SARS-CoV-2 another kind of liver aggressor, how does it do that?

Lozano-Sepúlveda, Sonia Amelia; Galán-Huerta, Kame; Martínez-Acuña, Natalia; Arellanos-Soto, Daniel; Rivas-Estilla, Ana María

doi:10.1016/j.aohep.2020.08.062

Cited by 32 publications

(35 citation statements)

References 57 publications

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“…Higher incidence of acute cardiac injury was reported [ 113 ] HBV Body fluid Yes Increased liver tissue damage and inflammatory responses due to COVID-19 may aid HBV co-infection by overexpressing host cell receptors [ 114 ]. It may also fuel the reactivation of pre-existing chronic HBV [ 115 ]. Elevation of ALT, AST, TBIL, ALP, and γ-GT.…”

Section: Molecular Mechanism Of Co-infection In Covid-19mentioning

confidence: 99%

Microbial co-infections in COVID-19: Associated microbiota and underlying mechanisms of pathogenesis

Hoque

Akter

Mishu

et al. 2021

Microbial Pathogenesis

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The novel coronavirus infectious disease-2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has traumatized the whole world with the ongoing devastating pandemic. A plethora of microbial domains including viruses (other than SARS-CoV-2), bacteria, archaea and fungi have evolved together and interact in complex molecular pathogenesis along with SARS-CoV-2. However, the involvement of other microbial co-pathogens and underlying molecular mechanisms leading to extortionate ailment in critically ill COVID-19 patients has yet not been extensively reviewed. Although, the incidence of co-infections could be up to 94.2% in laboratory-confirmed COVID-19 cases, the fate of co-infections among SARS-CoV-2 infected hosts often depends on the balance between the host's protective immunity and immunopathology. Predominantly identified co-pathogens of SARS-CoV-2 are bacteria such as Streptococcus pneumoniae, Staphylococcus aureus, Klebsiella pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Acinetobacter baumannii , Legionella pneumophila and Clamydia pneumoniae followed by viruses including influenza, coronavirus, rhinovirus/enterovirus, parainfluenza, metapneumovirus, influenza B virus, and human immunodeficiency virus. The cross-talk between co-pathogens (especially lung microbiomes), SARS-CoV-2 and host is an important factor that ultimately increases the difficulty of diagnosis, treatment, and prognosis of COVID-19. Simultaneously, co-infecting microbiotas may use new strategies to escape host defense mechanisms by altering both innate and adaptive immune responses to further aggravate SARS-CoV-2 pathogenesis. Better understanding of co-infections in COVID-19 is critical for the effective patient management, treatment and containment of SARS-CoV-2. This review therefore necessitates the comprehensive investigation of commonly reported microbial co-pathogens amid COVID-19, their transmission pattern along with the possible mechanism of co-infections and outcomes. Thus, identifying the possible co-pathogens and their underlying molecular mechanisms during SARS-CoV-2 pathogenesis may shed light in developing diagnostics, appropriate curative and preventive interventions for suspected SARS-CoV-2 respiratory infections in the current pandemic.

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Section: Molecular Mechanism Of Co-infection In Covid-19mentioning

confidence: 99%

Microbial co-infections in COVID-19: Associated microbiota and underlying mechanisms of pathogenesis

Hoque

Akter

Mishu

et al. 2021

Microbial Pathogenesis

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“… 12 There have also been reports of coronavirus particles in hepatocytes without a defined mechanism for infection. 13 …”

Section: Introductionmentioning

confidence: 99%

“…12 There have also been reports of coronavirus particles in hepatocytes without a defined mechanism for infection. 13 In a recent report studying the receptome of spike binding, ACE-2 was confirmed as the primary receptor for the spike protein via the binding domain (RBD) on the spike 1 portion of the molecule and the N-terminaldomain as the sites critical for virus-host interaction. 14 Additionally, the report described binding of the spike protein with ectopically expressed ASGR1 and KREMEN1 in transfected non-liver cells.…”

Section: Introductionmentioning

confidence: 99%

Binding of the SARS-CoV-2 Spike Protein to the Asialoglycoprotein Receptor on Human Primary Hepatocytes and Immortalized Hepatocyte-Like Cells by Confocal Analysis

Collins¹,

Steer²

2021

HMER

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Background The SARS-CoV-2 virus may have direct or indirect effects on other human organs beyond the respiratory system and including the liver, via binding of the spike protein. This study investigated the potential direct interactions with the liver by comparing the binding of SARS-CoV-2 spike proteins to human AT2-like cells, primary human hepatocytes and immortalized hepatocyte-like hybrid cells. Receptors with binding specificity for SARS-CoV-2 spike protein on AT2 cells and hepatocytes were identified. Methods The specific binding of biotinylated spike and spike 1 proteins to undifferentiated human E12 MLPC (E12), E12 differentiated alveolar type 2 (AT2) cells, primary human hepatocytes (PHH) and E12 human hepatocyte-like hybrid cells (HLC) was studied by confocal microscopy. We investigated the expression of ACE-2, binding of biotinylated spike protein, biotinylated spike 1 and inhibition of binding by unlabeled spike protein, two neutralizing antibodies and an antibody directed against the hepatocyte asialoglycoprotein receptor 1 (ASGr1). Results E12 MLPC did not express ACE-2 and did not bind either of spike or spike 1 proteins. AT2-like cells expressed ACE-2 and bound both spike and spike 1. Both PHH and HLC did not express ACE-2 and did not bind spike 1 protein. However, both PHH and HLC actively bound the spike protein. Biotinylated spike protein binding was inhibited by unlabeled spike but not spike 1 protein on PHH and HLC. Two commercial neutralizing antibodies blocked the binding of the spike to PHH and HLC but only one blocked binding to AT2. An antibody to the hepatocyte ASGr1 blocked the binding of the spike protein to PHH and HLC. Conclusion The absence of ACE-2 receptors and inhibition of spike binding by an antibody to the ASGr1 on both PHH and HLC suggested that the spike protein interacts with the ASGr1. The differential antibody blocking of spike binding to AT2, PHH and HLC indicated that neutralizing activity of SARS-CoV-2 binding might involve additional mechanisms beyond RBD binding to ACE-2.

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“…COVID-19 was first reported (2). Besides the respiratory system, entry receptor angiotensin-converting enzyme 2 (ACE2) receptors are also expressed in cholangiocytes, allowing SARS-CoV-2 to enter and replicate in the liver (3). There are case reports of liver-related serious adverse outcomes among patients with COVID-19 (4), and observational studies have reported that SARS-CoV-2 can result in abnormal liver enzymes in patients with HBV (5).…”

mentioning

confidence: 99%

HBV coinfection and in-hospital outcomes for COVID-19: a systematic review and meta-analysis

Zhu

Peltekian

2021

CanLivJ

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BACKGROUND: Since December 2019, there are 30 million confirmed cases of a novel coronavirus disease secondary to severe acute respiratory syndrome coronavirus 2. As of 2020, hepatitis B virus (HBV) affects more than 200 million people worldwide. Both are caused by viral agents. The short-term mortality rate from COVID-19 is much higher than that of HBV. OBJECTIVE: We sought to understand the impact of HBV coinfection on hospitalized patients with COVID-19. SEARCH METHODS: Searches of the literature were conducted in the PubMed, Cochrane Library, and Embase electronic databases. SELECTION CRITERIA: We included cohort studies and randomized studies with information on rates of mortality and intensive care unit (ICU) admission from individuals coinfected by HBV and COVID-19. DATA COLLECTION AND ANALYSIS: Data from six cohort studies with 2,015 patients were collected between January and April 2020, and the results were analyzed by meta-analysis. MAIN RESULTS: HBV coinfection did not lead to increased mortality or ICU admission rates among individuals hospitalized for COVID-19 (risk ratio 0.79, 95% CI 0.333-1.83, N = 2,015; adjusted OR = 0.79, 95% CI 0.31-1.98). During their hospital stay, coinfected patients did not appear to have an increased hospital length of stay or risk of hepatitis B reactivation. CONCLUSIONS: This systematic review and meta-analysis provides support that HBV is not a significant risk factor for serious adverse outcomes among patients hospitalized for COVID-19 infection.

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SARS-CoV-2 another kind of liver aggressor, how does it do that?

Cited by 32 publications

References 57 publications

Microbial co-infections in COVID-19: Associated microbiota and underlying mechanisms of pathogenesis

Microbial co-infections in COVID-19: Associated microbiota and underlying mechanisms of pathogenesis

Binding of the SARS-CoV-2 Spike Protein to the Asialoglycoprotein Receptor on Human Primary Hepatocytes and Immortalized Hepatocyte-Like Cells by Confocal Analysis

HBV coinfection and in-hospital outcomes for COVID-19: a systematic review and meta-analysis

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