Impact of the Interaction of Hepatitis B Virus with Mitochondria and Associated Proteins

Hossain, Md. Golzar; Akter, Sharmin; Ohsaki, Eriko; Ueda, Keiji

doi:10.3390/v12020175

Cited by 29 publications

(32 citation statements)

References 118 publications

(163 reference statements)

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“…A plausible metabolic link between mitochondria and influenza A, and with herpes viruses was shown in the 1950s by Ackerman and colleagues [ 13 , 14 ]. Recent studies showed how hepatitis B virus (HBV) [ 15 , 16 ] and hepatitis C virus (HCV) adopt the changes in mitochondrial dynamics for persistent infection [ 17 , 18 ]. Our laboratory has also shown that respiratory syncytial virus (RSV) infection affects mitochondrial function, leading to an altered immune response in lungs [ 19 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

Role of Mitochondria in Viral Infections

Elesela

Lukacs

2021

Life

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Viral diseases account for an increasing proportion of deaths worldwide. Viruses maneuver host cell machinery in an attempt to subvert the intracellular environment favorable for their replication. The mitochondrial network is highly susceptible to physiological and environmental insults, including viral infections. Viruses affect mitochondrial functions and impact mitochondrial metabolism, and innate immune signaling. Resurgence of host-virus interactions in recent literature emphasizes the key role of mitochondria and host metabolism on viral life processes. Mitochondrial dysfunction leads to damage of mitochondria that generate toxic compounds, importantly mitochondrial DNA, inducing systemic toxicity, leading to damage of multiple organs in the body. Mitochondrial dynamics and mitophagy are essential for the maintenance of mitochondrial quality control and homeostasis. Therefore, metabolic antagonists may be essential to gain a better understanding of viral diseases and develop effective antiviral therapeutics. This review briefly discusses how viruses exploit mitochondrial dynamics for virus proliferation and induce associated diseases.

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Section: Introductionmentioning

confidence: 99%

Role of Mitochondria in Viral Infections

Elesela

Lukacs

2021

Life

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“…Mutations in the hepatitis B virus genome have been reported worldwide, and these mutations have been affecting the diagnosis of hepatitis B, the effectiveness of hepatitis B vaccination, and occasionally patient resistance to antiviral drugs for hepatitis B [27,30,[38][39][40]. Such mutations are known to influence the viral replication and pathophysiology, and thereby to be involved in occult HBV infection and persistence [9,12,[41][42][43]. On the other…”

Section: Discussionmentioning

confidence: 99%

Analysis of the Physicochemical Properties, Replication and Pathophysiology of a Massively Glycosylated Hepatitis B Virus HBsAg Escape Mutant

Hossain

Suwanmanee

et al. 2021

Viruses

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Mutations in HBsAg, the surface antigen of the hepatitis B virus (HBV), might affect the serum HBV DNA level of HBV-infected patients, since the reverse transcriptase (RT) domain of HBV polymerase overlaps with the HBsAg-coding region. We previously identified a diagnostic escape mutant (W3S) HBV that produces massively glycosylated HBsAg. In this study, we constructed an HBV-producing vector that expresses W3S HBs (pHB-W3S) along with a wild-type HBV-producing plasmid (pHB-WT) in order to analyze the physicochemical properties, replication, and antiviral drug response of the mutant. Transfection of either pHB-WT or W3S into HepG2 cells yielded similar CsCl density profiles and eAg expression, as did transfection of a glycosylation defective mutant, pHB-W3S (N146G), in which a glycosylation site at the 146aa asparagine (N) site of HBs was mutated to glycine (G). Virion secretion, however, seemed to be severely impaired in cases of pHB-W3S and pHB-W3S (N146G), compared with pHB-WT, as determined by qPCR and Southern blot analysis. Furthermore, inhibition of glycosylation using tunicamycinTM on wild-type HBV production also reduced the virion secretion. These results suggested that the HBV core and Dane particle could be formed either by massively glycosylated or glycosylation-defective HBsAg, but reduced and/or almost completely blocked the virion secretion efficiency, indicating that balanced glycosylation of HBsAg is required for efficient release of HBV, and mutations inducing an imbalanced glycosylation of HBs would cause the virion to become stuck in the cells, which might be associated with various pathogeneses due to HBV infection.

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“…Other reports identify alternative virus-host interactions that could be targeted. Hossain et al review the reported interactions between HBV proteins and mitochondrial signalling, with particular focus on innate immunity and viral replication [12]. They highlight several reported interactions between HBV and mitochondria that could be targeted to inhibit HBV replication, although exactly how this can be achieved remains unclear and is the subject of ongoing research.…”

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confidence: 99%