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

Zhan XY, Wang N, Liu G, Qin L, Xu W, Zhao S, Qin L, Chen X - Retrovirology (2014)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Pathogen Biology, State Key Laboratory of Respiratory Disease, Center for Infection and Immunity, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, No. 190 Kaiyuan Avenue, Luogang District, Guangzhou Science Park, Guangzhou, 510530, Guangdong Province, China. zhan_xiaoyong@gibh.ac.cn.

ABSTRACT

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.

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Related in: MedlinePlus

Animal study design. At week 0, 12 monkeys in the 2 groups were infected with SIV. At week 15, all monkeys started to receive ART (downward black arrow). During weeks 49–66, 6 monkeys in the ART + Pc group were co-infected with Pc (red arrows and box). At week 75, ART was terminated in all monkeys (upward black arrow). The light gray boxes indicate ART, and the light red box indicates Pc infection.
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Fig1: Animal study design. At week 0, 12 monkeys in the 2 groups were infected with SIV. At week 15, all monkeys started to receive ART (downward black arrow). During weeks 49–66, 6 monkeys in the ART + Pc group were co-infected with Pc (red arrows and box). At week 75, ART was terminated in all monkeys (upward black arrow). The light gray boxes indicate ART, and the light red box indicates Pc infection.

Mentions: The design of the animal experiments is shown in Figure 1. Twelve Chinese-origin rhesus macaques (Macaca mulatta) were inoculated intravenously with 10,000 50% tissue culture infectious doses of SIVmac251 and were randomly divided into two groups (n = 6 per group): the ART group (ART only) and the ART + Pc group (ART plus Pc infection). SIV infection resulted in certain typical virological and immunological changes in the monkeys that were similar to those reported previously (Additional file 1: Figure S1) [15]. The animals in the ART + Pc group displayed typical clinical manifestations of malaria during Pc infection (data not shown).Figure 1


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

Zhan XY, Wang N, Liu G, Qin L, Xu W, Zhao S, Qin L, Chen X - Retrovirology (2014)

Animal study design. At week 0, 12 monkeys in the 2 groups were infected with SIV. At week 15, all monkeys started to receive ART (downward black arrow). During weeks 49–66, 6 monkeys in the ART + Pc group were co-infected with Pc (red arrows and box). At week 75, ART was terminated in all monkeys (upward black arrow). The light gray boxes indicate ART, and the light red box indicates Pc infection.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4269176&req=5

Fig1: Animal study design. At week 0, 12 monkeys in the 2 groups were infected with SIV. At week 15, all monkeys started to receive ART (downward black arrow). During weeks 49–66, 6 monkeys in the ART + Pc group were co-infected with Pc (red arrows and box). At week 75, ART was terminated in all monkeys (upward black arrow). The light gray boxes indicate ART, and the light red box indicates Pc infection.
Mentions: The design of the animal experiments is shown in Figure 1. Twelve Chinese-origin rhesus macaques (Macaca mulatta) were inoculated intravenously with 10,000 50% tissue culture infectious doses of SIVmac251 and were randomly divided into two groups (n = 6 per group): the ART group (ART only) and the ART + Pc group (ART plus Pc infection). SIV infection resulted in certain typical virological and immunological changes in the monkeys that were similar to those reported previously (Additional file 1: Figure S1) [15]. The animals in the ART + Pc group displayed typical clinical manifestations of malaria during Pc infection (data not shown).Figure 1

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Pathogen Biology, State Key Laboratory of Respiratory Disease, Center for Infection and Immunity, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, No. 190 Kaiyuan Avenue, Luogang District, Guangzhou Science Park, Guangzhou, 510530, Guangdong Province, China. zhan_xiaoyong@gibh.ac.cn.

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus