RNA interference and HIV‐1 infection

Abstract

Life-prolonging antiretroviral therapy remarkably reduces viral load, but it does not eradicate the virus. An important obstacle preventing virus clearance is the presence of latent virion reservoirs in the host. However, new promising antiviral approaches are emerging, and a number of host cell factors involved in the disease progression and control of HIV-1 replication have been recently discovered. For instance, the RNA interference (RNAi) mechanism, besides many functions conserved throughout evolution, works as a defence mechanism against noxious transcripts which may provide a new tool to block viral replication. The recent definition of basic RNAi mechanisms, as well as the discovery of micro RNAs (microRNAs) encoded by the host cell genome and by HIV-1, also suggest that RNAi may be involved in the control of HIV replication.

Inhibition of Feline Leukemia Virus Replication in Chronically Infected Cell Line Utilizing RNA Interference

“…[23][24][25][26][27][28][29] Recent studies have demonstrated that RNAi can be exploited in order to target genetic sequences of a variety of human and animal viruses including HIV-1, Poliovirus, Human Papillomavirus (HPV), Hepatitis C Virus (HCV), Hepatitis B Virus (HBV), Influenza Virus, Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV), and Feline Immunodeficiency Virus (FIV). 9,[30][31][32][33][34][35][36][37][38][39] These studies confirmed that RNAi technology represents a promising gene therapeutic approach to control viral infection and disease progression. Previous studies applying RNAi directed to structural genes inhibited viral replication of HIV and FIV.…”

“…The inhibition of HIV-1 and FIV [29][30][31][32][33]40,45,46 replication among other viruses could be accomplished by the shRNA expression in established and primary cell lines. Here, we investigated the feasibility of using RNAi technology, based in shRNA expression, aiming at controlling FeLV infection in feline cell lines.…”

“…2), indicating that a region of FeLV gag gene can be targeted by shRNA, as can other types of retrovirus like HIV and FIV, for example. [30][31][32][33]40,41 The F3 vector expressing anti-FeLV shRNA failed to reduce p27 protein expression, despite its complementarity to the gag sequence. Distinct factors could influence the inhibition mechanisms exerted by the anti-FeLV shRNA, including technical errors.…”

“…Previous studies applying RNAi directed to structural genes inhibited viral replication of HIV and FIV. [30][31][32][33]40 In this study, in order to investigate the potential use of RNAi technology as a therapeutic strategy for the control of FeLV replication, we first examined the expression of shRNAs against FeLV gag gene by the pSUPER vector system in FeLV replication in fibroblastic cells. Sequentially, we generated a retrovirus vector expressing a FeLV-specific shRNA and examined its effect on virus replication in a chronically FeLV-infected feline T lymphoid cell line, aiming to evaluate the efficient delivery and expression of FeLV-specific shRNA and certify the persistent inhibitory effect of FeLV in these cells.…”

microRNA in Cutaneous Wound Healing

“…Accordingly, several large DNA mammalian viruses have been shown to encode their own miRNAs. RNAi is directly implicated in HIV replication [33]. Dicer mutant mice are hypersusceptible to infection by the RNA virus vesicular stomatitis virus [57].…”