Plasmodium infection reduces the volume of the viral reservoir in SIV-infected rhesus macaques receiving antiretroviral therapy

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• 作者：Xiao-Yong Zhan ; Nina Wang ; Guangjie Liu ; Limei Qin ; Wanwan Xu ; Siting Zhao…
• 关键词：HIV ; 1 ; SIV ; AIDS ; Plasmodium ; Malaria ; Rhesus macaque model ; Co ; infection ; ART ; Viral reservoir
• 刊名：Retrovirology
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：11
• 期：1
• 全文大小：2,816 KB
• 参考文献：1. WHO Joint United Nations Program on HIV/AIDS (UNAIDS): UNAIDS report on the global AIDS epidemic in 2013. http://www.unaids.org/en/media/unaids/contentassets/documents/epidemiology/2013/gr2013/UNAIDS_Global_Report_2013_en.pdf.
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• 刊物主题：Virology; Infectious Diseases; Cancer Research;
• 出版者：BioMed Central
• ISSN：1742-4690

文摘

Background Previous studies indicated that Plasmodium infection activates the immune system, including memory CD4+ T cells, which constitute the reservoir of human immunodeficiency virus type-1 (HIV-1). Therefore, we postulated that co-infection with malaria might activate the reservoir of HIV-1. To test this hypothesis, we used a rhesus macaque model of co-infection with malaria and simian immunodeficiency virus (SIV), along with antiretroviral therapy (ART). Results Our results showed that Plasmodium infection reduced both the replication-competent virus pool in resting CD4+ T cells and the integrated virus DNA (iDNA) load in peripheral blood mononuclear cells in the monkeys. This reduction might be attributable to malaria-mediated activation and apoptotic induction of memory CD4+ T cells. Further studies indicated that histone acetylation and NF-kappaB (NF-κB) activation in resting CD4+ T cells may also play an important role in this reduction. Conclusions The findings of this work expand our knowledge of the interaction between these two diseases. As more HIV-1-infected individuals in malaria-endemic areas receive ART, we should explore whether any of the patients co-infected with Plasmodium experience virologic benefits.