Autophagy is activated by virus-driven energy theft. Click on the term “Autophagy” That fact is clear in the diagram of systems complexity and in my model.
A key question in virology, that is potentially answerable using paleovirological analyses, is what caused the elimination of extinct viral lineages?
The selection pressures acting on hsaHTenv, its orthologs and progenitors might have been complex. Loss of fusogenicity but retention of receptor binding activity are, in a sense, opposing influences in terms of maintenance of the ORF and its function. Moreover, although some purifying selective pressure (low dN/dS) can be detected in hsaHTenv and its orangutan ortholog, a relaxation of those forces might be expected to have occurred after HERV-T extinction, perhaps leading to reduced antiviral activity observed in modern hsaHTenv. Finally, as MCT-1 is a moncaboxylate transporter that is upregulated in human cancers (Halestrap, 2013), the ability of hsaHTenv to deplete MCT1 from cell surfaces may suggest an additional or alternative metabolism-related cellular or even anti-tumor functions and selective pressures. Such an activity might have continued to shape hsaHTenv sequence independent of anti-HERV-T activity. In either case, this study highlights the potential importance of ERV proteins as raw material for the innovation of new functions in human ancestors.
All energy-dependent cell type differentiation is receptor-mediated. The nutrient energy-dependent de novo creation of receptors in cell types links metabolic networks to genetic networks via RNA-mediated protein folding chemistry, which biophysically constrains virus-driven energy theft. The energy theft links viral replication to the degradation of messenger RNA and mutations, which are linked to all pathology.
Reported as: Virology: Pushing the envelope