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Chapter 16 : Retrovirus Variation and Evolution

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Abstract:

In this chapter, the author discusses two topics: the long-term association of virus and host as revealed by the study of endogenous proviruses and the short-term "evolution" that characterizes the association of some viruses, most notably human immunodeficiency virus (HIV), with their host. Ancient endogenous proviruses were inserted into the germ line of a species prior to separation of that species from related species. To understand the host-provirus relationship better, the proviruses of mice is chosen as a model, in particular the C-type proviruses, which form the largest group related to known viruses. In some species of mice, the predominant endogenous proviruses are recombinant relative to those that had been studied in laboratory mice. Infection of the germ line is a rare event, yet endogenous proviruses have many times been independently fixed in the genomes of mice and other species. A final point concerning the evolution of endogenous viruses is an interesting correlation between virus lifestyle and endogenization. Retroviruses differ considerably in the amount of genetic variation observed among individuals within species. Divergence of up to 25% within the most variable regions (in ) has been observed, even when infection was initiated with known clonal virus. These observations are consistent with the evolution of HIV in vivo into a complex quasispecies. The high rate of replication of HIV during the entire course of the infection has important consequences for understanding genetic variation and its role in evolution, pathogenesis, and therapy.

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16

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Figures

Image of Figure 1
Figure 1

Polymorphism among endogenous murine leukemia viruses. The provirus maps show linked sequence differences useful for distinguishing the four groups. These include sequences in and the long terminal repeat that generate useful oligonucleotide probes, restriction site polymorphisms, receptor utilization differences, and an insertion of a small transposable element into the long terminal repeat ( ). emv, ecotropic murine virus; pmv, polytropic murine virus; mpmv, modified polytropic murine virus; xmv, xenotropic murine virus.

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Image of Figure 2
Figure 2

Mapping of endogenous murine leukemia viruses. All polytropic, modified polytropic, and xenotropic proviruses were mapped onto the mouse genome by using the proviral DNA distribution in recombinant inbred and intercross mice. The proviruses are shown on the left side of each chromosome, and standard markers are shown on the right side ( ).

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Figure 3

Distribution of some endogenous proviruses among common inbred strains of mice. The chart on the right depicts the relationships of some strains inferred from the historical record ( ).

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Image of Figure 4
Figure 4

Phylogeny of inbred strains. (Left) Tree derived from the endogenous provirus distribution by using PAUP ( ); (right) relationships of inbred strains derived by analysis of biochemical polymorphisms ( ). Branches depicted by heavy lines are consistent with the historical record.

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Image of Figure 5
Figure 5

Phylogeny of retroviruses. The figure shows a phylogenetic tree based on comparison of reverse transcriptases and relating the presently defined genera ( ) (listed on the left). Heavy curved arrows indicate probable recombination events. Retrovirus genera with endogenous members are shown in boldface. MLV, murine leukemia virus; ALV, avian leukemia virus; HSRV, human spuma-retrovirus; HERV-C, human endogenous retrovirus C; EIAV, equine infectious anemia virus; SMRV, squirrel monkey retrovirus; IAP, intracisternal A particle; RSV, Rous sarcoma virus; BLV, bovine leukemia virus; HTLV, human T-lymphotropic leukemia virus.

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Image of Figure 6
Figure 6

Protocol for in vitro rapid passage of Rous sarcoma virus. A biologically cloned sample of the Prague strain of Rous sarcoma virus (subgroup B) was subjected to undiluted passage in cultures of chicken embryo fibroblasts (CEF) every 3 to 4 days. At selected passages, a sample was taken for analysis, initially by quantitative RNase T1 fingerprinting (30) and later by PCR amplification, cloning, and sequencing of a selected region on ( ).

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Figure 7

Selected changes in the Rous sarcoma virus genome as a function of passage. (Top) Biological properties: transformation (measured by focus assay) and cytopathicity (measured by plaque assay); (bottom) genome changes measured by quantitative fingerprinting, including loss of the gene, overgrowth of a highly defective variant, and appearance of selected point mutations in the SU portion of ( ).

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Image of Figure 8
Figure 8

Selected point mutations in the Rous sarcoma virus gene. The region of the SU portion of shown in the top lines was amplified, cloned, and sequenced from selected passages of the experiment shown in Fig. 6 and 7 . The two most prominent selected changes are indicated in the nucleotide and amino acid sequences shown at the bottom, and the same region from a number of avian leukemia virus isolates of chickens and pheasants is shown for comparison. RAV-1, Rous-associated virus-1; Pr-C, Prague strain RSV, subgroup C; SR-D, Schmidt-Ruppin RSV, subgroup D; RPV-F, ring-necked pheasant virus, subgroup F.

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Figure 9

Genetic change as a function of time in Rous sarcoma virus passaged in vitro and SIV growing in vivo. The genetic distance of the passaged virus from the experiment shown in Fig. 6 was calculated from the sequences of at least 50 clones from each selected passage (closed circles). For comparison, the data of Burns and Desrosiers ( ) for molecularly cloned SIV growing in monkeys are shown by open circles.

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Image of Figure 10
Figure 10

Effect of mutation and selection on a virus population. The curves were obtained by a simple computer simulation in which the frequency of a given mutation was incremented by the effects of forward mutation () and selective advantage (5 if positive), and decremented by reverse mutation (assumed to be equal to ) and .v (if negative). (A) Effect of varying from 10 to 10 while holding .5 constant at 10; (B and C) effects of varying positive (B) and negative (C) s while holding constant at 10 ( ).

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Figure 11

Kinetics of HIV infection after inhibitor treatment in vivo. Shown is a compilation of data from a number of studies ( ) in which the concentration of virus (as genome RNA) and the CD4 cell number were monitored after administration of one of a number of (nucleoside or nonnucleoside) reverse transcriptase or protease inhibitors ( ). wt, wild type.

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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Image of Figure 12
Figure 12

Types of HIV-infected cells in vivo. At steady state, the rate of creation of each cell type by infection matches its rate of death, and the overall rate of replenishment matches the death rates of all types combined. The horizontal axis is labeled “time” to indicate that at steady state, the number of cells in each state (nonproducing or virus producing) is proportional to the time spent in that state ( ).

Citation: Coffin J. 1995. Retrovirus Variation and Evolution, p 221-244. In Cooper G, Temin R, Sugden B (ed), The DNA Provirus. ASM Press, Washington, DC. doi: 10.1128/9781555818302.ch16
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