期刊
PATHOGENS AND DISEASE
卷 73, 期 7, 页码 -出版社
OXFORD UNIV PRESS
DOI: 10.1093/femspd/ftv044
关键词
HIV-1; virus; lymphomagenesis; antiretroviral drugs; immune activation; chronic infection
资金
- University of Maryland School of Medicine Deans Challenge Award
- National Institute of Neurological Disorders and Stroke (NINDS) National Institute of Health (NIH) [NS-066842]
HIV infection increases the risk of many types of cancer, including lymphoma. Combination antiretroviral therapy (cART) has reduced, but not eliminated, the risk of HIV-associated lymphoma. There has been a substantial shift in the subtypes of lymphoma observed in HIV-infected patients treated with cART. In this review, we will first outline these changes based on epidemiological studies and describe the impact of cART on lymphoma risk and mortality. Then, we will discuss some immunological factors that may contribute to the increased risk of lymphoma persisting after the administration of cART, including immunological non-response to therapy, chronic B-cell activation and dysfunction, T follicular helper cells, natural killer cells and altered lymphopoiesis. A better understanding of the pathophysiologic mechanisms of HIV-associated lymphoma under effective cART will inform future treatment strategies.
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