Since COVID-19 was declared a pandemic, Brazil has become one of the countries most affected by this disease. A year into the pandemic, a second wave of COVID-19 emerged, with a rapid spread of a new SARS-CoV-2 lineage of concern. Several vaccines have been granted emergency-use authorization, leading to a decrease in mortality and severe cases in many countries. However, the emergence of SARS-CoV-2 variants raises the alert for potential new waves of transmission and an increase in pathogenicity. We compared the demographic and clinical data of critically ill patients infected with COVID-19 hospitalized in Rio de Janeiro during the first and second waves between July 2020 and October 2021. In total, 106 participants were included in this study; among them, 88% had at least one comorbidity, and 37% developed severe disease. Disease severity was associated with older age, pre-existing neurological comorbidities, higher viral load, and dyspnea. Laboratory biomarkers related to white blood cells, coagulation, cellular injury, inflammation, renal, and liver injuries were significantly associated with severe COVID-19. During the second wave of the pandemic, the necessity of invasive respiratory support was higher, and more individuals with COVID-19 developed acute hepatitis, suggesting that the progression of the second wave resulted in an increase in severe cases. These results can contribute to understanding the behavior of the COVID-19 pandemic in Brazil and may be helpful in predicting disease severity, which is a pivotal for guiding clinical care, improving patient outcomes, and defining public policies.
COVID-19 pandemic affected the global population in an unprecedented scale, with long-term consequences of SARS CoV-2 infection now emerging as a serious concern. Cognitive dysfunction is often reported in post-COVID patients, but its underlying mechanisms remain unknown. Here we demonstrated that brain exposure to SARS-CoV-2 spike (S) protein through its infusion into the lateral ventricle of adult mice induced late cognitive impairment, hippocampal synapse loss, and microglial engulfment of presynaptic terminals. Additionally, TLR4 blockage prevented Sassociated detrimental effects on memory in mice and TLR4 single nucleotide polymorphism (SNP) rs10759931 was associated with late cognitive outcome in mild COVID-19-recovered patients. Collectively, these findings indicate that S protein directly impacts the brain and identify TLR4 as a key target to prevent cognitive dysfunction. To our knowledge, this is the first animal model that recapitulates postCOVID cognitive impairment, opening new avenues for developing new strategies to prevent or treat the neurological outcomes of COVID-19.
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