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JUNK DNA SAVED THE HOST. "The presence of incomplete viral elements in host genomes are not simply the remnants of past viral infection and disease (virus sweeps), but should be considered as the savior of the host lineage by providing the capacity for self regulation and persistence of viruses that can still threaten related species. Virus persistence provides a large selective advantage in the virosphere." https://lnkd.in/etdQ9rN View in LinkedIn

OPPOSING LYTIC INFECTION. "Even ‘defective’ (and parasitic) components of viruses (and transposons) can express virus-specific regulatory (opposing) molecules (including ncRNA), clearly promote virus–host persistence, and respond to oppose lytic virus infection." https://lnkd.in/etdQ9rN View in LinkedIn

VIRAL DRIVER. "I am asserting that most initial genetic and selective events that transform host regulatory complexity are usually ‘pushed’ by virus action in a general direction of increasing complexity. In this way, viruses present an omnipresent and ancient issue." https://lnkd.in/etdQ9rN View in LinkedIn

PERFECT EVOLUTIONARY SUBSTRATE. "Viruses possess all the advantages of evolution relative to host: extreme genetic adaptability, extreme diversity, extreme numbers, extreme rates of genetic exchange, tolerance for ‘unfit’ variation, and the ability to reassemble from cryptic or ‘dead’ parts. They can transition between the chemical and living world." http://onlinelibrary.wiley.com/doi/10.1111/apm.12485/full View in LinkedIn

VIRAL EDITORS OF HOST SYSTEMS. "The concept is that viruses are fully competent agents and editors of all host systems of instruction (DNA, RNA, epigenetic, translational etc.). Thus, they provide the host with new sources of instruction systems (not errors). In addition, they promote network formation by providing coherent societies (quasispecies populations) of agents able to edit host code content (and add new identity) in a diffuse, distributed manner, which promotes the creation of and editing of host regulatory networks." http://onlinelibrary.wiley.com/doi/10.1111/apm.12485/full View in LinkedIn

NEW EXPLANATIONS NEEDED. “Clearly, our results contradict the ‘molecular piracy hypothesis’ where viral genes are assumed to be transferred from their hosts; thus alternative explanations are required.” https://lnkd.in/dsexZC2 View in LinkedIn

POTASSIUM CHANNELS. “The viral K+ channels are small and basically consist of the pore module shared by all K+ channels. Our analyses indicate that viral-encoded K+ channel proteins do not have a close phylogenetic relationship with their host-encoded K+ channel proteins. A similar scenario was recently discovered for a chlorovirus encoded cation transporter which occurs in different virus species independent of their host.” https://lnkd.in/dsexZC2 View in LinkedIn

VIRAL GENE SWAPS. “Hence their ancestor probably exchanged vast pools of genetic elements horizontally and generated a reticulated network of genes at an early stage of their evolution. This view is consistent with the genetics of phycodnavirus evolution as these viruses have both prokaryotic and eukaryotic homologs in addition to many other genes with no cellular homologs.” https://lnkd.in/dsexZC2 View in LinkedIn

STILL CONSIDERED NEUTRAL. "Synonymous variation is therefore still often thought to lack any major functional or evolutionary importance." https://lnkd.in/dU2Q65U View in LinkedIn

HORIZONTAL NOT VERTICAL. “Comparative genomics studies further suggest that virus evolution can best be understood in terms of reticulated ‘trees’ and mosaic evolution. This means that large DNA viruses fundamentally have a network-based history that does not trace back to a single gene or set of genes.” https://lnkd.in/dsexZC2 View in LinkedIn