On 2017 Oct 02, Donald Forsdyke commented:

VIRAL REPRODUCTIVE ISOLATION WITHIN A COMMON HOST CELL

This otherwise admirable article (Hunter P, 2017) begins with the curious assertion that, "since they depend on their host for replication," then viruses cannot "be categorized as species on the basis of reproductive isolation." The latter prevents recombination between organisms and so forms the most generally accepted definition of species. Virus species whose members share a common host cell, and depend on that cell for their replication, are still able to retain their species individuality. Their members do not mutually destroy each other by recombinational blending of their genomes. They are reproductively isolated from each other.

When we compare two viral species that have a common host cell, with two viral species that, even within a common host, do not share a common cell, we would expect to observe a fundamental difference related to their reproductive isolation mechanisms. If that difference is found to apply to other viral pairs that occupy a common host cell, then a fundamental isolation mechanism has been identified.

Such a difference was first related to the base compositions of insect viruses (1), a then to the base compositions of herpes viruses (2). A more extreme example arose from studies of retroviruses that share a T-lymphocyte host. The AIDS virus (HIV1) and human T cell leukaemia virus (HTLV1), can be assumed to have evolved from a common ancestor. Differentiation of members of that ancestral species within a common host cell into two independent populations would have required some mechanism to prevent their blending. Thus, we see today a wide divergence in base compositions. HIV1 is one of the highest AT-rich species know. HTLV1 is one of the highest GC-rich species known (3). There is high differentiation of chromosomal nucleic acids.

In these viruses there has been no opportunity for other reproductive isolation mechanisms to supersede chromosomal mechanisms. Diffusible cytoplasmic products make the subsequent evolution of genic incompatibilities less likely, and being in a common host cell there is no equivalent of prezygotic isolation as conventionally understood (4).

1. Wyatt GR (1952) The nucleic acids of some insect viruses. J Gen Physiol 36:201-205. WYATT GR, 1952
2. Schachtel GA et al. (1991) Evidence for selective evolution of codon usage in conserved amino acid segments of human alphaherpesvirus proteins. J Mol Evol 33:483-494. Schachtel GA, 1991
3. Bronson EC, Anderson JN (1994) Nucleotide composition as a driving force in the evolution of retroviruses. J Mol Evol 38:506-532. Bronson EC, 1994
4. Forsdyke DR (1996) Different biological species broadcast their DNAs at different (G+C)% wavelengths. J Theoret Biol 178:405-417. Forsdyke DR, 1996% "wavelengths".")

On 2017 Oct 02, Donald Forsdyke commented:

VIRAL REPRODUCTIVE ISOLATION WITHIN A COMMON HOST CELL

This otherwise admirable article (Hunter P, 2017) begins with the curious assertion that, "since they depend on their host for replication," then viruses cannot "be categorized as species on the basis of reproductive isolation." The latter prevents recombination between organisms and so forms the most generally accepted definition of species. Virus species whose members share a common host cell, and depend on that cell for their replication, are still able to retain their species individuality. Their members do not mutually destroy each other by recombinational blending of their genomes. They are reproductively isolated from each other.

When we compare two viral species that have a common host cell, with two viral species that, even within a common host, do not share a common cell, we would expect to observe a fundamental difference related to their reproductive isolation mechanisms. If that difference is found to apply to other viral pairs that occupy a common host cell, then a fundamental isolation mechanism has been identified.

Such a difference was first related to the base compositions of insect viruses (1), a then to the base compositions of herpes viruses (2). A more extreme example arose from studies of retroviruses that share a T-lymphocyte host. The AIDS virus (HIV1) and human T cell leukaemia virus (HTLV1), can be assumed to have evolved from a common ancestor. Differentiation of members of that ancestral species within a common host cell into two independent populations would have required some mechanism to prevent their blending. Thus, we see today a wide divergence in base compositions. HIV1 is one of the highest AT-rich species know. HTLV1 is one of the highest GC-rich species known (3). There is high differentiation of chromosomal nucleic acids.

In these viruses there has been no opportunity for other reproductive isolation mechanisms to supersede chromosomal mechanisms. Diffusible cytoplasmic products make the subsequent evolution of genic incompatibilities less likely, and being in a common host cell there is no equivalent of prezygotic isolation as conventionally understood (4).

1. Wyatt GR (1952) The nucleic acids of some insect viruses. J Gen Physiol 36:201-205. WYATT GR, 1952
2. Schachtel GA et al. (1991) Evidence for selective evolution of codon usage in conserved amino acid segments of human alphaherpesvirus proteins. J Mol Evol 33:483-494. Schachtel GA, 1991
3. Bronson EC, Anderson JN (1994) Nucleotide composition as a driving force in the evolution of retroviruses. J Mol Evol 38:506-532. Bronson EC, 1994
4. Forsdyke DR (1996) Different biological species broadcast their DNAs at different (G+C)% wavelengths. J Theoret Biol 178:405-417. Forsdyke DR, 1996% "wavelengths".")