This may be partially explained by their different abilities in propagation and supporting viral replication and protein expression that would require more detailed studies.
Proviral factors are host proteins hijacked by viruses for processes essential for virus propagation such as cellular entry and replication.
The relevance of these findings is closely related to the role of apoptosis as a host cell mechanism which, in contrast to necrosis, limits viral replication, propagation, and inflammation [42], [43].
In addition, a previous computational study of HCV signaling pathways suggested a critical role for miRNAs in the replication, propagation, and latency of viruses in the host cell [ 10].
Because DNA oncoviruses rely on the cellular DNA replication machinery for propagation and most of them infect quiescent cells, which are not optimal for viral DNA replication, they evolved oncoproteins targeting the central cellular hubs regulating cell growth.
This mosaic organization is the product of the combination of a limited number of constitutive modules [ 17]: intracellular mobility modules (recombination and replication functions), intercellular mobility modules (transformation, phage propagation and conjugative transfer) and stability modules.
Analysis of EST abundance in a contig can provide insights to gene expression levels, although this information must be taken with caution due to cloning and replication bias resulting form library construction and propagation steps.
In metazoans, early replication has been correlated with gene transcription, and replication timing has been proposed to facilitate the propagation of alternative epigenetic chromatin states during chromosome duplication [12].
DNMT1 is a maintenance methylase that recognises and methylates hemi-methylated CpG dinucleotides during DNA replication allowing the propagation and conservation of the DNA methylation patterns through the future generations [ 14, 15].
DNA replication origins have not yet been identified in N. castellii, and we investigated the propagation of pRS306 and pRS316 plasmids, on which an S. cerevisiae centromere and replication origin are absent and present, respectively [ 23]. pRS306 and pRS316 were maintained at high copy number in N. castellii cells (>70 per cell; see Figure 3E).
