Differential Expression of Human MicroRNAs During Dengue Virus Infection in THP-1 Monocytes

被引:3
作者
Rossi, Atila Duque [1 ]
Higa, Luiza Mendonca [1 ,2 ]
Herlinger, Alice Laschuk [1 ]
Ribeiro-Alves, Marcelo [3 ]
de Menezes, Mariane Talon [1 ]
Giannini, Ana Lucia Moraes [4 ]
Cardoso, Cynthia Chester [1 ]
Da Poian, Andrea T. T. [2 ]
Tanuri, Amilcar [1 ]
Aguiar, Renato Santana [1 ,5 ]
机构
[1] Univ Fed Rio de Janeiro, Inst Biol, Dept Genet, Lab Virol Mol, Rio De Janeiro, Brazil
[2] Univ Fed Rio de Janeiro, Inst Bioquim Med Leopoldo Meis, Lab Bioquim Virus, Rio De Janeiro, Brazil
[3] Fiocruz MS, Inst Nacl Infectol Evandro Chagas, Lab Pesquisa Clin DST AIDS, Rio De Janeiro, Brazil
[4] Univ Fed Rio de Janeiro, Inst Biol, Dept Genet, Lab Genom Func & Transducao Sinal, Rio De Janeiro, Brazil
[5] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Genet Ecol & Evolucao, Lab Biol Integrat, Belo Horizonte, MG, Brazil
来源
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY | 2021年 / 11卷
关键词
microRNA; monocyte; dengue; gene expression; virus-host; NECROSIS-FACTOR-ALPHA; NS1; PROTEIN; REPLICATION; ACTIVATION; APOPTOSIS; GLYCOSYLATION; CELLS;
D O I
10.3389/fcimb.2021.714088
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Dengue virus (DENV) is the most widespread arbovirus, responsible for a wide range of clinical manifestations, varying from self-limited illness to severe hemorrhagic fever. Dengue severity is associated with host intense proinflammatory response and monocytes have been considered one of the key cell types involved in the early steps of DENV infection and immunopathogenesis. To better understand cellular mechanisms involved in monocyte infection by DENV, we analyzed the expression levels of 754 human microRNAs in DENV-infected THP-1 cells, a human monocytic cell line. Eleven human microRNAs showed differential expression after DENV infection and gene ontology and enrichment analysis revealed biological processes potentially affected by these molecules. Five downregulated microRNAs were significantly linked to cellular response to stress, four to cell death/apoptosis, two to innate immune responses and one upregulated to vesicle mediated, TGF-beta signaling, phosphatidylinositol mediated signaling, lipid metabolism process and blood coagulation.
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页数:8
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