Viral apoptotic mimicry: an immune evasion strategy developed by the hepatitis B virus?

Vanlandschoot, Peter; Leroux‐Roels, Geert

doi:10.1016/s1471-4906(03)00026-7

Cited by 62 publications

(54 citation statements)

References 40 publications

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“…9 These subviral particles may play a role in evading host immune response. 10 There is greater excess of spherical and filament particles in hepatitis B 'e' antigen (HBeAg) viremic individuals as compared to low viremic anti-HBe-positive carriers in whom the decline of filaments parallels that of the virions while a relative excess of spherical particles remains.…”

Section: Structure and Molecular Virology Of Hepatitis B Surface Antigenmentioning

confidence: 99%

HBsAg Quantification in Clinical Practice

Seth¹

2012

Journal of Clinical and Experimental Hepatology

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Section: Structure and Molecular Virology Of Hepatitis B Surface Antigenmentioning

confidence: 99%

HBsAg Quantification in Clinical Practice

Seth¹

2012

Journal of Clinical and Experimental Hepatology

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“…1) (7). These subviral particles may play a role in evading the host immune response (8), and may also co-exist with anti-HBs as part of circulating immune complexes (9).…”

Section: Hbsag: Virologymentioning

confidence: 99%

Quantification of hepatitis B surface antigen: a new concept for the management of chronic hepatitis B

Moucari

Marcellin

2011

Liver International

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HBsAg is a very important clinical test that might not only indicate active hepatitis B virus (HBV) infection but might also be used to predict clinical and treatment outcome. Clearance of HBsAg in patients with chronic HBV infection is associated with a much better clinical outcome, although surveillance for early detection of hepatocellular carcinoma (HCC) should continue. HBV DNA quantification is currently used for selecting candidates for therapy, monitoring response to therapy and detecting the emergence of drug resistance. Assays for HBsAg quantification are less expensive than HBV DNA and fully automated with a high throughput capacity. HBsAg titering may be a useful tool to manage patients with chronic HBV, to more clearly define which patients may, and more importantly, may not, benefit from treatment. Baseline and on-treatment HBsAg quantification may help to refine future treatment algorithms for both immune-modulator therapy and nucleos(t)ide analogues. Both HBV markers provide complementary information on the status of HBV infection. However, the relevance of serum HBsAg levels and its use as a reliable replacement for both covalently closed circular DNA and HBV DNA remain unclear.

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“…Such apoptotic mimicry has been characterized rigorously with several viruses 16,17 and trypanosomatids. [18][19][20] For example, viral internalization and the suppression of host immune responsiveness associated with vaccinia and hepatitis B viruses appear to follow apoptoticlike mechanisms of PS-dependent macropinocytosis and antiinflammatory cytokine induction.…”

Section: Open Questionsmentioning

confidence: 99%

Exploiting death: apoptotic immunity in microbial pathogenesis

Ucker

2016

Cell Death Differ

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Innate immunity typically is responsible for initial host responses against infections. Independently, nucleated cells that die normally as part of the physiological process of homeostasis in mammals (including humans) suppress immunity. Specifically, the physiological process of cell death (apoptosis) generates cells that are recognized specifically by viable cells of all types and elicit a profound transient suppression of host immunity (termed 'innate apoptotic immunity' (IAI)). IAI appears to be important normally for the maintenance of self-tolerance and for the resolution of inflammation. In addition, pathogens are able to take advantage of IAI through a variety of distinct mechanisms, to enable their proliferation within the host and enhance pathogenicity. For example, the protist pathogen Leishmania amazonensis, at its infective stage, mimics apoptotic cells by expressing apoptotic-like protein determinants on the cell surface, triggering immunosuppression directly. In contrast, the pathogenic bacterium Listeria monocytogenes triggers cell death in host lymphocytes, relying on those apoptotic cells to suppress host immune control and facilitate bacterial expansion. Finally, although the inhibition of apoptotic cell death is a common attribute of many viruses which facilitates their extended replication, it is clear that adenoviruses also reprogram the non-apoptotic dead cells that arise subsequently to manifest apoptotic-like immunosuppressive properties. These three instances represent diverse strategies used by microbial pathogens to exploit IAI, focusing attention on the potency of this facet of host immune control. Further examination of these cases will be revealing both of varied mechanisms of pathogenesis and the processes involved in IAI control.

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Viral apoptotic mimicry: an immune evasion strategy developed by the hepatitis B virus?

Cited by 62 publications

References 40 publications

HBsAg Quantification in Clinical Practice

HBsAg Quantification in Clinical Practice

Quantification of hepatitis B surface antigen: a new concept for the management of chronic hepatitis B

Exploiting death: apoptotic immunity in microbial pathogenesis

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