Dendritic Cells in HIV-1 and HCV Infection: Can They Help Win the Battle?

Sehgal, Mohit; Khan, Zafar K.; Talal, Andrew H.

doi:10.4137/vrt.s11046

Cited by 9 publications

(7 citation statements)

References 318 publications

(340 reference statements)

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“…Thus, HCV Agloaded DC may restore impaired T cell specific immune responses and may constitute an efficient and important anti-viral therapy for HCV. 43…”

Section: Hdcs and Immune Escape In Hcv Infectionmentioning

confidence: 99%

Hepatic Dendritic Cells, the Tolerogenic Liver Environment, and Liver Disease

et al. 2018

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The unique liver immune microenvironment favors resistance to inflammation that promotes normal physiological function. At the same time, it endows the liver with tolerogenic properties that may promote pathological processes. Hepatic dendritic cells (HDCs) initiate and orchestrate immune responses depending on signals they receive from the local environment and are thought to contribute to liver tolerance. Thus, HDCs facilitate impaired T cell responses that are observed in persistent hepatitis C virus (HCV) infection, hepatocellular carcinoma progression, and liver allograft transplantation. HDCs also participate in anti-inflammatory responses in liver ischemia-reperfusion injury (IRI). Moreover, they promote the regression of fibrosis from various fibrogenic liver injuries. These findings suggest that HDCs regulate intrahepatic immune responses, allowing the liver to maintain homeostasis and integrity even under pathological conditions. This review focuses on the tolerogenic properties of HDCs based on recent research and in relation to liver disease pathogenesis and its therapy.

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“…Thus, HCV Agloaded DC may restore impaired T cell specific immune responses and may constitute an efficient and important anti-viral therapy for HCV. 43…”

Section: Hdcs and Immune Escape In Hcv Infectionmentioning

confidence: 99%

Hepatic Dendritic Cells, the Tolerogenic Liver Environment, and Liver Disease

et al. 2018

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“…IL‐2‐activated NK cells eliminate iDCs and thus may also play a role in downregulation of immune responses, as IL‐2 is primarily produced by activated inflammatory T cells . Bidirectional crosstalk between DCs and NK cells is important for the priming, activation, and expansion of T‐cell responses , and disruption of this pathway is emerging as an important immune evasion mechanism employed by several viruses and direct infection of DCs appears to be an important factor . It is unlikely that DCs support replication of HCV, although HCV RNA has been detected in both mDCs and pDCs while other studies have not been able to detect viral replication or protein synthesis in DCs after co‐culture with infectious recombinant HCV .…”

Section: Regulatory Natural Killer Cellsmentioning

confidence: 99%

Natural killer cells: multifaceted players with key roles in hepatitis C immunity

Golden-Mason

Rosen

2013

Immunological Reviews

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Summary Natural killer cells (NKs) are involved in every stage of hepatitis C viral (HCV) infection, from protection against HCV acquisition and resolution in the acute phase to treatment-induced clearance. In addition to their direct antiviral actions, NKs are involved in the induction and priming of appropriate downstream T-cell responses. In the setting of chronic HCV, overall NK cell levels are decreased, altered subset distribution is altered, and changes in NK receptor (NKR) expression have been demonstrated, although the contribution of individual NKRs to viral clearance or persistence remains to be clarified. Enhanced NK cell cytotoxicity accompanied by insufficient interferon-γ production may promote liver damage in the setting of chronic infection. Treatment-induced clearance is associated with activation of NK cells, and it will be of interest to monitor NK cell responses to triple therapy. Activated NK cells also have antifibrotic properties, and the same hepatic NK cell populations that are actively involved in control of HCV may also be involved in control of HCV-associated liver damage. We still have much to learn, in particular: how do liver-derived NKs influence the outcome of HCV infection? Do NK receptors recognize HCV-specific components? And, are HCV-specific memory NK populations generated?

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“…Several viral proteins also appear to play a role in the evasion of host immune responses. In addition to infecting hepatocytes, HCV has been reported to infect dendritic cells (DCs) [16,17], B cells [18,19], and peripheral blood mononuclear cells [20,21]. NS3, NS4A, NS4B, NS5A, and NS5B forms the replicase machinery and NS2 and p7 are essential for viral assembly and release [22].…”

Section: Characteristics Structure and Pathogenesismentioning

confidence: 99%

Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence

Chigbu

Loonawat

Sehgal

et al. 2019

Cells

Self Cite

118

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Hepatitis C (HCV) is a major cause of liver disease, in which a third of individuals with chronic HCV infections may develop liver cirrhosis. In a chronic HCV infection, host immune factors along with the actions of HCV proteins that promote viral persistence and dysregulation of the immune system have an impact on immunopathogenesis of HCV-induced hepatitis. The genome of HCV encodes a single polyprotein, which is translated and processed into structural and nonstructural proteins. These HCV proteins are the target of the innate and adaptive immune system of the host. Retinoic acid-inducible gene-I (RIG-I)-like receptors and Toll-like receptors are the main pattern recognition receptors that recognize HCV pathogen-associated molecular patterns. This interaction results in a downstream cascade that generates antiviral cytokines including interferons. The cytolysis of HCV-infected hepatocytes is mediated by perforin and granzyme B secreted by cytotoxic T lymphocyte (CTL) and natural killer (NK) cells, whereas noncytolytic HCV clearance is mediated by interferon gamma (IFN-γ) secreted by CTL and NK cells. A host–HCV interaction determines whether the acute phase of an HCV infection will undergo complete resolution or progress to the development of viral persistence with a consequential progression to chronic HCV infection. Furthermore, these host–HCV interactions could pose a challenge to developing an HCV vaccine. This review will focus on the role of the innate and adaptive immunity in HCV infection, the failure of the immune response to clear an HCV infection, and the factors that promote viral persistence.

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Dendritic Cells in HIV-1 and HCV Infection: Can They Help Win the Battle?

Cited by 9 publications

References 318 publications

Hepatic Dendritic Cells, the Tolerogenic Liver Environment, and Liver Disease

Hepatic Dendritic Cells, the Tolerogenic Liver Environment, and Liver Disease

Natural killer cells: multifaceted players with key roles in hepatitis C immunity

Hepatitis C Virus Infection: Host–Virus Interaction and Mechanisms of Viral Persistence

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