Abstract
African swine fever virus (ASFV) represents a severe threat to global agriculture with the world's domestic pig population reduced by a quarter following recent outbreaks in Europe and Asia. Like other nucleocytoplasmic large DNA viruses, ASFV encodes a transcription apparatus including a eukaryote-like RNA polymerase along with a combination of virus-specific, and host-related transcription factors homologous to the TATA-binding protein (TBP) and TFIIB. Despite its high impact, the molecular basis and temporal regulation of ASFV transcription is not well understood. Our lab recently applied deep sequencing approaches to characterise the viral transcriptome and gene expression during early and late ASFV infection. We have characterised the viral promoter elements and termination signatures, by mapping the RNA-5′ and RNA-3′ termini at single nucleotide resolution. In this review, we discuss the emerging field of ASFV transcripts, transcription, and transcriptomics.
Highlights
Introduction to African swine feverThe emergence of African Swine Fever (ASF), caused by African swine fever virus (ASFV), was first documented almost 100 years ago in Kenya after the disease transferred from warthogs to domestic pigs, which developed a highly lethal haemorrhagic fever; ASFV remains endemic in Sub-Saharan Africa [1]
The emergence of African Swine Fever (ASF), caused by ASFV, was first documented almost 100 years ago in Kenya after the disease transferred from warthogs to domestic pigs, which developed a highly lethal haemorrhagic fever; ASFV remains endemic in Sub-Saharan Africa [1]
Most differences between the genomes of virulent and attenuated lab strains reside in pathogenicity islands, often encoding genes belonging to multigene families (MGF) whose function remain poorly understood [11]
Summary
The emergence of African Swine Fever (ASF), caused by ASFV, was first documented almost 100 years ago in Kenya after the disease transferred from warthogs to domestic pigs, which developed a highly lethal haemorrhagic fever; ASFV remains endemic in Sub-Saharan Africa [1]. Research on attenuated virus-based vaccines, carrying deletions of virulence-associated genes, show promise, but have not yet been exploited commercially. Nor is it clear whether they can be developed and applied in time to circumvent further demise of domesticated pig populations [6]. Most differences between the genomes of virulent and attenuated lab strains reside in pathogenicity islands, often encoding genes belonging to multigene families (MGF) whose function remain poorly understood [11]
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