19: From Dysregulated Immunity to Vaccination Status Quo

Cited by 6 publications

References 95 publications

Effects of vaccination on COVID-19 infection symptoms in multiple sclerosis patients

Effects of vaccination on COVID-19 infection symptoms in multiple sclerosis patients

Insights Into the Changing Landscape of Coronavirus Disease 2019

Could SARS-CoV-2 Spike Protein Be Responsible for Long-COVID Syndrome?

Contact Info

Product

Resources

About