Foot-and-mouth disease virus(FMDV) rapidly causes cytopathic effects in susceptible cells. Incomplete viral clearance during the acute infection leads to persistent infection. The relationship between host gene expression and the persistent infection remains unclear. In this study, we analyzed the transcriptome profiles of BHK-21 cells acutely and persistently infected with FMDV to identify differences in gene expression. GO and KEGG enrichment analyses showed that the 8,378 differentially expressed genes were significantly enriched in categories including metabolism, biosynthesis, ribosome function, and endocytosis. In persistently infected BHK-21 cells, ribosome-and translation-related genes were significantly down-regulated. There were more differentially expressed immune-related genes during persistent infection than during acute infection. Two hundred and seventy-four genes were differentially expressed in both acutely and persistently infected BHK-21 cells. Among these genes, heat shock protein family B member 1(Hspb1) knockdown significantly inhibited FMDV replication. Our research provides a basis for further research to understand the mechanisms of persistent FMDV infection including the genes involved in FMDV replication.
Kaposi's sarcoma-associated herpesvirus(KSHV) is a double stranded DNA virus.It was found to be related to Kaposi's sarcoma(KS),primary effusion lymphoma(PEL) and multicentric Castleman's disease(MCD),which cause severe illness in AIDS patients.As a member of human herpesvirus family,KSHV displays two distinct phases in its life cycle,the default latent and lytic replication phase.Following primary infection,the virus can quickly establish latent infection in the host.However,it is still not fully understood up to date how KSHV establishes and maintains viral latency in the host cells.KSHV mainly infects endothelial cells in the host,promoting proliferation and angiogenesis.Abundant angiogenesis is the key feature of KS and is the critical factor for KS progression.The mechanism of KSHV mediated pathogenesis is also largely unknown.In this review,we summarize the recent progress in the mechanisms of KSHV latency and pathogenesis,with particular views from our work.
