Possible involvement of miRNAs in tropism of Parvovirus B19

Abstract

Human Parvovirus B19 (PVB19) is one of the most important pathogens that targets erythroid lineage. Many factors were mentioned for restriction to erythroid progenitor cells (EPCs). Previous studies showed that in non-permissive cells VP1 and VP2 (structural proteins) mRNAs were detected but could not translate to proteins. A bioinformatics study showed that this inhibition might be due to specific microRNAs (miRNAs) present in non-permissive cells but not in permissive EPCs. To confirm the hypothesis, we evaluated the effect of miRNAs on VP expression. CD34(+) HSCs were separated from cord blood. Then, CD34(+) cells were treated with differentiation medium to obtain CD36(+) EPCs. To evaluate the effect of miRNAs on VP expression in MCF7 and HEK-293 cell lines (non-permissive cells) and CD36(+) EPCs, dual luciferase assay was performed in presence of shRNAs against Dicer and Drosha to disrupt miRNA biogenesis. QRT-PCR was performed to check down-regulation of Dicer and Drosha after transfection. All measurements were done in triplicate. Data means were compared using one-way ANOVAs. MicroRNA prediction was done by the online microRNA prediction tools. No significant difference was shown in luciferase activity of CD36(+) EPCs after co-transfection with shRNAs, while it was significant in non-permissive cells. Our study revealed that miRNAs may be involved in inhibition of VP expression in non-permissive cells, although further studies are required to demonstrate which miRNAs exactly are involved in regulation of PVB19 replication.

Research update for articles published in EJCI in 2014

“…Since our paper has been published, interesting studies have explored the possible mechanisms involved in the tropism of Parvovirus (PV) B19 for different cell types [39], including endothelial cells [40,41], erythroid progenitor cells [42] and T cells [43]. Altered function of these cell types might be responsible for the occurrence of major adverse cardiac events (MACE) after coronary stenting in different ways, thus supporting the main observation of our paper.…”

“…In particular, Anbarlou et al . have shown that miRNAs may be involved in regulation of PVB19 replication in different cell types, allowing structural protein expression in nonpermissive cells. PVB19 uptake into endothelial cells seems to be enhanced by an antibody‐mediated mechanism that involves a receptor for complement factor C1q .…”

“…Altered function of these cell types might be responsible for the occurrence of major adverse cardiac events (MACE) after coronary stenting in different ways, thus supporting the main observation of our paper. In particular, Anbarlou et al [39] have shown that miRNAs may be involved in regulation of PVB19 replication in different cell types, allowing structural protein expression in nonpermissive cells. PVB19 uptake into endothelial cells seems to be enhanced by an antibody-mediated mechanism that involves a receptor for complement factor C1q [40].…”

Viral Metagenomics of Blood Donors and Blood-Derived Products Using Next-Generation Sequencing

“…RBCU and PC are predominantly constituted of nonnucleated cells containing RNA of human/viral origin. For example, parvovirus B19 has a tropism for red blood cells [22], whereas dengue virus[23] and hepatitis C virus [24] can directly infect megakaryocytes and platelets, respectively. Residual plasma is more or less abundant in RBCU and PC and contains nucleic acids.…”