CD8<sup>+</sup>T Cell Depletion Amplifies Hepatitis C Virus Replication in Peripheral Blood Mononuclear Cells

Li, Yuan; Xu, Wenju; Douglas, Steven D.; Metzger, David S.; Woody, George; Zhang, Ting; Song, Li; Ho, Wen‐Zhe

doi:10.1086/432957

Cited by 24 publications

(23 citation statements)

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“…In the case of HCV infection, CD8 þ T cells also are likely to produce the soluble factors that suppress HCV replication. Our recent study [6] showed that removal of CD8 þ T cells from HCVinfected and HCV RNA undetectable PBMCs resulted in HCV RNA expression. The anti-HCV activity of CD8 þ T cell-produced soluble factors was also confirmed in the hepatic cells.…”

Section: T Zhang T Zhang Et Al Et Almentioning

confidence: 99%

“…The anti-HCV activity of CD8 þ T cell-produced soluble factors was also confirmed in the hepatic cells. CD8 þ T cells isolated from both HCV-infected and normal subjects release soluble factors that powerfully inhibited HCV replicon expression in the hepatic cells [6]. IFN-produced by CD8 þ T cells is partially responsible for CD8 þ T cell-mediated noncytotoxic anti-HCV activity [6].…”

Section: T Zhang T Zhang Et Al Et Almentioning

confidence: 99%

“…CD8 þ T cells isolated from both HCV-infected and normal subjects release soluble factors that powerfully inhibited HCV replicon expression in the hepatic cells [6]. IFN-produced by CD8 þ T cells is partially responsible for CD8 þ T cell-mediated noncytotoxic anti-HCV activity [6]. Liu et al [140] reported that the CD8 þ antiviral effect in HCV replicon cells was markedly reduced by blocking IFN-but was unaffected by blocking TNF-.…”

Section: T Zhang T Zhang Et Al Et Almentioning

confidence: 99%

“…These data highlight the critical role of CD8 þ T cell-produced IFN-in the control of HCV replication. Because IFN-is only partially responsible for the noncytotoxic anti-HCV activity of CD8 þ T cells [6], other unknown anti-HCV soluble factor(s) produced by CD8 þ T cells should be the subject of future studies. These data highlight the vital role of CD8 þ T cells in the host anti-HCV innate immunity.…”

Section: T Zhang T Zhang Et Al Et Almentioning

confidence: 99%

“…The liver is its primary target organ, and the hepatocyte is its primary target cell. HCV, however, also infects other cell types, for example, peripheral blood mononuclear cells (PBMCs) [2][3][4][5][6], macrophages [7], T and B cells [8]. HCV has six distinct genotypes, which show marked differences in geographic distribution, disease progression and response to IFN--based therapy [9].…”

Section: Introductionmentioning

confidence: 99%

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Drug abuse, innate immunity and hepatitis C virus

Zhang

2006

Reviews in Medical Virology

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Since its discovery in 1989, hepatitis C virus (HCV) has become a major public health problem. HCV chronically infects an estimated 170 million people worldwide. The seroprevalence of anti-HCV antibody in the United States has been estimated at 1.8%, which corresponds to approximately 4 million people. HCV is the most common chronic blood borne infection in the United States, and the leading cause of liver transplantation in developed countries. Injection drug use is the dominant mode of HCV transmission and accounts for up to 90% of current infections. Opiates and other drug abuse, such as alcohol, have been implicated as cofactors in the pathogenesis of HCV disease. Injection drug use has been the most common risk factor identified in alcoholics with HCV infection. Both opiates and alcohol contribute significantly to morbidity and mortality from HCV disease. These drugs most likely act synergistically to promote the development and progression of HCV disease. However, there is limited information available concerning the interaction of the drug abuse with the host cell innate immunity against HCV infection, which is a major barrier to fundamental understanding of the immunopathogenesis of HCV disease. Therefore, defining the role of the drug abuse in the development of chronic HCV infection is of crucial importance and should provide practical guidance toward the reduction of risk factors that interfere with therapeutic approaches for HCV infection and disease. This review paper focuses on the interplay between drug abuse (opiates and alcohol), innate immunity and HCV in the context of the development of HCV disease.

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Section: T Zhang T Zhang Et Al Et Almentioning

confidence: 99%

Section: T Zhang T Zhang Et Al Et Almentioning

confidence: 99%

Section: T Zhang T Zhang Et Al Et Almentioning

confidence: 99%

Section: T Zhang T Zhang Et Al Et Almentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Drug abuse, innate immunity and hepatitis C virus

Zhang

2006

Reviews in Medical Virology

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CD56+ T cells inhibit hepatitis C virus replication in human hepatocytes†

Wang

et al. 2009

Hepatology

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Hepatitis C virus reactivation in patients receiving cancer treatment: A prospective observational study

et al. 2017

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Hepatitis C virus (HCV) reactivation in patients receiving cancer treatment has been reported in retrospective studies. We sought to determine prospectively the incidence, predictors, and clinical significance of HCV reactivation during cancer treatment. HCV-infected patients receiving cancer treatment at our institution between November 2012 and July 2016 were studied. Reactivation was defined as an increase in HCV-RNA 1 log 10 IU/mL over baseline and hepatitis flare as an increase in alanine aminotransferase to 3 times the upper limit of normal. One hundred patients were studied, 50 with hematologic malignancies and 50 with solid tumors. Reactivation occurred in 23 (23%) patients, including 18 (36%) patients with hematologic malignancies and 5 (10%) patients with solid tumors. In univariate analysis, patients with reactivation were more likely than those without reactivation to have prolonged lymphopenia (median, 95 versus 22 days; P 5 0.01) and to have received rituximab (44% versus 9%; P < 0.0001), bendamustine (22% versus 0%; P < 0.001), high-dose steroids (57% versus 21%; P 5 0.001), or purine analogs (22% versus 5%; P 5 0.02). Rituximab (odds ratio 5 9.52; P 5 0.001), and high-dose steroids (odds ratio 5 5.05; P 5 0.01) retained significance in multivariable analysis. Of the 23 patients with reactivation, 10 (43%) had hepatitis flare. No patient with reactivation experienced liver failure or liverrelated death within 36 weeks after initiation of cancer treatment. Fourteen patients with hepatitis flare, six of whom had reactivation, required discontinuation or dose reduction of cancer treatment. Conclusion: HCV reactivation occurred in 23% of HCV-infected patients receiving cancer treatment, and most had an unremarkable clinical course. However, reactivation can affect the cancer treatment plan. Our findings suggest that HCV infection should not contraindicate cancer therapy and infected patients should have access to multiple cancer treatments with close monitoring while receiving regimens associated with HCV reactivation. (HEPATOLOGY 2018;67:36-47). SEE EDITORIAL ON PAGE 4H epatitis C virus (HCV) infection is the most common blood-borne infection in the United States, where at least 3.5 million people are currently infected. (1) HCV infection is observed in 1.5% to 32% of cancer patients around the world, depending on the geographic area and type of cancer studied. (2)(3)(4)(5) Among patients with cancer receiving chemotherapy, liver dysfunction caused by hepatitis B virus (HBV) reactivation is a significant problem, (6)(7)(8) occurring in 14% to 72% of patients who did not receive prophylactic antiviral therapy and leading to liver failure in 13% of cases and death in 6% of cases. (6,(8)(9)(10) In contrast, the incidence and consequences of HCV reactivation (HCVr) during cancer treatment remain poorly defined. HCVr appears to be less common and to have less severe consequences than HBV reactivation, (3,7,(11)(12)(13) with only a few fatal cases of fulminant hepatitis attributed to HCV having been rep...

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CD8⁺T Cell Depletion Amplifies Hepatitis C Virus Replication in Peripheral Blood Mononuclear Cells

Cited by 24 publications

References 58 publications

Drug abuse, innate immunity and hepatitis C virus

Drug abuse, innate immunity and hepatitis C virus

CD56+ T cells inhibit hepatitis C virus replication in human hepatocytes†

Hepatitis C virus reactivation in patients receiving cancer treatment: A prospective observational study

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CD8+T Cell Depletion Amplifies Hepatitis C Virus Replication in Peripheral Blood Mononuclear Cells

Cited by 24 publications

References 58 publications

Drug abuse, innate immunity and hepatitis C virus

Drug abuse, innate immunity and hepatitis C virus

CD56+ T cells inhibit hepatitis C virus replication in human hepatocytes†

Hepatitis C virus reactivation in patients receiving cancer treatment: A prospective observational study

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Product

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CD8⁺T Cell Depletion Amplifies Hepatitis C Virus Replication in Peripheral Blood Mononuclear Cells