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• KSHV is etiologically associated with KS, MCD, and PEL. • MicroRNAs (miRNAs) are a class of highly conserved small non-coding RNAs. • miRNAs are gene regulators for about 60% of protein-coding genes. • miRNAs regulate KSHV entry, lytic cycle, and latent phase of replication. Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent of Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman Disease (MCD). Recent mechanistic advances have discerned the importance of microRNAs in the virus–host relationship. KSHV has two modes of replication: lytic and latent phase. KSHV entry into permissive cells, establishment of infection, and maintenance of latency are contingent upon successful modulation of the host miRNA transcriptome. Apart from host cell miRNAs, KSHV also encodes viral miRNAs. Among various cellular and molecular targets, miRNAs are appearing to be key players in regulating viral pathogenesis. Therefore, the use of miRNAs as novel therapeutics has gained considerable attention as of late. This innovative approach relies on either mimicking miRNA species by identical oligonucleotides, or selective silencing of miRNA with specific oligonucleotide inhibitors. Here, we provide an overview of KSHV pathogenesis at the molecular level with special emphasis on the various roles miRNAs play during virus infection. [ABSTRACT FROM AUTHOR]

• Expression patterns of 10 DEGs were diametrically opposite in Z8R and Z8S group. • DHAV-3 infection results in cell growth suppression may be associated with IFITM1. • Conserved regions of IFITM1 (213–317 bp) could affected the cell cycle of DEF cells. Duck viral hepatitis (DVH) has a significant economic impact on duck industry, and duck hepatitis A virus genotype 3 (DHAV-3) is the most prevalent pathogen of DVH in Asian duck industry. The detailed study connecting differentially expressed genes (DEGs) and the differential resistance to DHAV-3 have not been accurately described, although a large numbers of DEGs have been identified by transcriptomic studies. Here, a resistant Pekin duck line (Z8R) and a susceptible Pekin duck line (Z8S) as models, high mortality and dramatically increased aspartate aminotransferase (AST), alanine aminotransferase (ALT) and the expression of immune-related genes of Z8S group were shown to be noticeable signs of cases caused by DHAV-3 infection. Compared with the control (Con) group, 1117 down-regulated DEGs and 612 up-regulated DEGs were found in the Z8S group and 37 down-regulated DEGs and 82 up-regulated DEGs were found in the Z8R group. Ultimately, the expression patterns of 10 DEGs were found to be diametrically opposite in Z8R and Z8S group. Functional analysis revealed that IFITM1 was associated with cell growth suppression, which was considered a key candidate gene. Results of flow cytometry showed that the conserved regions of IFITM1 (213–317 bp) could affected the cell cycle of duck embryo fibroblast (DEF) cells after infection with DHAV-3. Transcriptome and western blot analysis suggested that the CCND1, CCNE1 and CDK6 were significantly up-regulated in susceptible ducks by comparing with Con group. The hepatic injury and pathogenic outcomes caused by DHAV-3 infection were more severe in Z8S group compared to Z8R. Results of transcriptomics analysis and flow cytometry suggested that DHAV-3 infection can induce cell cycle changes that may be associated with IFITM1 expression level. These data will greatly enhance our understanding of the pathogenesis of DHAV-3 infection in ducklings and have implications for development of resistance breeding. [ABSTRACT FROM AUTHOR]

Porcine reproductive and respiratory syndrome virus (PRRSV) has been recognized to modulate the innate immune response of host. However, little is known about the effects of PRRSV infection on porcine intrinsic virus-restriction factors. This study presents the first demonstration that the nonstructural protein 3 (Nsp3) or envelope (E) protein of PRRSV interacted with porcine intrinsic virus-restriction factor IFITM1 or Tetherin. Next, in PRRSV-infected MARC-145 cells and the transfected cells with the IFITM1- or Tetherin-expressing plasmid, IFITM1 was shown to be mainly distributed perinuclear, and Tetherin was proposed to be partially removed away from cell surface. Moreover, the overexpression of IFITM1 and Tetherin were shown to have no obvious effects on the replication of PRRSV in MARC-145 cells. The Nsp3 of PRRSV was demonstrated to induce the proteasome-dependent degradation of IFITM1 upon PRRSV infection. These findings suggest that PRRSV might counteract the antiviral functions of IFITM1 and Tetherin by the interaction of the Nsp3 with IFITM1 and the E protein with Tetherin, providing a novel clue for exploring possible mechanisms associated with the evasion of PRRSV from immune recognition of host. [ABSTRACT FROM AUTHOR]