The Role of human herpesvirus and GBV-C coinfections in the development of non-Hodgkin's lymphoma in HIV-1 positive individuals in the multicenter AIDS cohort studySuder, Natalie (2014) The Role of human herpesvirus and GBV-C coinfections in the development of non-Hodgkin's lymphoma in HIV-1 positive individuals in the multicenter AIDS cohort study. Master's Thesis, University of Pittsburgh. (Unpublished)
AbstractIntroduction: Infection with the human immunodeficiency virus (HIV) can result in severe immune suppression, often allowing infections that would normally be controlled by the immune system to persist in HIV-positive individuals. Many of these infections can in turn affect the dynamics of HIV disease progression. Specifically, we hypothesize that herpesvirus infections are associated with more rapid progression of HIV-1 disease, and chronic immune activation that can lead to the development of HIV/AIDS-associated cancers. Alternatively, we postulate that GB Virus C coinfection has been shown to have a protective effect against HIV-1 disease progression, and may reduce chronic immune activation in HIV-1 positive individuals. Methods: This study investigated the associations of cytomegalovirus, Epstein-Barr virus, human herpesvirus 6, human herpesvirus 8, and GB Virus C viral coinfections on the development of non-Hodgkin’s lymphoma in MACS HIV-1 seroconverters pre-combination antiretroviral therapy (cART). 536 seroconverters pre-cART were included in the investigation, including 22 who developed non-Hodgkin’s lymphoma. Results: HIV-1 seroconverters who developed non-Hodgkin’s lymphoma pre-cART experienced CMV and EBV viremia significantly more frequently than those who did not develop non-Hodgkin’s lymphoma. HIV-1 seroconverters who did not develop non-Hodgkin’s lymphoma pre-cART were more frequently viremic for GBV-C. Levels of EBV viremia were significantly higher in HIV-1 seroconverters who developed non-Hodgkin’s lymphoma, and levels of GBV-C viremia were significantly higher in the HIV-1 seroconverters who did not develop non-Hodgkin’s lymphoma. Additionally, HIV-1 seroconverters who had experienced EBV viremia progressed from HIV-1 seroconversion to lymphoma diagnosis more rapidly than those from whom EBV viremia was never detected. Conversely, those who experienced GBV-C viremia, but never experienced EBV viremia progressed more slowly from HIV-1 seroconversion to non-Hodgkin’s lymphoma. Discussion: This investigation supports the hypothesis that EBV and CMV coinfections drive HIV-1 disease progression and the development of HIV-associated non-Hodgkin’s lymphoma. The results also suggest that GBV-C plays a protective role against the development of non-Hodgkin’s lymphoma in HIV-1 positive individuals. These findings are of public health significance, because knowledge gained regarding the risks associated with non-Hodgkin’s lymphoma development can contribute to the prevention and early detection of non-Hodgkin’s lymphoma. Share
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