The balance of power between HIV and the immune system

McLean, Angela R.

doi:10.1016/0966-842x(93)90018-m

Cited by 30 publications

(6 citation statements)

References 34 publications

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“…4. The Associated model underlies a few of recent suggestions for HIV virulence (reviewed nicely by McLean 1993). The course of an HIV infection follows the curious pattern of exhibiting two viremias, a brief one within a few months of acquiring the virus, and another much longer one years later during AIDS and AIDS Related Complex.…”

Section: Ila the Associated Modelmentioning

confidence: 98%

Perspective: Virulence

Bull¹

1994

Evolution

386

277

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Why do parasites harm their hosts? Intuition suggests that parasites should evolve to be benign whenever the host is needed for transmission. Yet a growing theoretical literature offers several models to explain why natural selection may favor virulent parasites over avirulent ones. This perspective first organizes these models into a simple framework and then evaluates the empirical evidence for and against the models. There is relatively scant evidence to support any of the models rigorously, and indeed, there are only a few unequivocal observations of virulence actually evolving in parasite populations. These shortcomings are surmountable, however, and empirical models of host-parasite interactions have been developed for many kinds of pathogens so that the relevant data could be acquired in the near future.

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Section: Ila the Associated Modelmentioning

confidence: 98%

Perspective: Virulence

Bull¹

1994

Evolution

386

277

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“…The progression from widespread infection but few symptoms to the later, lethal stages of immunodeficiency is not fully understood. Levin and Bull summarize three models that can explain the course of infection and disease: (i) more virulent HIVs evolve within the host (Miedema et al 1990), (ii) HIV variation accumulates and eventually exceeds a "diversity threshold" beyond which the immune system cannot control the viral population (Nowak et al 1991), and (iii) mutant viruses arise that cannot be recognized by the immune system (McLean 1993).…”

Section: Dynamics Of Parasite Populations Within Hostsmentioning

confidence: 99%

Models of Parasite Virulence

Frank

1996

The Quarterly Review of Biology

1,241

1,305

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Several evolutionary processes influence virulence, the amount of damage a parasite causes to its host. For example, parasites are favored to exploit their hosts prudently to prolong infection and avoid killing the host. Parasites also need to use some host resources to reproduce and transmit infections to new hosts. Thus parasites face a tradeoff between prudent exploitation and rapid reproduction-a life history tradeoff between longevity and fecundity. Other tradeoffs among components of parasite fitness also influence virulence. For example, competition among parasite genotypes favors rapid growth to achieve greater relative success within the host. Rapid growth may, however, lower the total productivity of the local group by overexploiting the host, which is a potentially renewable food supply. This is a problem of kin selection and group selection. I summarize models of parasite virulence with the theoretical tools of life history analysis, kin selection, and epidemiology. I then apply the theory to recent empirical studies and models of virulence. These applications, to nematodes, to the extreme virulence of hospital epidemics, and to bacterial meningitis, show the power of simple life history theory to highlight interesting questions and to provide a rich array of hypotheses. These examples also show the kinds of conceptual mistakes that commonly arise when only a few components of parasite fitness are analysed in isolation. The last part of the article connects standard models of parasite virulence to diverse topics, such as the virulence of bacterial plasmids, the evolution of genomes, and the processes that influenced conflict and cooperation among the earliest replicators near the origin of life.

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“…You would be better placed to compare theories about the maintenance of peripheral tolerance. The formulation of hypotheses on the pathogenesis of infectious agents like human immunodeficiency virus and human T-cell leukemia virus I and of T-cell-mediated autoimmune disorders would also be helped (1,2). In short, not knowing whether T lymphocytes usually live for weeks or months or years is an important gap in our knowledge.…”

mentioning

confidence: 99%

In vivo estimates of division and death rates of human T lymphocytes.

McLean

Michie

1995

Proc. Natl. Acad. Sci. U.S.A.

248

135

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We present data on the decay, after radiotherapy, of naive and memory human T lymphocytes with stable chromosome damage. These data are analyzed in conjunction with existing data on the decay of naive and memory T lymphocytes with unstable chromosome damage and older data on unsorted lymphocytes. The We use two data sets from which to estimate life-history parameters of human T lymphocytes in vivo. Both come from cross-sectional studies of the number of lymphocytes with radiation-induced chromosomal damage. The data of Buckton et at (6) record the proportion of lymphocytes with stable and unstable damage in men given radiation therapy as treatment for ankylosing spondylitis. The data of Michie (7) record the proportion of T lymphocytes of primed and unprimed subsets with stable and unstable damage. By using these two data sets, we are able to estimate death rates, proliferation rates, and interconversion rates for primed and unprimed T lymphocytes. We then use these rate estimates as parameters for a simple mathematical model of the population dynamics of peripheral T cells. Investigation of the behavior of this simple model allows us to make some inferences about the broader implications of the data. METHODSBuckton's Data. Full details concerning the methods for collecting these data are given in the original paper (6). We give a brief summary. One hundred and twenty-nine venous blood samples were taken from 66 men between 0 and 3700 days after they had received x-ray treatment for ankylosing spondylitis. Chromosome preparations were made from lymphocytes and classified into groups by the method of Buckton and Pike (4). Data were then aggregated into 14 groups of 8-12 observations. Only the aggregated data were reported and it is these aggregated data that we use. Although Buckton's samples must have contained small numbers of B cells, we assume that they are present in such small proportions that we can ignore them. We therefore treat Buckton's data (6)

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The balance of power between HIV and the immune system

Cited by 30 publications

References 34 publications

Perspective: Virulence

Perspective: Virulence

Models of Parasite Virulence

In vivo estimates of division and death rates of human T lymphocytes.

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