AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research)


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Achieving Long-Term Viral Suppression May Reduce Risk of AIDS-Related Cancers

Accessed September 23, Download citation file: RIS Zotero. Reference Manager. Autosuggest Results. Expand All Sections. It would appear that most non-viral cancers are not recognised as foreign and are not simply kept at bay by immune surveillance. This appears paradoxical as neo-antigens have been detected on certain tumours, e. Indeed, these tumour antigens are targets for immunotherapy. Probably the immune system does play some role in surveillance of such tumours. Our modern knowledge of oncogenesis, however, tells us that somatic mutations — switching on oncogenes, inactivating tumour suppressor genes, and suppressing default, apoptotic pathways — are also required for tumour development, and without such genetic lesions, cells will not exert uncontrolled growth, even in the absence of immune surveillance.

In human transplant recipients and AIDS patients, two tumour types stand out above all others as having greatly increased incidence compared to immunocompetent but otherwise matched controls. They are B-cell lymphoma and Kaposi's sarcoma. EBV was originally linked with Burkitt's lymphoma BL in children, a tumour of small B-lymphocytes which also bear c- myc -Ig fusions on account of chromosome translocation.

BL is clearly increased in immunodeficiency, but there are few data so far for NPC. The most frequent lymphoma in AIDS and transplant recipients is immunoblastic lymphoma, of large B-lymphoblasts [2]. This may start as a polyclonal lymphoproliferative disease and progress to a monoclonal malignancy. Thus in early stages it resembles infectious mononucleosis, which represents primary EBV infection of adults, and also Duncan's syndrome in infants, an X-linked inherited disorder of a failure to mount an immune response to EBV infection.

A small percentage of lymphomas may be caused by HHV In particular it is associated with a lymphoma known as primary effusion lymphoma PEL , or body cavity-based lymphoma, rare among AIDS patients, a tumour lacking c- myc rearrangement [3]. Multicentric Castleman's disease, another lymphoproliferative syndrome seen in AIDS, is also associated with HHV-8 infection [4] , and the herpesvirus can be detected in immunoblasts [5].

Virology Lectures 2017 #18: Transformation and Oncogenesis

Although these might perhaps contain a novel, currently unknown oncogenic virus, an alternative pathway to oncogenesis could be that in HIV infection, in contrast to transplant patients, there is chronic activation of B cells. Thus much research remains to be done to elucidate the aetiology and pathogenesis of lymphomas in AIDS.

Long before AIDS, KS was suspected of having an infectious aetiology, but the incriminating virus, KSHV or HHV-8, was not discovered until [6] , when novel herpesvirus sequences were detected by using representational difference analysis, a subtractive DNA hybridisation technique involving PCR amplification of non-hybridised fragments. HHV-8 is a gamma herpesvirus distantly related to EBV; it is more closely related to herpesvirus saimiri of new world squirrel monkeys, and to recently discovered viruses in macaques.

The viral DNA sequences can be detected as latent infection in the spindle and endothelial tumour cells in KS [8] , as well as the primary effusion lymphoma cells already discussed. Using a monoclonal antibody to the major latent nuclear antigen, we recently demonstrated the expression of latent viral antigen in the nuclei of tumour cells [5]. KS is an unusual tumour of endothelioblasts. The cells express the vascular endothelial growth factor receptor type 3 VEGF-R3 , which is a marker of lymphatic endothelium rather than of mature vascular endothelium [5].

It remains controversial whether KS tumours are monoclonal. Early lesions may not be, but nodules within advanced KS lesions may represent clonal proliferation.

Cancer in the HIV-Infected Population | TheBodyPro

It is rarely seen in people who have acquired their HIV parenterally, such as injecting drug users and men with haemophilia [9]. Recent serological surveys for antibodies to HHV-8 indicate that by and large the presence of HHV-8 antibodies in risk groups or populations reflects the incidence of KS, although the prevalence of HHV-8 infection is much higher than the risk of disease.

HHV-8 can be transmitted sexually, and this appears to be the major route among gay men. In endemic areas such as the Mediterranean and Africa, however, a steadily rising seroprevalence is seen throughout childhood and adulthood. The mode of transmission is unknown, although infants generally have HHVpositive mothers infected with the same strain.

Saliva is a possible source of infection. The HHV-8 genome carries several homologues of cellular genes that may well contribute to its oncogenic potential [7].


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  8. For example, a cyclin D homologue interacts with cellular CDK6 to phosphorylate and inactivate Rb protein, and the HHVencoded cyclin escapes the network of CDK inhibitors that regulate cellular cyclins [11]. Other HHV-8 genes such as a G-protein coupled receptor [12] and an interferon response factor [13] will transform NIH-3T3 cells into tumorigenic counterparts.

    An overall picture of the major AIDS-linked tumours has emerged in which two viruses play different roles in the disease process. The major role of HIV is to cause immune deficiency. The herpesvirus, either EBV or HHV-8, may then act as the directly oncogenic agent, one that is normally kept in check by cell-mediated immunity.

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    This is well known for EBV infection [2] and we have recently identified cytotoxic T-lymphocyte responses for some HHV-8 antigens [16]. It is also possible that HIV plays a more direct role through a secreted form of the viral Tat protein. In vitro, Tat acts synergistically with basic fibroblast growth factor to stimulate proliferation of endothelial cells [17].

    AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research) AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research)
    AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research) AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research)
    AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research) AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research)
    AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research) AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research)
    AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research) AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research)
    AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research) AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research)
    AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research) AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research)
    AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research) AIDS-Associated Viral Oncogenesis (Cancer Treatment and Research)

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