Prevalence of Hepatitis B Virus, Genotypes, and Mutants in HBsAg-Positive Patients in Meerut, India

Khan, Salman; Madan, Molly; Virmani, S. K.

doi:10.29252/ibj.23.5.7

Cited by 6 publications

(1 citation statement)

References 40 publications

(47 reference statements)

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“…Hepatitis B virus (HBV) causes acute and chronic hepatitis in humans . Chronic HBV infection is a worldwide public health challenge, influencing nearly 240 million people . Patients with chronic HBV infection are more vulnerable to severe liver illness, hepatocellular cancer, and cirrhosis .…”

Section: Introductionmentioning

confidence: 99%

The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

Chen

Ming

et al. 2020

Cell Biochemistry & Function

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As small conserved RNAs without a coding function, microRNAs are expressed in multicellular organisms and contribute to the modulation of multiple cellular reactions, such as viral replication, as well as autophagy. microRNAs can regulate host gene expression and inhibit or reinforce hepatitis B virus (HBV) replication. Hepatic cells express miR-155 noticeably. Consequently, our study explored miR-155 modulation of HBV replication and investigated the potential mechanism involved. miR-155 was inhibited on HBV infection. miR-155 transfection remarkably reinforced HBV replication, antigen expression, and progeny secretion in HepG2215 cells. Moreover, miR-155 impaired the inhibition of the cytokine signalling 1 (SOCS1)/Akt/ mTOR axis and reinforced HepG2215 autophagy. Additionally, the autophagy inhibitor (3-MA) eliminated HBsAg secretion triggered by miR-155. Taken together, miR-155 reinforced HBV replication by reinforcing SOCS1-triggered autophagy.Significance of the study: The research studied the potential mechanism involved in HBV replication and miR-155 that miR-155 reinforces HBV replication by reinforcing the SOCS1/Akt/mTOR axis-stimulated autophagy, and therefore, it can provide medical practitioners with the inspiration that chronic HBV might be cured or improved by regulating the activation of miR-155 in cells. In the study, the experiments show that autophagy inhibitors (3-MA) counteracted miR-155 contribution to HBV replication, and it might be a practicable way to improve HBV through some therapies that can repress the autophagy in related cells. K E Y W O R D S autophagy, HBV replication, infection, miR-155, SOCS1

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Section: Introductionmentioning

confidence: 99%

The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

Chen

Ming

et al. 2020

Cell Biochemistry & Function

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Cell death pathways and viruses: Role of microRNAs

Nahand

Shojaie

Akhlagh

et al. 2021

Molecular Therapy - Nucleic Acids

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Viral infections lead to the death of more than a million people each year around the world, both directly and indirectly. Viruses interfere with many cell functions, particularly critical pathways for cell death, by affecting various intracellular mediators. MicroRNAs (miRNAs) are a major example of these mediators because they are involved in many (if not most) cellular mechanisms. Virus-regulated miRNAs have been implicated in three cell death pathways, namely, apoptosis, autophagy, and anoikis. Several molecules (e.g., BECN1 and B cell lymphoma 2 [BCL2] family members) are involved in both apoptosis and autophagy, while activation of anoikis leads to cell death similar to apoptosis. These mechanistic similarities suggest that common regulators, including some miRNAs (e.g., miR-21 and miR-192), are involved in different cell death pathways. Because the balance between cell proliferation and cell death is pivotal to the homeostasis of the human body, miRNAs that regulate cell death pathways have drawn much attention from researchers. miR-21 is regulated by several viruses and can affect both apoptosis and anoikis via modulating various targets, such as PDCD4, PTEN, interleukin (IL)-12, Maspin, and Fas-L. miR-34 can be downregulated by viral infection and has different effects on apoptosis, depending on the type of virus and/or host cell. The present review summarizes the existing knowledge on virus-regulated miRNAs involved in the modulation of cell death pathways. Understanding the mechanisms for virus-mediated regulation of cell death pathways could provide valuable information to improve the diagnosis and treatment of many viral diseases.

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Exchanges in the ‘a’ determinant of the hepatitis B virus surface antigen revisited

Pondé,

Amorim

2024

Virology

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Prevalence of Hepatitis B Virus, Genotypes, and Mutants in HBsAg-Positive Patients in Meerut, India

Cited by 6 publications

References 40 publications

The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

Cell death pathways and viruses: Role of microRNAs

Exchanges in the ‘a’ determinant of the hepatitis B virus surface antigen revisited

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