网范文：“Punctuated interpenetration and pathogen virulence ” 信息动态形式适用于生物之间互相贯通的视觉认知，凝结包括免疫功能嵌入社会和文化结构。这篇医学范文讲述的是艾滋病毒的问题，我们迭代参数,从认知凝结和病原体之间的直接交互,然后将略论扩展到二阶的突变机制。基于大偏差的措施,产生协同认知。我们认为,艾滋病毒和疟疾等进化的病原体,嵌入环境整体的生活和工作条件，可能构成选择性压力，触发疾病的发生。开始检查变异疟疾病理学，英语论文范文，和异性恋的艾滋病的传播。
艾滋病毒对免疫挑战,并躲避反击。恶性疟原虫从事类似的快速克隆抗原变异,主要机制是逃避宿主免疫系统的抗体介入。下面的范文进行论述。
Abstract
We apply an information dynamics formalism to the Levins and Lewontin vision of biological interpenetration between a ‘cognitive condensation’ including immune function embedded in social and cultural structure on the one hand, and an established, highly adaptive, parasite population on the other. We iterate the argument, beginning with direct interaction between cognitive condensation and pathogen, then extend the analysis to second order ‘mutator’ mechanisms inherent both to immune function and to certain forms of rapid pathogen antigenic variability.
The methodology, based on the Large Deviations Program of applied probability, produces synergistic cognitive/adaptive ‘learning plateaus’ that represent stages of chronic infection, and, for human populations, is able to encompass the fundamental embedding biological reality of culture omitted by other approaches. We conclude that, for ‘evolution machine’ pathogens like HIV and malaria, simplistic magic bullet ‘medical’ drug, vaccine, or behavior modification interventions which do not address the critical embedding context of overall living and working conditions may constitute selection pressures triggering adaptations in life history strategy resulting in marked increase of pathogen virulence.
Key words: adaptation, chronic infection, cognition, immune, interpenetration, mutator, phase transition, renormalization, virulence
Introduction
The first s in this series (Wallace and Wallace, 2017; Wallace, 2017a), began our examination of culturally-driven variation in malaria pathology and rates of heterosexual HIV transmission. HIV responds to immune challenge as an evolution machine, generating copious variation and hiding from counterattack in refugia at multiple scales of space, time, and population. P. falciparum engages in analogous rapid clonal antigenic variation, and cyto-adherence and sequestration in the deep vasculature, primary mechanisms for escaping from antibody-mediated mechanisms of the host’s immune system (e.g. Alred, 1998). Something much like the mutator mechanism, in the sense of Thaler (1999), or ‘second order selection’ in the sense of Tenallion et al. (2017), appears to generate antigenic variation in the face of immune attack for a large class of pathogens. On the other hand, recent work by DiNoia and Neuberger (2017) outlines the mechanisms by which the immune system’s antibody-producing B-cells engage in a secondorder fine tuning of antibody production through an exceedingly high rate of mutation-like transformations, a hypermutation which allows us to respond quickly and effectively to pathogens that we have encountered previously (Gearhart, 2017).
Many chronic infections, particularly those which cloak themselves in antigenic ‘coats of many colors’, are very often marked by distinct ‘stages’ over the course of the disease. For HIV this typically involves an initial viremia triggering an immune response which drives the virus into refugia during an extended asymptomatic period whose ending is characterized by the start of a third phase, AIDS. Malaria’s most evident ‘stages’ are expressed as explosive outbursts of rapid parasite replication which facilitate insect-mediated transmission between hosts. Such evasive pathogens presently account for a very large fraction of human deaths by infectious disease, and represent, for a broad range of organisms, the evolutionary success of multiple-stage chronicity as a life history strategy, in the particular context of rapid antigenic variation. Here we extend the earlier theoretical analysis of Wallace (2017a), which focused on infection as a sudden ‘perturbation’.
We will analyze how pathogen life history stages represent a kind of evolutionary punctuation (e.g. Eldredge, 1985) for chronic infection in the face of relentless immune and other selection pressure, both directly, as is the likely case for HIV, and by means of a ‘second order punctuation’ through the mutator mechanism (Thaler, 1999) associated with rapid antigenic variation, as is the case with malaria. Elsewhere we study clonal selection in tumorigenesis from a similar ‘second order’ perspective (Wallace, Wallace, and Wallace, 2017). Recently Adami et al. (2017) applied an information theoretic approach to conclude that genomic complexity resulting from evolutionary adaptation can be identified with the amount of information a gene sequence stores about its environment. Lewontin (2017) might be said to argue for something of a reverse process, in which environmental complexity is the amount of information organisms introduce into their environment as a result of their collective actions and interactions.
We shall find this to be a persuasive perspective. Wallace (2017b) has applied a Rate Distortion argument in the context of imposed renormalization symmetry to obtain evolutionary ‘punctuated equilibrium’ (Eldredge, 1985) as a consequence of Ademi’s mechanism. Here we use the more general Joint Asymptotic Equipartition Theorem to conclude that pathogenic adaptive response and coupled cognitive immune challenge will be jointly linked in chronic infection, and subject to a transient ‘punctuated interpenetration’ very similar to evolutionary punctuation. Multiple punctuated transitions, perhaps of mixed ‘order’, are seen as constituting shifts to the different stages of chronic infection.
Since the joint system of host and pathogen passes through such phase transition analogs fairly rapidly, and may be stable for a relatively long time thereafter – ‘piecewise adiabatic memoryless ergodic’ – this is very far indeed from ‘edge of chaos’ arguments which rather implausibly imprison biological systems at transition. Similarly, our approach can be said to subsume ‘self organized criticality’ approaches which see punctuated extinctions as generated entirely by forces internal to defined communities: biology may not be a pile of sand after all. Examining paths in parameter space for the renormalization properties of such transitions (i.e. ‘universality class tuning’ in the sense of Albert and Barabasi, 2017) produces a second order punctuation in the rate at which the selection pressure of the immune system imposes a distorted image of itself onto pathogen structure.
This is our version of the mutator, or what Tenallion et al. (2017) call ‘second order selection’. Recognizably similar matters have long been under scrutiny: interactions between the central nervous system (CNS) and the immune system, and between the genetic heritage and the immune system have become academically codified through journals with titles such as Neuroimmunology and Immunogenetics. Elsewhere (Wallace and Wallace, 2017) we introduce another complication by arguing that the culture in which humans are socially embedded also interacts with individual immune systems to form a composite entity that might well be labeled an immunocultural condensation, (ICC). It is, we will argue here, the joint entity of immune, CNS, and embedding sociocultural cognition which engages in orders of ‘punctuated interpenetration’ with an adaptive chronic infectious challenge. Similar arguments are already in the French literature (e.g. Combes, 2017). Before entering the formal thicket, it is important to highlight some general considerations.
First, the information theory approach we adopt is notorious for providing ‘existence theorems’ whose ‘representation’, to use physics jargon, is arduous. For example, although the Shannon Coding Theorem implied the possibility of highly efficient coding schemes as early as 1949, it took more than forty years for practical ‘turbo codes’ to be created. The program we propose is unlikely to be any less difficult. Second, we are invoking information theory variants of the fundamental limit theorems of probability. These are independent of exact mechanisms, but constrain the behavior of those mechanisms.
For example, although not all processes involve long sums of independent stochastic variables, those that do, regardless of the individual variable distribution, collectively follow a Normal distribution as a consequence of the Central Limit Theorem. Similarly, the games of chance in a Las Vegas casino are all quite different, but nonetheless the success of ‘strategies’ for playing them is strongly and systematically constrained by the Martingale Theorem, regardless of game details. We similarly propose that languages-on-networks and languages-that-interact, as a consequence of the limit theorems of information theory, will be subject to regularities of punctuation and ‘generalized Onsager relations’, regardless of detailed mechanism. Finally, just as we often impose parametric statistics, at least as a first approximation, on sometimes questionable experimental situations, relying on the robustness of the Central Limit Theorem to carry us through, here we will invoke a similar heuristic approach for our versions of the information theory limit theorems. We begin with a description of cognitive process, including Cohen’s (2017) immune cognition, in terms of an information source, a ‘language’ constrained by the Shannon-McMillan or Asymptotic Equipartition Theorem, and its Rate Distortion or Joint Asymptotic Equipartition and other variants for interacting sources.()
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