Are microRNAs Important Players in HIV-1 Infection? An Update

Abstract

HIV-1 has already claimed over 35 million human lives globally. No curative treatments are currently available, and the only treatment option for over 36 million people currently living with HIV/AIDS are antiretroviral drugs that disrupt the function of virus-encoded proteins. However, such virus-targeted therapeutic strategies are constrained by the ability of the virus to develop drug-resistance. Despite major advances in HIV/AIDS research over the years, substantial knowledge gaps exist in many aspects of HIV-1 replication, especially its interaction with the host. Hence, understanding the mechanistic details of virus–host interactions may lead to novel therapeutic strategies for the prevention and/or management of HIV/AIDS. Notably, unprecedented progress in deciphering host gene silencing processes mediated by several classes of cellular small non-coding RNAs (sncRNA) presents a promising and timely opportunity for developing non-traditional antiviral therapeutic strategies. Cellular microRNAs (miRNA) belong to one such important class of sncRNAs that regulate protein synthesis. Evidence is mounting that cellular miRNAs play important roles in viral replication, either usurped by the virus to promote its replication or employed by the host to control viral infection by directly targeting the viral genome or by targeting cellular proteins required for productive virus replication. In this review, we summarize the findings to date on the role of miRNAs in HIV-1 biology.

The HIV-1 capsid-binding host factor CPSF6 is post-transcriptionally regulated by the cellular microRNA miR-125b

“…There are two key mechanisms by which miRNAs can confer antiviral activity (57)(58)(59). Through a direct-mechanism, miRNAs can inhibit viral protein translation by targeting HIV-1 mRNAs.…”

MicroRNA Involvement in Signaling Pathways During Viral Infection

“…The means by which HIV manages to evade the host's immune strategies involves the reshaping of the host cells with the aid of viral accessory proteins and RNA (Fruci et al, 2017). However, while host miRNAs can play either positive or negative roles in viral replication and disease evolution (Balasubramaniam et al, 2018), the existence of viral miRNAs has only relatively recently been demonstrated and their role in pathogenesis is still disputed (Omoto et al, 2004).…”

MiR-10a-5p-Mediated Syndecan 1 Suppression Restricts Porcine Hemagglutinating Encephalomyelitis Virus Replication

“…For instance, cellular miR-17 promotes the stability and translation of viral RNA by targeting the 3 -UTR of RNA viruses (Scheel et al, 2016). The latter affects virus replication by targeting host cellular mRNAs (Balasubramaniam et al, 2018). For example, miR-200b and miR-429 suppress the expression of zinc finger E-box binding homeobox 1 (ZEB1) and zinc finger E-box binding homeobox 2 (ZEB2), the two cellular proteins that have key roles to establish and maintain latent infections of Epstein-Barr virus, thus leading to lytic reactivation of latently infected cells (Ellis-Connell et al, 2010).…”