Should COVID-19 be branded to viral thrombotic fever?

Filho, Rubens Carmo Costa; Neto, Hugo Caire Castro-Faria; Mengel, José; Pelajo-Machado, Marcelo; Martins, Marco A.; Leite, Érica Távora; Mendonça-Filho, Hugo Tannus Furtado de; Souza, Tatiana de Arruda Campos Brasil de; Bello, Gonzalo; Leite, José Paulo Gagliardi

doi:10.1590/0074-02760200552

Cited by 6 publications

(4 citation statements)

References 69 publications

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“…Severe COVID-19 is characterised by systemic thrombosis, pulmonary venous congestion and embolism. 28 , 29 In addition, several studies have identified D-dimer and coagulation factors as biomarkers of severe disease. 30 , 31 , 32 Herein, we identified high levels of circulating D-dimer associated with anti-NP and anti-RBD IgG only in severely infected patients.…”

Section: Discussionmentioning

confidence: 99%

Coagulopathy and the humoral response against viral proteins in patients at different stages of COVID-19

Monteiro

Tavares

Souza

et al. 2022

Mem. Inst. Oswaldo Cruz

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BACKGROUND Patients with severe coronavirus disease 2019 (COVID-19) often present with coagulopathies and have high titres of circulating antibodies against viral proteins. OBJECTIVES Herein, we evaluated the association between D-dimer and circulating immunoglobulin levels against viral proteins in patients at different clinical stages of COVID-19. METHODS For this, we performed a cross-sectional study involving patients of the first wave of COVID-19 clinically classified as oligosymptomatic (n = 22), severe (n = 30), cured (n = 27) and non-infected (n = 9). Next, we measured in the plasma samples the total and fraction of immunoglobulins against the nucleoprotein (NP) and the receptor-binding domain (RBD) of the spike proteins by enzyme-linked immunosorbent assay (ELISA) assays. FINDINGS Patients with severe disease had a coagulation disorder with high levels of D-dimer as well as circulating IgG against the NP but not the RBD compared to other groups of patients. In addition, high levels of D-dimer and IgG against the NP and RBD were associated with disease severity among the patients in this study. MAIN CONCLUSIONS Our data suggest that IgG against NP and RBD participates in the worsening of COVID-19. Although the humoral response against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is partially understood, and more efforts are needed to clarify gaps in the knowledge of this process.

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Section: Discussionmentioning

confidence: 99%

Coagulopathy and the humoral response against viral proteins in patients at different stages of COVID-19

Monteiro

Tavares

Souza

et al. 2022

Mem. Inst. Oswaldo Cruz

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“…Vascular alterations, such as endothelial rupture by direct signaling effects or indirectly by increasing the production of inflammatory mediators accompanied by coagulation cascade dysregulation, have been reported in infections with other coronaviruses [ 55 , 56 ]. In fact, the coagulation phenotype of COVID-19 is so remarkable that it was proposed that this disease should be in fact named as viral thrombotic fever [ 57 ]. Similar to COVID-19, SARS-CoV infection was associated with endothelial dysfunction, thrombotic complications, and hematological manifestations.…”

Section: Effects Of Sars-cov-2 On Neural Endotheliummentioning

confidence: 99%

Role of aging in Blood–Brain Barrier dysfunction and susceptibility to SARS-CoV-2 infection: impacts on neurological symptoms of COVID-19

Adesse

Gladulich

Alvarez-Rosa

et al. 2022

Fluids Barriers CNS

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COVID-19, which is caused by Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2), has resulted in devastating morbidity and mortality worldwide due to lethal pneumonia and respiratory distress. In addition, the central nervous system (CNS) is well documented to be a target of SARS-CoV-2, and studies detected SARS-CoV-2 in the brain and the cerebrospinal fluid of COVID-19 patients. The blood–brain barrier (BBB) was suggested to be the major route of SARS-CoV-2 infection of the brain. Functionally, the BBB is created by an interactome between endothelial cells, pericytes, astrocytes, microglia, and neurons, which form the neurovascular units (NVU). However, at present, the interactions of SARS-CoV-2 with the NVU and the outcomes of this process are largely unknown. Moreover, age was described as one of the most prominent risk factors for hospitalization and deaths, along with other comorbidities such as diabetes and co-infections. This review will discuss the impact of SARS-CoV-2 on the NVU, the expression profile of SARS-CoV-2 receptors in the different cell types of the CNS and the possible role of aging in the neurological outcomes of COVID-19. A special emphasis will be placed on mitochondrial functions because dysfunctional mitochondria are also a strong inducer of inflammatory reactions and the “cytokine storm” associated with SARS-CoV-2 infection. Finally, we will discuss possible drug therapies to treat neural endothelial function in aged patients, and, thus, alleviate the neurological symptoms associated with COVID-19.

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“…In the recent publication "Should COVID-19 be branded to Viral Thrombotic Fever?," the authors intended to frame COVID-19 in more clinical terminology, making an analogy to Viral Hemorrhagic Fever (VHF). In this article, the authors reported: "We found irrefutable evidence in the current literature that COVID-19 is the first viral disease that can be marketed as a viral thrombotic fever" [5]. Although this is a very categorical statement, considering the small number of studies exclusively dedicated to the characterization of COVID-19 as a thrombotic fever, it is very important to consider this designation.…”

Section: Potential Impact Of Thrombotic Complications On Covid-19 Prognosismentioning

confidence: 99%

DNA Polymorphisms as Potential Biomarkers of Thrombophilic Prognosis for COVID-19 Patients

Fucci¹,

Pitliuk²,

Nunes³

2021

Biomarkers and Bioanalysis Overview

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Coronavirus disease 2019 (COVID-19) is a major issue of our times. Many aspects and features of this new and complex disease are being described on a daily basis. Major endpoints are systemic inflammation, markedly characterized by the cytokine storm, respiratory failure, and coagulation disorders, such as thrombophilia. In its terms, thrombophilia has a major impact on the COVID-19 prognosis. With regard to this, paying attention on molecular variants, such as DNA polymorphisms, epigenetic factors, and other biomarkers, could be an important approach to optimizing and personalizing the treatment of patients according to their inherited thrombotic features. This chapter brings an overview on the three major DNA polymorphisms associated with thrombophilia and proposes that these same biomarkers could be used in pretreatment screenings of patients with COVID-19 to seek the most appropriate therapy for each individual molecular profile.

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Should COVID-19 be branded to viral thrombotic fever?

Cited by 6 publications

References 69 publications

Coagulopathy and the humoral response against viral proteins in patients at different stages of COVID-19

Coagulopathy and the humoral response against viral proteins in patients at different stages of COVID-19

Role of aging in Blood–Brain Barrier dysfunction and susceptibility to SARS-CoV-2 infection: impacts on neurological symptoms of COVID-19

DNA Polymorphisms as Potential Biomarkers of Thrombophilic Prognosis for COVID-19 Patients

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