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hsa-miR-181-5p inhibits human immunodeficiency virus type 1 replication by downregulating DDX3X expression
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Abstract
The adverse effects of antiviral therapy have prompted research into novel treatment strategies. miR-181 has been shown to be negatively correlated with the HIV viral load. We predicted that miR-181 could target DDX3X, a host factor involved in HIV nuclear export leading to the inhibiting of HIV replication. To verify our hypothesis, an miR-181 mimic was transfected into Jurkat cells infected with pNL4-3 wild strain and HIV replication-competent H9-IIIB cells. Besides the reporter gene plasmid containing the DDX3x mRNA sequence was transfected into 293T cells. We found that miR-181 significantly reduced HIV viral protein Gag(p24) Tat and Rev and downregulated the expression of mRNAs and protein targeting DDX3X. Our results confirmed that miR-181 was indeed involved in regulating the level of HIV viral replication in lymphocytes by downregulating the level of DDX3X expression. Our research results provide a research basis for the future development of new antiviral drugs for HIV.
Title: hsa-miR-181-5p inhibits human immunodeficiency virus type 1 replication by downregulating DDX3X expression
Description:
Abstract
The adverse effects of antiviral therapy have prompted research into novel treatment strategies.
miR-181 has been shown to be negatively correlated with the HIV viral load.
We predicted that miR-181 could target DDX3X, a host factor involved in HIV nuclear export leading to the inhibiting of HIV replication.
To verify our hypothesis, an miR-181 mimic was transfected into Jurkat cells infected with pNL4-3 wild strain and HIV replication-competent H9-IIIB cells.
Besides the reporter gene plasmid containing the DDX3x mRNA sequence was transfected into 293T cells.
We found that miR-181 significantly reduced HIV viral protein Gag(p24) Tat and Rev and downregulated the expression of mRNAs and protein targeting DDX3X.
Our results confirmed that miR-181 was indeed involved in regulating the level of HIV viral replication in lymphocytes by downregulating the level of DDX3X expression.
Our research results provide a research basis for the future development of new antiviral drugs for HIV.
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