  Extreme enrichment of the human immunodeficiency virus (HIV-1) RNA genome for
the purine A parallels the mild purine-loading of the RNAs of most organisms.
This should militate against loop-loop "kissing" interactions between the
structured viral genome and structured host RNAs, which can generate segments
of double-stranded RNA sufficient to trigger intracellular alarms. However,
human T cell leukaemia virus (HTLV-1), with the potential to invade the same
host cell, shows extreme enrichment for the pyrimidine C. Assuming the low GC%
HIV and the high GC% HTLV-1 to share a common ancestor, it was postulated that
differences in GC% arose to prevent homologous recombination between these
emerging lentiviral species. Sympatrically isolated by this intracellular
reproductive barrier, prototypic HIV-1 seized the AU-rich (low GC%) high ground
(thus committing to purine A rather than purine G). Prototypic HTLV-1 forwent
this advantage and evolved an independent evolutionary strategy. Evidence
supporting this hypothesis since its elaboration in the 1990s is growing. The
conflict between the needs to encode accurately both a protein, and nucleic
acid structure, is often resolved in favour of the nucleic acid because, apart
from regulatory roles, structure is critical for recombination. However, above
a sequence difference threshold, structure (and hence recombination) is
impaired. New species can then arise.
