Immunology of EBV-Related Lymphoproliferative Disease in HIV-Positive Individuals
Epstein-Bar virus (EBV) can directly cause lymphoproliferative disease (LPD), including AIDS-defining lymphomas such as Burkitt’s lymphoma and other non-Hodgkin lymphomas (NHL), as well as human immunodeficiency virus (HIV)-related Hodgkin lymphoma (HL). The prevalence of EBV in HL and NHL is elevat...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2020-09-01
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| Series: | Frontiers in Oncology |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fonc.2020.01723/full |
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| author | Polina Shindiapina Polina Shindiapina Elshafa H. Ahmed Anna Mozhenkova Tamrat Abebe Robert A. Baiocchi Robert A. Baiocchi |
| author_facet | Polina Shindiapina Polina Shindiapina Elshafa H. Ahmed Anna Mozhenkova Tamrat Abebe Robert A. Baiocchi Robert A. Baiocchi |
| author_sort | Polina Shindiapina |
| collection | DOAJ |
| description | Epstein-Bar virus (EBV) can directly cause lymphoproliferative disease (LPD), including AIDS-defining lymphomas such as Burkitt’s lymphoma and other non-Hodgkin lymphomas (NHL), as well as human immunodeficiency virus (HIV)-related Hodgkin lymphoma (HL). The prevalence of EBV in HL and NHL is elevated in HIV-positive individuals compared with the general population. Rates of incidence of AIDS-defining cancers have been declining in HIV-infected individuals since initiation of combination anti-retroviral therapy (cART) use in 1996. However, HIV-infected persons remain at an increased risk of cancers related to infections with oncogenic viruses. Proposed pathogenic mechanisms of HIV-related cancers include decreased immune surveillance, decreased ability to suppress infection-related oncogenic processes and a state of chronic inflammation marked by alteration of the cytokine profile and expanded numbers of cytotoxic T lymphocytes with down-regulated co-stimulatory molecules and increased expression of markers of senescence in the setting of treated HIV infection. Here we discuss the cooperation of EBV-infected B cell- and environment-associated factors that may contribute to EBV-related lymphomagenesis in HIV-infected individuals. Environment-derived lymphomagenic factors include impaired host adaptive and innate immune surveillance, cytokine dysregulation and a pro-inflammatory state observed in the setting of chronic, cART-treated HIV infection. B cell factors include distinctive EBV latency patterns and host protein expression in HIV-associated LPD, as well as B cell-stimulating factors derived from HIV infection. We review the future directions for expanding therapeutic approaches in targeting the viral and immune components of EBV LPD pathogenesis. |
| first_indexed | 2024-12-21T00:07:15Z |
| format | Article |
| id | doaj.art-15fff3b5358c4eef88ee3bd4f00267bf |
| institution | Directory Open Access Journal |
| issn | 2234-943X |
| language | English |
| last_indexed | 2024-12-21T00:07:15Z |
| publishDate | 2020-09-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Oncology |
| spelling | doaj.art-15fff3b5358c4eef88ee3bd4f00267bf2022-12-21T19:22:26ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2020-09-011010.3389/fonc.2020.01723529601Immunology of EBV-Related Lymphoproliferative Disease in HIV-Positive IndividualsPolina Shindiapina0Polina Shindiapina1Elshafa H. Ahmed2Anna Mozhenkova3Tamrat Abebe4Robert A. Baiocchi5Robert A. Baiocchi6Division of Hematology, Department of Internal Medicine, The Ohio State University, Columbus, OH, United StatesComprehensive Cancer Center, The James Cancer Hospital and Solove Research Institute, The Ohio State University, Columbus, OH, United StatesComprehensive Cancer Center, The James Cancer Hospital and Solove Research Institute, The Ohio State University, Columbus, OH, United StatesComprehensive Cancer Center, The James Cancer Hospital and Solove Research Institute, The Ohio State University, Columbus, OH, United StatesDepartment of Microbiology, Immunology, and Parasitology, School of Medicine Tikur Anbessa Specialized Hospital, College of Health Sciences, Addis Ababa University, Addis Ababa, EthiopiaDivision of Hematology, Department of Internal Medicine, The Ohio State University, Columbus, OH, United StatesComprehensive Cancer Center, The James Cancer Hospital and Solove Research Institute, The Ohio State University, Columbus, OH, United StatesEpstein-Bar virus (EBV) can directly cause lymphoproliferative disease (LPD), including AIDS-defining lymphomas such as Burkitt’s lymphoma and other non-Hodgkin lymphomas (NHL), as well as human immunodeficiency virus (HIV)-related Hodgkin lymphoma (HL). The prevalence of EBV in HL and NHL is elevated in HIV-positive individuals compared with the general population. Rates of incidence of AIDS-defining cancers have been declining in HIV-infected individuals since initiation of combination anti-retroviral therapy (cART) use in 1996. However, HIV-infected persons remain at an increased risk of cancers related to infections with oncogenic viruses. Proposed pathogenic mechanisms of HIV-related cancers include decreased immune surveillance, decreased ability to suppress infection-related oncogenic processes and a state of chronic inflammation marked by alteration of the cytokine profile and expanded numbers of cytotoxic T lymphocytes with down-regulated co-stimulatory molecules and increased expression of markers of senescence in the setting of treated HIV infection. Here we discuss the cooperation of EBV-infected B cell- and environment-associated factors that may contribute to EBV-related lymphomagenesis in HIV-infected individuals. Environment-derived lymphomagenic factors include impaired host adaptive and innate immune surveillance, cytokine dysregulation and a pro-inflammatory state observed in the setting of chronic, cART-treated HIV infection. B cell factors include distinctive EBV latency patterns and host protein expression in HIV-associated LPD, as well as B cell-stimulating factors derived from HIV infection. We review the future directions for expanding therapeutic approaches in targeting the viral and immune components of EBV LPD pathogenesis.https://www.frontiersin.org/article/10.3389/fonc.2020.01723/fullEpstein-Barr viruslymphoproliferative diseaseHIVImmunologyimmunodeficiency |
| spellingShingle | Polina Shindiapina Polina Shindiapina Elshafa H. Ahmed Anna Mozhenkova Tamrat Abebe Robert A. Baiocchi Robert A. Baiocchi Immunology of EBV-Related Lymphoproliferative Disease in HIV-Positive Individuals Frontiers in Oncology Epstein-Barr virus lymphoproliferative disease HIV Immunology immunodeficiency |
| title | Immunology of EBV-Related Lymphoproliferative Disease in HIV-Positive Individuals |
| title_full | Immunology of EBV-Related Lymphoproliferative Disease in HIV-Positive Individuals |
| title_fullStr | Immunology of EBV-Related Lymphoproliferative Disease in HIV-Positive Individuals |
| title_full_unstemmed | Immunology of EBV-Related Lymphoproliferative Disease in HIV-Positive Individuals |
| title_short | Immunology of EBV-Related Lymphoproliferative Disease in HIV-Positive Individuals |
| title_sort | immunology of ebv related lymphoproliferative disease in hiv positive individuals |
| topic | Epstein-Barr virus lymphoproliferative disease HIV Immunology immunodeficiency |
| url | https://www.frontiersin.org/article/10.3389/fonc.2020.01723/full |
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