Acute Liver Failure Secondary to Yellow Fever: A Challenging Scenario

Song, Alice; D’Albuquerque, Luiz Augusto Carneiro

doi:10.1002/cld.784

Cited by 12 publications

(7 citation statements)

References 15 publications

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“…Tissue tropism for the manifestation of vascular hyperpermeability is different among flaviviruses. DENV causes systemic vascular leakage affecting organs such as the liver, brain, lungs, umbilical vein, and skin. − ZIKV preferentially infects neural stem cells, astrocytes, oligodendrocyte precursor cells, and microglia and can cause Guillain-Barré syndrome, neuropathy, and myelitis, which predominantly affect adults and older children. , ZIKV RNA has also been found in the tissues of both mothers and fetuses, including cord blood, different placental cells, amniotic fluid, and the developing fetal brain, and is known to cause microcephaly in fetuses and infants. − YFV infections are characterized by jaundice, and in most cases symptoms are accompanied by hepatocyte damage, resulting in liver disease. − WNV and JEV, being neurotropic viruses, tend to affect the CNS, and Japanese encephalitis is characterized by extensive inflammation in the CNS and disruption of the blood–brain barrier. ,− …”

Section: Tissue-specific Tropism Of Ns1 and Its Impact On Flavivirus ...mentioning

confidence: 99%

Roles of NS1 Protein in Flavivirus Pathogenesis

Perera,

Ranadeva,

Sirisena

et al. 2023

ACS Infect. Dis.

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Flaviviruses such as dengue, Zika, and West Nile viruses are highly concerning pathogens that pose significant risks to public health. The NS1 protein is conserved among flaviviruses and is synthesized as a part of the flavivirus polyprotein. It plays a critical role in viral replication, disease progression, and immune evasion. Post-translational modifications influence NS1's stability, secretion, antigenicity, and interactions with host factors. NS1 protein forms extensive interactions with host cellular proteins allowing it to affect vital processes such as RNA processing, gene expression regulation, and cellular homeostasis, which in turn influence viral replication, disease pathogenesis, and immune responses. NS1 acts as an immune evasion factor by delaying complement-dependent lysis of infected cells and contributes to disease pathogenesis by inducing endothelial cell damage and vascular leakage and triggering autoimmune responses. Anti-NS1 antibodies have been shown to cross-react with host endothelial cells and platelets, causing autoimmune destruction that is hypothesized to contribute to disease pathogenesis. However, in contrast, immunization of animal models with the NS1 protein confers protection against lethal challenges from flaviviruses such as dengue and Zika viruses. Understanding the multifaceted roles of NS1 in flavivirus pathogenesis is crucial for effective disease management and control. Therefore, further research into NS1 biology, including its host protein interactions and additional roles in disease pathology, is imperative for the development of strategies and therapeutics to combat flavivirus infections successfully. This Review provides an in-depth exploration of the current available knowledge on the multifaceted roles of the NS1 protein in the pathogenesis of flaviviruses.

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Section: Tissue-specific Tropism Of Ns1 and Its Impact On Flavivirus ...mentioning

confidence: 99%

Roles of NS1 Protein in Flavivirus Pathogenesis

Perera,

Ranadeva,

Sirisena

et al. 2023

ACS Infect. Dis.

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“…Yellow Fever (YF) is a significant public health concern in tropical regions of Africa and South America, accounting for an estimated 29,000 to 60,000 deaths annually (Garske et al 2014;Paules and Fauci 2017;Song and Carneiro D'Albuquerque 2019). The disease can manifest as a spectrum of clinical presentations, from self-limiting, flu-like symptoms to severe forms characterized by hemorrhage and liver disease.…”

Section: Introductionmentioning

confidence: 99%

Systems Immunology Approaches to Understanding Immune Responses in Acute Infection of Yellow Fever Patients

Gonçalves,

Costa,

Thomazella

et al. 2024

Preprint

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In the 2018 yellow fever (YF) outbreak in Brazil, we generated new transcriptomic data and combined it with clinical and immunological data to decode the pathogenesis of YF. Our analysis of 79 patients highlighted distinct gene expression patterns between acute YF infections, other viral infections, and the milder infection induced by the live-attenuated YF-17D vaccine. We identified a critical role for low-density, immature neutrophils in severe outcomes, marked by the downregulation of genes such as PADI4, CSF3R, and ICAM1 in deceased patients. These genes are essential for neutrophil migration and maturation, suggesting their pivotal role in disease progression. Furthermore, our study revealed a complex interaction among inflammation-related genes: increased expression of CXCL10 in the acute phase was accompanied by decreased expression of IL-1b and an increase in IL1R2, a decoy receptor that binds to IL-1 to inhibit its activity. The diminished expression of HLA class II genes suggests an impairment in antigen presentation. These insights underscore the delicate balance of immune responses in YF pathogenesis and provide a foundation for future therapeutic and diagnostic advancements in managing YF.

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“…In the beginning of 2018, a YF outbreak occurred on the outskirts of Sao Paulo; 538 cases were confirmed between January and December 2018, with a lethality rate of 34.6% [4]. The pathophysiology of the disease involves viral tropism and acute direct damage to vital organs such as liver and kidneys [5][6][7], in severe cases leading to fulminant hepatitis and acute renal failure (often requiring replacement therapies) [8][9][10][11], with high in-hospital case fatality rates (of up to 67%, according to recent studies [12][13][14]).…”

Section: Introductionmentioning

confidence: 99%

Staging liver fibrosis after severe yellow fever with ultrasound elastography in Brazil: A six-month follow-up study

et al. 2021

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Background Yellow fever (YF) is a hemorrhagic disease caused by an arbovirus endemic in South America, with recent outbreaks in the last years. Severe cases exhibit fulminant hepatitis, but there are no studies regarding its late-term effects on liver parenchyma. Thus, the aim of this study was to determine the frequency and grade of liver fibrosis in patients who recovered from severe YF and to point out potential predictors of this outcome. Methodology/Principal findings We followed-up 18 patients who survived severe YF during a recent outbreak (January-April 2018) in Brazil using ultrasound (US) with shear-wave elastography (SWE) at 6 months after symptoms onset. No patient had previous history of liver disease. Median liver stiffness (LS) was 5.3 (4.6–6.4) kPa. 2 (11.1%) patients were classified as Metavir F2, 1 (8.3%) as F3 and 1 (8.3%) as F4; these two last patients had features of cardiogenic liver congestion on Doppler analysis. Age and cardiac failure were associated with increased LS (p = 0.036 and p = 0.024, respectively). SAPS-3 at ICU admission showed a tendency of association with significant fibrosis (≥ F2; p = 0.053). 7 patients used sofosbuvir in a research protocol, of which none showed liver fibrosis (p = 0.119). Conclusions/Significance We found a low frequency of liver fibrosis in severe YF survivors. US with SWE may have a role in the follow up of patients of age and / or with comorbidities after hospital discharge in severe YF, a rare but reemergent disease.

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Acute Liver Failure Secondary to Yellow Fever: A Challenging Scenario

Abstract: http://aasldpubs.onlinelibrary.wiley.com/hub/journal/10.1002/(ISSN)2046-2484/video/13-2-reading-song a video presentation of this article Answer questions and earn https://www.wileyhealthlearning.com/Activity/6692506/disclaimerspopup.aspx

Cited by 12 publications

References 15 publications

Roles of NS1 Protein in Flavivirus Pathogenesis

Roles of NS1 Protein in Flavivirus Pathogenesis

Systems Immunology Approaches to Understanding Immune Responses in Acute Infection of Yellow Fever Patients

Staging liver fibrosis after severe yellow fever with ultrasound elastography in Brazil: A six-month follow-up study

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