Abstract
When stringent criteria have been used, the Epstein Barr virus (EBV), the Kaposi's sarcoma herpesvirus (KSHV), human immunodeficiency virus type 1 (HIV-1) and human hepatitis C virus (HCV) have been identified with sufficient evidence to be causative agents of non-Hodgkin's Lymphomas. Initially, single viral infection was considered fully responsible for the oncogenic properties of each virus, while it is now established that in many cases, multiple viral agents collaborate as cofactors in inducing lymphomas, especially in the presence of HIV-dependent immunodeficiency. Viruses cooperate by using their specific pathogenetic mechanisms in different combinations. The aim of this review is to describe the cooperation between different viruses in the development of lymphomas including the evidences supporting their pathogenetic role. Viral cooperation, a mechanism by which different viruses coinfecting human tissues have synergistic or regulatory effects on carcinogenesis, targets neoplastic B cells as well as cells of the microenvironment, such as reactive T-cells, B cells and macrophages, as well as non-immune cells such as endothelial cells, that contribute to tumor microenvironment. The most important viral genes involved in cooperation include HIV-1 tat and vpu, EBV LMP-1 and EBNA-2 and KSHV KIE2, Rta and LANA. Lymphomagenesis related to viral cooperation represents an interesting topic where microenvironmental abnormalities may be particularly relevant, particularly because antiviral targeted therapies and therapies producing the reconstitution of the immune system may constitute areas of interest aiming at improving the outcome of virus associated lymphomas. While the immune component of the lymphoma microenvironment can be easily studied by immunological and molecular techniques, the definition of the non-immune component of the lymphoma microenvironment is largely incomplete and may be the issue of future investigations. Understanding the pathogenetic role of viral infection in specific malignancies and defining microenvironmental abnormalities and mechanisms of viral carcinogenesis are important steps toward precise diagnosis and accurate treatment strategies for HIV-associated cancers.
| Original language | English |
|---|---|
| Pages (from-to) | 70-80 |
| Number of pages | 11 |
| Journal | Seminars in Cancer Biology |
| Volume | 34 |
| DOIs | |
| Publication status | Published - Oct 1 2015 |
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Keywords
- Epstein Barr virus
- Human immunodeficiency virus
- Kaposi's sarcoma herpesvirus
- Lymphomagenesis
- Viral cooperation
ASJC Scopus subject areas
- Cancer Research
Cite this
Microenvironmental abnormalities induced by viral cooperation : Impact on lymphomagenesis. / De Paoli, Paolo; Carbone, Antonino.
In: Seminars in Cancer Biology, Vol. 34, 01.10.2015, p. 70-80.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Microenvironmental abnormalities induced by viral cooperation
T2 - Impact on lymphomagenesis
AU - De Paoli, Paolo
AU - Carbone, Antonino
PY - 2015/10/1
Y1 - 2015/10/1
N2 - When stringent criteria have been used, the Epstein Barr virus (EBV), the Kaposi's sarcoma herpesvirus (KSHV), human immunodeficiency virus type 1 (HIV-1) and human hepatitis C virus (HCV) have been identified with sufficient evidence to be causative agents of non-Hodgkin's Lymphomas. Initially, single viral infection was considered fully responsible for the oncogenic properties of each virus, while it is now established that in many cases, multiple viral agents collaborate as cofactors in inducing lymphomas, especially in the presence of HIV-dependent immunodeficiency. Viruses cooperate by using their specific pathogenetic mechanisms in different combinations. The aim of this review is to describe the cooperation between different viruses in the development of lymphomas including the evidences supporting their pathogenetic role. Viral cooperation, a mechanism by which different viruses coinfecting human tissues have synergistic or regulatory effects on carcinogenesis, targets neoplastic B cells as well as cells of the microenvironment, such as reactive T-cells, B cells and macrophages, as well as non-immune cells such as endothelial cells, that contribute to tumor microenvironment. The most important viral genes involved in cooperation include HIV-1 tat and vpu, EBV LMP-1 and EBNA-2 and KSHV KIE2, Rta and LANA. Lymphomagenesis related to viral cooperation represents an interesting topic where microenvironmental abnormalities may be particularly relevant, particularly because antiviral targeted therapies and therapies producing the reconstitution of the immune system may constitute areas of interest aiming at improving the outcome of virus associated lymphomas. While the immune component of the lymphoma microenvironment can be easily studied by immunological and molecular techniques, the definition of the non-immune component of the lymphoma microenvironment is largely incomplete and may be the issue of future investigations. Understanding the pathogenetic role of viral infection in specific malignancies and defining microenvironmental abnormalities and mechanisms of viral carcinogenesis are important steps toward precise diagnosis and accurate treatment strategies for HIV-associated cancers.
AB - When stringent criteria have been used, the Epstein Barr virus (EBV), the Kaposi's sarcoma herpesvirus (KSHV), human immunodeficiency virus type 1 (HIV-1) and human hepatitis C virus (HCV) have been identified with sufficient evidence to be causative agents of non-Hodgkin's Lymphomas. Initially, single viral infection was considered fully responsible for the oncogenic properties of each virus, while it is now established that in many cases, multiple viral agents collaborate as cofactors in inducing lymphomas, especially in the presence of HIV-dependent immunodeficiency. Viruses cooperate by using their specific pathogenetic mechanisms in different combinations. The aim of this review is to describe the cooperation between different viruses in the development of lymphomas including the evidences supporting their pathogenetic role. Viral cooperation, a mechanism by which different viruses coinfecting human tissues have synergistic or regulatory effects on carcinogenesis, targets neoplastic B cells as well as cells of the microenvironment, such as reactive T-cells, B cells and macrophages, as well as non-immune cells such as endothelial cells, that contribute to tumor microenvironment. The most important viral genes involved in cooperation include HIV-1 tat and vpu, EBV LMP-1 and EBNA-2 and KSHV KIE2, Rta and LANA. Lymphomagenesis related to viral cooperation represents an interesting topic where microenvironmental abnormalities may be particularly relevant, particularly because antiviral targeted therapies and therapies producing the reconstitution of the immune system may constitute areas of interest aiming at improving the outcome of virus associated lymphomas. While the immune component of the lymphoma microenvironment can be easily studied by immunological and molecular techniques, the definition of the non-immune component of the lymphoma microenvironment is largely incomplete and may be the issue of future investigations. Understanding the pathogenetic role of viral infection in specific malignancies and defining microenvironmental abnormalities and mechanisms of viral carcinogenesis are important steps toward precise diagnosis and accurate treatment strategies for HIV-associated cancers.
KW - Epstein Barr virus
KW - Human immunodeficiency virus
KW - Kaposi's sarcoma herpesvirus
KW - Lymphomagenesis
KW - Viral cooperation
UR - http://www.scopus.com/inward/record.url?scp=84942295101&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84942295101&partnerID=8YFLogxK
U2 - 10.1016/j.semcancer.2015.03.009
DO - 10.1016/j.semcancer.2015.03.009
M3 - Article
C2 - 25837157
AN - SCOPUS:84942295101
VL - 34
SP - 70
EP - 80
JO - Seminars in Cancer Biology
JF - Seminars in Cancer Biology
SN - 1044-579X
ER -