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52 - Immunobiology and host response to KSHV infection
- from Part III - Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses
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- By Dimitrios Lagos, Cancer Research UK Viral Oncology Group, Wolfson Institute for Biomedical Research, University College London, London, UK, Chris Boshoff, Cancer Research UK Viral Oncology Group, Wolfson Institute for Biomedical Research, University College London, London, UK
- Edited by Ann Arvin, Stanford University, California, Gabriella Campadelli-Fiume, Università degli Studi, Bologna, Italy, Edward Mocarski, Emory University, Atlanta, Patrick S. Moore, University of Pittsburgh, Bernard Roizman, University of Chicago, Richard Whitley, University of Alabama, Birmingham, Koichi Yamanishi, University of Osaka, Japan
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- Book:
- Human Herpesviruses
- Published online:
- 24 December 2009
- Print publication:
- 16 August 2007, pp 915-928
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Summary
Introduction
The interplay between malignancy, infection and immunity is best illustrated by the neoplasms related to KSHV (Boshoff and Weiss, 2002): Kaposi sarcoma (KS) is approximately 100 times more common during immunosuppression and can be resolved when iatrogenic immunosuppression is stopped (Euvrard et al., 2003) and during highly active antiretroviral treatment (HAART) of HIV-1 infected individuals (Boshoff and Weiss, 2002). Primary effusion lymphoma (PEL) and plasmablastic multicentric Castleman's disease (MCD) also occur predominantly during immunosuppression. Like other gammaherpesviruses, KSHV persists as a latent episome in B-lymphocytes (Ambroziak et al., 1995; Cesarman et al., 1995; Renne et al., 1996), without provoking host responses that would eliminate infected cells. KSHV acquired a fascinating repertoire of decoys to trick the host immune response enabling establishment of lifelong infection in humans with very few clinical manifestations. When the balance between viral infection and host immunity is disturbed, some of the molecular pathways employed by KSHV to evade host immune responses are directly involved in driving oncogenesis (Moore and Chang, 2003). KSHV is an excellent model to study the coevolution of pathogen attack and mechanisms of host counter attack.
KS is most aggressive in the immunosuppressed and resolves with partial restoration of the immune system (Gill et al., 2002). Since the introduction of HAART, there has also been a dramatic fall in the incidence of KS (Jacobson et al., 1999).
11 - Gammaherpesviral infections and neoplasia in immunocompromised populations
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- By Chris Boshoff, Departments of Oncology and Molecular Pathology, The CRC Viral Oncology Group, Wolfson Institute for Biomedical Research, Cruciform Building, Gower Street, University College London, London WC1E 6BT, UK
- Edited by G. L. Smith, Imperial College of Science, Technology and Medicine, London, W. L. Irving, University of Nottingham, J. W. McCauley, Institute for Animal Health, Compton, Berkshire, D. J. Rowlands, University of Leeds
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- Book:
- New Challenges to Health
- Published online:
- 06 July 2010
- Print publication:
- 19 April 2001, pp 213-232
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Summary
INTRODUCTION
A substantial burden of human cancer worldwide is attributable to infection. Viral infections account for approximately 15 % of all human cancers. Cervical cancer, hepatocellular carcinoma and Kaposi's sarcoma, all caused by viruses, are some of the most important tumours in sub-Saharan Africa.
The interface between infection and malignancy is highlighted by the cancers prevalent in immunocompromised patients (Table 1). Human immunodeficiency virus (HIV)- infected individuals are specifically prone to cancer caused by viruses, e.g. Epstein–Barr virus (lymphomas), papillomaviruses (squamous carcinomas of skin and ano-genital carcinoma) and Kaposi's sarcoma-associated herpesvirus (lymphomas, multicentric Castleman's disease and Kaposi's sarcoma). The tumours increased in HIV-infected individuals where a virus has not yet been described (Table 1) may nevertheless have a viral aetiology. Carcinogenesis is a multifactorial process and not all persons infected with oncogenic viruses will develop a cancer: in fact, only a fraction of infected individuals will develop a tumour, particularly in the absence of immunosuppression. Certain tumours with a known viral aetiology (e.g. nasopharyngeal and hepatocellular carcinoma) are not increased in AIDS, indicating that viral infection and immunosuppression, without co-factors, are not enough to precipitate those specific cancers. Efficacious immunization against the primary infection would virtually eliminate the occurrence of the tumour with which the virus is associated. A successful vaccine against hepatitis B is available, whereas vaccines against Epstein–Barr virus and human papillomaviruses are currently in clinical studies.
This review will focus on the neoplasia associated with the gammaherpesviruses Epstein–Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV).