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Downregulation of miRNA-26a by HIV-1 Enhances CD59 Expression and Packaging, Impacting Virus Susceptibility to Antibody-Dependent Complement-Mediated Lysis
被引:2
作者:

Bellini, Nicolas
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Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada
Univ Montreal, Fac Med, Dept Microbiol Infect Dis & Immunol, Montreal, PQ H3C 3J7, Canada Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada

Ye, Chengyu
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Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada

Ajibola, Oluwaseun
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Univ Manitoba, Rady Fac Hlth Sci, Dept Immunol, Winnipeg, MB R3E 0T5, Canada Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada

Murooka, Thomas T.
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Univ Manitoba, Rady Fac Hlth Sci, Dept Immunol, Winnipeg, MB R3E 0T5, Canada Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada

Lodge, Robert
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Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada

Cohen, eric A.
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Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada
Univ Montreal, Fac Med, Dept Microbiol Infect Dis & Immunol, Montreal, PQ H3C 3J7, Canada Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada
机构:
[1] Inst Rech Clin Montreal, Lab Human Retrovirol, Montreal, PQ H2W 1R7, Canada
[2] Univ Montreal, Fac Med, Dept Microbiol Infect Dis & Immunol, Montreal, PQ H3C 3J7, Canada
[3] Univ Manitoba, Rady Fac Hlth Sci, Dept Immunol, Winnipeg, MB R3E 0T5, Canada
来源:
VIRUSES-BASEL
|
2024年
/
16卷
/
07期
基金:
加拿大健康研究院;
关键词:
CD59;
HIV-1;
complement-mediated lysis;
miRNA-26a;
innate immunity;
viral evasion;
T-CELLS;
NEUTRALIZING ANTIBODIES;
FEEDBACK LOOP;
TYPE-1;
ACTIVATION;
ENVELOPE;
BINDING;
DIFFERENTIATION;
INACTIVATION;
TRANSLATION;
D O I:
10.3390/v16071076
中图分类号:
Q93 [微生物学];
学科分类号:
071005 ;
100705 ;
摘要:
MicroRNAs (miRNAs) play important roles in the control of HIV-1 infection. Here, we performed RNA-seq profiling of miRNAs and mRNAs expressed in CD4+ T lymphocytes upon HIV-1 infection. Our results reveal significant alterations in miRNA and mRNA expression profiles in infected relative to uninfected cells. One of the miRNAs markedly downregulated in infected cells is miRNA-26a. Among the putative targets of miRNA-26a are CD59 receptor transcripts, which are significantly upregulated in infected CD4+ T cells. The addition of miRNA-26a mimics to CD4+ T cells reduces CD59 at both the mRNA and surface protein levels, validating CD59 as a miRNA-26a target. Consistent with the reported inhibitory role of CD59 in complement-mediated lysis (CML), knocking out CD59 in CD4+ T cells renders both HIV-1-infected cells and progeny virions more prone to antibody-dependent CML (ADCML). The addition of miRNA-26a mimics to infected cells leads to enhanced sensitivity of progeny virions to ADCML, a condition linked to a reduction in CD59 packaging into released virions. Lastly, HIV-1-mediated downregulation of miRNA-26a expression is shown to be dependent on integrated HIV-1 expression but does not involve viral accessory proteins. Overall, these results highlight a novel mechanism by which HIV-1 limits ADCML by upregulating CD59 expression via miRNA-26a downmodulation.
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页数:22
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h-index: 0
机构:
Univ Amsterdam, Acad Med Ctr, Dept Expt Immunol M01 120, Landsteiner Lab, NL-1105 AZ Amsterdam, Netherlands Univ Amsterdam, Acad Med Ctr, Dept Expt Immunol M01 120, Landsteiner Lab, NL-1105 AZ Amsterdam, Netherlands