Micro RNAs—The Small Big Players in Hepatitis E Virus Infection: A Comprehensive Review

Golkocheva-Markova, Еlitsa

doi:10.3390/biom12111543

Cited by 2 publications

(1 citation statement)

References 70 publications

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“…miRNAs are small (up to 25 nt), non-coding highly conserved RNAs, which represent 1% of the human genome but interact with about 60% of messenger RNAs. The matured mi-RNAs recognize their complementary mRNAs through base-pairing, which occurs between the so-called miRNA’s “seed region” (located on the 2nd to 7th nt of 5′-end) and the miRNA binding site within 3′UTR ( 29 ). Host miRNAs are essentially involved in the life cycles of multiple viruses and their associated pathogenesis via interacting directly with viral genomes or host genes.…”

Section: Discussionmentioning

confidence: 99%

miR-26a exerts broad-spectrum antiviral effects via the enhancement of RIG-I-mediated type I interferon response by targeting USP15

Zhang,

Li,

Hou

et al. 2024

Microbiol Spectr

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Host innate immunity is an important defense line against virus infection and is precisely regulated by various factors. Studying the mechanism of virus-host interaction is essential to developing novel antivirals. Being one of the key host natural antiviral responses, host small non-coding RNAs (miRNAs) possess promising antiviral potential worthy of study. Herein, we found that miR-26a exerted broad-spectrum antiviral effect against multiple viruses, e.g., Hepatitis E virus, Vesicular Stomatitis Virus, and Sendai Virus. Mechanistically, miR-26a specifically targets 3′UTR of mRNA to inhibit USP15 expression. USP15 interacted directly with RIG-I to deubiquitinate K63-linked RIG-I, thus negatively regulating type I interferon (IFN) signaling. Consequently, miR-26a, by downregulating USP15, promotes K63 ubiquitination of RIG-I to enhance type I IFN responses, resulting in an active antiviral state against virus infection. Intriguingly, the activation of type I IFN responses could suppress miR-26a expression, serving as an intrinsic negative feedback loop to avoid dysregulated signal activation. Hence, the broad-spectrum antiviral effects of miR-26a and its mode-of-action enriched the interaction networks between miRNAs and innate immunity, providing insights for the development of broad-spectrum antivirals against viral infection. IMPORTANCE miR-26a serves as a potent positive regulator of type I interferon (IFN) responses. By inhibiting USP15 expression, miR-26a promotes RIG-I K63-ubiquitination to enhance type I IFN responses, resulting in an active antiviral state against viruses. Being an intricate regulatory network, the activation of type I IFN responses could in turn suppress miR-26a expression to avoid the disordered activation that might result in the so-called “type I interferonopathy.” The knowledge gained would be essential for the development of novel antiviral strategies against viral infection.

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Section: Discussionmentioning

confidence: 99%

miR-26a exerts broad-spectrum antiviral effects via the enhancement of RIG-I-mediated type I interferon response by targeting USP15

Zhang,

Li,

Hou

et al. 2024

Microbiol Spectr

View full text Add to dashboard Cite

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From discovery to treatment: tracing the path of hepatitis E virus

Letafati,

Taghiabadi,

Roushanzamir

et al. 2024

Virol J

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The hepatitis E virus (HEV) is a major cause of acute viral hepatitis worldwide. HEV is classified into eight genotypes, labeled HEV-1 through HEV-8. Genotypes 1 and 2 exclusively infect humans, while genotypes 3, 4, and 7 can infect both humans and animals. In contrast, genotypes 5, 6, and 8 are restricted to infecting animals. While most individuals with a strong immune system experience a self-limiting infection, those who are immunosuppressed may develop chronic hepatitis. Pregnant women are particularly vulnerable to severe illness and mortality due to HEV infection. In addition to liver-related complications, HEV can also cause extrahepatic manifestations, including neurological disorders. The immune response is vital in determining the outcome of HEV infection. Deficiencies in T cells, NK cells, and antibody responses are linked to poor prognosis. Interestingly, HEV itself contains microRNAs that regulate its replication and modify the host's antiviral response. Diagnosis of HEV infection involves the detection of HEV RNA and anti-HEV IgM/IgG antibodies. Supportive care is the mainstay of treatment for acute infection, while chronic HEV infection may be cleared with the use of ribavirin and pegylated interferon. Prevention remains the best approach against HEV, focusing on sanitation infrastructure improvements and vaccination, with one vaccine already licensed in China. This comprehensive review provides insights into the spread, genotypes, prevalence, and clinical effects of HEV. Furthermore, it emphasizes the need for further research and attention to HEV, particularly in cases of acute hepatitis, especially among solid-organ transplant recipients.

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Micro RNAs—The Small Big Players in Hepatitis E Virus Infection: A Comprehensive Review

Cited by 2 publications

References 70 publications

miR-26a exerts broad-spectrum antiviral effects via the enhancement of RIG-I-mediated type I interferon response by targeting USP15

miR-26a exerts broad-spectrum antiviral effects via the enhancement of RIG-I-mediated type I interferon response by targeting USP15

From discovery to treatment: tracing the path of hepatitis E virus

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