Viruses, Immunity, and Cancer: Lessons from Hepatitis B

Chisari, Francis V.

doi:10.1016/s0002-9440(10)64980-2

Cited by 281 publications

(231 citation statements)

References 105 publications

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“…The molecular mechanisms that underlie the pathogenesis of inflammation-associated cancer are complex, and involve both the innate and adaptive immune systems 3,133,134,135 . Although viral oncogenes can contribute directly to neoplastic transformation, neither infection nor pathogen-encoded oncogenes are required for inflammatory cells to induce cancer 136 . Indeed, highly reactive chemical compounds, including superoxide, hydrogen peroxide, singlet oxygen and nitric oxide are released from activated phagocytic inflammatory cells of the innate immune system, and can cause oxidative or nitrosative damage to DNA in the epithelial cells, or react with other cellular components such as phospholipids, initiating a free-radical chain reaction 2 .…”

Section: Box 1 | Molecular Mechanisms Of Inflammation-induced Cancersmentioning

confidence: 99%

Inflammation in prostate carcinogenesis

et al. 2007

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About 20% of all human cancers are caused by chronic infection or chronic inflammatory states. Recently, a new hypothesis has been proposed for prostate carcinogenesis. It proposes that exposure to environmental factors such as infectious agents and dietary carcinogens, and hormonal imbalances lead to injury of the prostate and to the development of chronic inflammation and regenerative 'risk factor' lesions, referred to as proliferative inflammatory atrophy (PIA). By developing new experimental animal models coupled with classical epidemiological studies, genetic epidemiological studies and molecular pathological approaches, we should be able to determine whether prostate cancer is driven by inflammation, and if so, to develop new strategies to prevent the disease. NIH Public Access Author ManuscriptNat Rev Cancer. Author manuscript; available in PMC 2013 January 23. $watermark-text $watermark-text $watermark-textProstate cancer is the most common non-cutaneous malignant neoplasm in men in Western countries, responsible for the deaths of approximately 30,000 men per year in the United States 1 . The number of afflicted men is increasing rapidly as the population of males over the age of 50 grows worldwide. Therefore, finding strategies for the prevention of prostate cancer is a crucial medical challenge. As men in South East Asian countries have a low incidence of prostate cancer that increases rapidly after immigration to the West, this disease is not an intrinsic feature of ageing. The pathogenesis of prostate cancer reflects both hereditary and environmental components. What are the environmental factors and genetic variations that have produced such an epidemic of prostate cancer? Approximately 20% of all human cancers in adults result from chronic inflammatory states and/or chronic inflammation 2-4 (BOX 1), which are triggered by infectious agents or exposure to other environmental factors, or by a combination thereof. There is also emerging evidence that inflammation is crucial for the aetiology of prostate cancer. This evidence stems from epidemiological, histopathological and molecular pathological studies. The objective of this Review is to take a multidisciplinary approach to present and analyse such studies. Because several reviews related to these topics have been published [5][6][7] , here we will focus on new findings and ideas with the purpose of sparking innovative areas of investigation that might ultimately lead to the prevention of prostate cancer. Enigmas in the aetiology of prostate cancerAs in other cancers, prostate cancer develops through the accumulation of somatic genetic and epigenetic changes, resulting in the inactivation of tumour-suppressor genes and caretaker genes, and the activation of oncogenes 8,9 (TABLE 1). There is also evidence for an underlying genetic instability that might facilitate tumour progression 10,11 . Although these genetic and epigenetic changes are crucial for our understanding of 'how' prostate cancer arises, another key remaining question is 'why'...

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Section: Box 1 | Molecular Mechanisms Of Inflammation-induced Cancersmentioning

confidence: 99%

Inflammation in prostate carcinogenesis

et al. 2007

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“…A series of investigations of the mechanisms by which Tcells control HBV replication showed the major role of cytokine-mediated, intracellular inactivation of HBV that does not require cell death. 8 This noncytolytic antiviral effect, first demonstrated in an HBV transgenic mouse model and subsequently in other animals, is primarily mediated by interferon-gamma (IFN-␥). [9][10][11] A detailed analysis of HBV clearance during acute infection in chimpanzees showed that the disappearance of viral DNA from the liver coincides with IFN-␥ induction before the increase of serum alanine aminotransferase (ALT), in other words, without destruction of hepatocytes.…”

Section: H Epatitis B Virus (Hbv) Is a Noncytopathic Dnamentioning

confidence: 99%

Lamivudine plus interleukin-12 combination therapy in chronic hepatitis B: Antiviral and immunological activity

et al. 2005

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H epatitis B virus (HBV) is a noncytopathic DNAvirus, which can cause acute, self-limited hepatitis or chronic hepatitis, cirrhosis, and/or hepatocellular carcinoma. 1 The diversity of clinical outcomes after exposure to HBV is determined primarily by the host immune response. 2,3 The resolution of HBV infection after acute self-limited hepatitis is associated with strong CD4ϩ and CD8ϩ T-cell responses, with a type 1 cytokine profile. [4][5][6][7] In contrast to this strong antiviral T-cell reactivity, which persists in the convalescent phase after hepatitis B surface antigen (HBsAg) clearance, patients with chronic HBV infection have weak or undetectable T-cell reactivity to HBV, which is the dominant factor that permits an ongoing, high level of viral replication. A series of investigations of the mechanisms by which Tcells control HBV replication showed the major role of cytokine-mediated, intracellular inactivation of HBV that does not require cell death. 8 This noncytolytic antiviral effect, first demonstrated in an HBV transgenic mouse model and subsequently in other animals, is primarily mediated by interferon-gamma (IFN-␥). 9-11 A detailed analysis of HBV clearance during acute infection in chimpanzees showed that the disappearance of viral DNA from the liver coincides with IFN-␥ induction before the increase of serum alanine aminotransferase (ALT), in other words, without destruction of hepatocytes. 11

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“…Resolution of acute infection is associated with a vigorous polyclonal helper (Th) and cytotoxic T lymphocyte (CTL) response to multiple viral antigens in the infected livers [2,10,62,63]. Moreover, although destruction of virally infected hepatocytes is evident during the resolution of acute infection, it has been elegantly demonstrated that the noncytolytical reduction of viral gene products in infected cells by cytokines, such as interferon gamma and tumor necrosis factor, released from activated T lymphocytes is likely to play an important role in terminating the infection [12,64].…”

Section: Immunological Basis Of Chronicitymentioning

confidence: 99%

Molecular Virology of Hepatitis B Virus for Clinicians

Block

Guo

2007

Clinics in Liver Disease

144

128

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SynopsisThis chapter reviews the molecular biology of the hepatitis B virus (HBV) in an effort to explain its natural history from a molecular perspective. The life cycle of the virus, with special attention to virus replication, polypeptide production and morphogenesis, is described. The way in which these steps may influence the natural history of viral pathogenesis, as well as the effectiveness of interventions, receives special consideration.

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Viruses, Immunity, and Cancer: Lessons from Hepatitis B

Abstract: Address reprint requests to Francis V.

Cited by 281 publications

References 105 publications

Inflammation in prostate carcinogenesis

Inflammation in prostate carcinogenesis

Lamivudine plus interleukin-12 combination therapy in chronic hepatitis B: Antiviral and immunological activity

Molecular Virology of Hepatitis B Virus for Clinicians

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