NS5B induces up-regulation of the BH3-only protein, BIK, essential for the hepatitis C virus RNA replication and viral release

Aweya, Jude Juventus; Sze, Ching Wooen; Bayega, Anthony; Mohd-Ismail, Nur Khairiah; Deng, Lin; Hotta, Hak; Tan, Yee‐Joo

doi:10.1016/j.virol.2014.10.027

Cited by 10 publications

(9 citation statements)

References 60 publications

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“…These studies demonstrated that HCV regulates host genes involved in oxidative stress, apoptosis, lipid metabolism, immunity, proliferation, and intracellular transport [ 24 ]. A recent study using an apoptosis-specific PCR array [ 52 ] identified BCL2-interacting killer (BIK) mRNA expression as up-regulated, consistent with our results, reported here ( Table 1 ). They showed that expression was also upregulated at the protein level and revealed its role in HCV replication through interaction with NS5B.…”

Section: Discussionsupporting

confidence: 92%

HCV-Mediated Apoptosis of Hepatocytes in Culture and Viral Pathogenesis

Silberstein¹,

Ulitzky²,

Lima³

et al. 2016

PLoS ONE

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Chronic Hepatitis C Virus (HCV) infection is associated with progressive liver injury and subsequent development of fibrosis and cirrhosis. The death of hepatocytes results in the release of cytokines that induce inflammatory and fibrotic responses. The mechanism of liver damage is still under investigation but both apoptosis and immune-mediated processes may play roles. By observing the changes in gene expression patterns in HCV-infected cells, both markers and the causes of HCV-associated liver injury may be elucidated. HCV genotype 1b virus from persistently infected VeroE6 cells induced a strong cytopathic effect when used to infect Huh7.5 hepatoma cells. To determine if this cytopathic effect was a result of apoptosis, ultrastructural changes were observed by electron microscopy and markers of programmed cell death were surveyed. Screening of a human PCR array demonstrated a gene expression profile that contained upregulated markers of apoptosis, including tumor necrosis factor, caspases and caspase activators, Fas, Bcl2-interacting killer (BIK) and tumor suppressor protein, p53, as a result of HCV genotype 1b infection. The genes identified in this study should provide new insights into understanding viral pathogenesis in liver cells and may possibly help to identify novel antiviral and antifibrotic targets.

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Section: Discussionsupporting

confidence: 92%

HCV-Mediated Apoptosis of Hepatocytes in Culture and Viral Pathogenesis

Silberstein¹,

Ulitzky²,

Lima³

et al. 2016

PLoS ONE

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“…5'-ACGAAC-3' [38,39] . Starting of replication phase, after viral entry into the host cell, uncoating of the viral particles with the incorporation of complete genetic material [15,[40][41][42] . Virus sub-genomic region of m-RNAs through translation, form the assembly of viral proteins.…”

Section: Mers-covmentioning

confidence: 99%

Review on Newly Identified Corona Virus and its Genomics Organization

Rao¹,

Verma²,

Kumar³

et al. 2020

SSR-IIJLS

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Human Coronaviruses (HCoV) exhibit positive single stranded RNA genome with enveloped nucleocapsid. Coronavirus belongs to the family Coronaviridae, originated from avian and mammalian species causes upper respiratory tract infection in humans by novel HCoVs viruses named as HCoV-HKU1, HCoV-NL63 but predominant species is Middle East respiratory syndrome (MERS-CoV) across the world. HCoV-HKU1 sp. is associated with chronic pulmonary disease, while HCoV-NL63 causes upper and lower respiratory tract disease in both children and adults, but most recent one was MERS-CoV, which caused acute pneumonia and occasional renal failure. The novel coronavirus SARS-CoV-2 is a new strain that causes the Coronavirus Disease 2019 (COVID-19) as named by the World Health Organization. According to the recent world statistics report about the COVID-19 cases approx. 101,500 confirmed cases and 3,500 death cases appeared. And mostly, a case of infection with CoV was identified in Wuhan, China. Structurally viral genome constitutes of 2/3rd of replicase gene encoding ORFs regions and rest of the 1/3rd region of genome form the structural proteins. The aim of the study was to understand the viral genetic systems in order to facilitate the genetic manipulation of the viral genome and to know the fundamental mechanism during the viral replication, facilitating the development of antidotes against the virus.

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“…96-well ELISA plates (Nunc™ Maxisorp™) were coated overnight at 4°C with 100 ng of purified haemagglutinin (HA) proteins of H5Nx [A/Vietnam/ 1194/2004(H5N1); A/chicken/Iowa/04-20/2015 (H5N2); A/duck/Guangdong/GD01/2014(H5N6); A/ broiler duck/Korea/Buan2/2014(H5N8)], A/Missouri/ 09/2014(H3N2), A/Netherlands/219/2003(H7N7), A/ Anhui/DEWH72-01/2013(H7N9), A/guinea fowl/ Hong Kong/WF10/99(H9N2) purchased from Sino Biological, washed with PBS containing 0.05% Tween-20 (PBST) and blocked with 5% FBS/PBST for 1 h. Serially diluted mAbs in 5% FBS/PBST were added to the plates and incubated for 1.5 h at 37°C. A mouse IgG2a mAb, 1A4, which was generated using the hepatitis C virus NS5B protein, was also used at the highest concentration (50 ng/ml) as an isotype control antibody [46]. The plates were washed and incubated with horseradish-peroxidase-conjugated goat anti-mouse IgG antibody (Thermo Fisher Scientific) for 1 h at 37°C.…”

Section: Enzyme-linked Immunosorbent Assay (Elisa)mentioning

confidence: 99%

Contribution of Fc-dependent cell-mediated activity of a vestigial esterase-targeting antibody against H5N6 virus infection

Zheng

Teo

Arularasu

et al. 2020

Emerging Microbes & Infections

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The highly pathogenic avian influenza A (H5N6) virus has caused sporadic human infections with a high case fatality rate. Due to the continuous evolution of this virus subtype and its ability to transmit to humans, there is an urgent need to develop effective antiviral therapeutics. In this study, a murine monoclonal antibody 9F4 was shown to display broad binding affinity against H5Nx viruses. Furthermore, 9F4 can neutralize H5N6 pseudotyped particles and prevent entry into host cells. Additionally, ADCC/ADCP deficient L234A, L235A (LALA) and CDC deficient K322A mutants were generated and displayed comparable binding affinity and neutralizing activity as wild type 9F4 (9F4-WT). Notably, 9F4-WT, 9F4-LALA and 9F4-K322A exhibit in vivo protective efficacies against H5N6 infections in that they were able to reduce viral loads in mice. However, only 9F4-WT and 9F4-K322A but not 9F4-LALA were able to reduce viral pathogenesis in H5N6 challenged mice. Furthermore, depletion of phagocytic cells in mice lungs nullifies 9F4-WT's protection against H5N6 infections, suggesting a crucial role of the host's immune cells in 9F4 antiviral activity. Collectively, these findings reveal the importance of ADCC/ADCP function for 9F4-WT protection against HPAIV H5N6 and demonstrate the potential of 9F4 to confer protection against the reassortant H5-subtype HPAIVs.

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NS5B induces up-regulation of the BH3-only protein, BIK, essential for the hepatitis C virus RNA replication and viral release

Cited by 10 publications

References 60 publications

HCV-Mediated Apoptosis of Hepatocytes in Culture and Viral Pathogenesis

HCV-Mediated Apoptosis of Hepatocytes in Culture and Viral Pathogenesis

Review on Newly Identified Corona Virus and its Genomics Organization

Contribution of Fc-dependent cell-mediated activity of a vestigial esterase-targeting antibody against H5N6 virus infection

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