Table 1 miRNAs function in viral infections

HBV

miR-155

Zinc fingers and homeoboxes 2 (ZHX2) levels were lowered by miR-155 overexpression through miR-155 seed sites in the ZHX2 3′UTR, but ZHX2 levels were raised by miR-155 inhibition. Therefore, data provide a potential treatment for HBV-related HCC by suggesting that HBV’s HCC-promoting features may involve silencing of ZHX2 through a miR-155-dependent route.

[37]

HBV

miR-122

By downregulating the Gld2 gene, HBV decreased the levels of miR-122, which may indicate a novel method for HBV to control the production of miRNAs. As a consequence of the Gld2 protein being downregulated by the HBV X (HBx) protein, the amount of miR-122 is lowered.

[38]

HAV

hsa-miR-146a-5p

hepatitis A virus (HAV) partly interferes with RIG-I/MDA5-mediated IFN-I signaling by cleaving TNF receptor-associated factor 6 (TRAF6), an important adaptor protein, through hsa-miR-146a-5p.

[39]

HCV

miR-122

Two locations in the 5’ UTR of the HCV genome are targeted by miR-122, which thus encourages viral RNA accumulation.

[40]

HCV

miR-199a∗

In two cell lines harboring HCV replicons (replicon cells), overexpression of miR-199a_* suppressed HCV genome replication. In contrast, suppression of miRNA by a particular ASO sped up viral multiplication. When miR-199a was overexpressed in HCV replicon cells, replicon RNA was deposited in RISC.

[41]

HEV

miR-214

Direct interactions between miR-214 and HEV RNA promote HEV replication and genome translation. The expression of protein C, the thrombin-negative regulator, is suppressed by miR-214. HEV ORF3, another viral component, similarly improves intracellular active thrombin levels. Furthermore, miR-214 specifically targets 2′-5′-oligoadenylate synthetase, an antiviral host factor.

[42]

SARS-CoV-2

miR-2392

It is essential for miR-2392 to drive downstream inhibition of mitochondrial gene expression, increase inflammation, glycolysis, and hypoxia, as well as support several COVID-19 infections-related symptoms. COVID-19 symptoms in the host are accompanied by overexpression of miR-2392.

[43]

HIV-1

miR-132

miR-132 is shown to be substantially increased after CD4 + T cell activation, and studies in the Jurkat CD4 + T cell line demonstrate that miR-132 promotes viral propagation. MeCP2, a miR-132 target, is upregulated, which boosts HIV-1 replication.

[44]

HIV-1

miR-29a

miR-29a suppresses viral replication by binding to and silencing a region in the 3′UTR of viral mRNAs. A cytokine-microRNA (i.e., IL-21/miR-29a) route was discovered by studying its effects on HIV-1 replication in vivo. MiR-29a has been shown to have a significant role in HIV-1 proliferation and latency.

[45]

Dengue virus

miR-548 g-3p

It was revealed that miR-548 g-3p inhibited DENV 1, 2, 3, and 4 replication and also inhibited the production of viral proteins by interfering with DENV translation.

[46]

Dengue virus

miR-21

miR-21 increases the replication of DENV 2. To study the role of miR-21 in DENV infection, we co-administered AMO-21 and a peptide nucleic acid-21 (PNA-21) construct having a nucleotide sequence complementary to AMO-21, and then infected the animals with DENV 2.

[47]