生物多样性与传染性疾病的关系: 进展、挑战与展望

在全球生物多样性快速丧失的背景下, 理解生物多样性如何影响传染性疾病风险具有重要意义。大量研究表明, 宿主多样性对传染性疾病可能存在稀释效应(即疾病风险随宿主生物多样性的增加而降低), 但是也有放大效应或者没有影响的证据。本文首先介绍了关于生物多样性与传染性疾病关系的研究进展, 以及该领域的热点研究问题, 包括宿主多样性-疾病关系的格局和空间依赖性、稀释效应的体系依赖性和系统发育稀释效应等。随后,介绍了相关研究伴随的争议和批判, 主要集中在: 稀释效应发生的普遍性、生物多样性-疾病关系实验研究的发表偏好性以及部分疾病生态学家对生物多样性和传染性疾病之间简单数字关系的过分关注。最后指出稀释效应与物种共存、全球变化对稀释效应的影响、进化与稀释效应、稀释效应在政策制定中的应用等领域可能是今后的主要研究方向。     

Does life history mediate changing disease risk when communities disassemble?

Biodiversity loss sometimes increases disease risk or parasite transmission in humans, wildlife and plants. Some have suggested that this pattern can emerge when host species that persist throughout community disassembly show high host competence – the ability to acquire and transmit infections. Here, we briefly assess the current empirical evidence for covariance between host competence and extirpation risk, and evaluate the consequences for disease dynamics in host communities undergoing disassembly. We find evidence for such covariance, but the mechanisms for and variability around this relationship have received limited consideration. This deficit could lead to spurious assumptions about how and why disease dynamics respond to community disassembly. Using a stochastic simulation model, we demonstrate that weak covariance between competence and extirpation risk may account for inconsistent effects of host diversity on disease risk that have been observed empirically. This model highlights the predictive utility of understanding the degree to which host competence relates to extirpation risk, and the need for a better understanding of the mechanisms underlying such relationships.     

植物遗传多样性与生态系统功能关系的研究进展

全球变化和人类活动导致物种生境的萎缩, 造成很多植物种群数量缩减, 遗传多样性快速丧失。对于物种多样性低的生态系统, 优势种的遗传多样性可能比物种多样性对生态系统功能产生更大的影响。因此, 了解遗传多样性和生态系统功能的关系(GD-EF)及其机制对生物多样性保护、应对环境变化和生态修复具有指导意义。该文综述了植物遗传多样性对生态系统结构(高营养级生物群落结构)和生态系统功能(初级生产力、养分循环和稳定性)的影响及机制、功能多样性对GD-EF的影响、遗传多样性效应和物种多样性效应的比较, 以及GD-EF在生态修复等实际应用的研究进展。最后指出当前研究的不足之处, 以期为后续研究提供参考: 1)还需深入研究GD-EF机制; 2)未评估遗传多样性对生态系统多功能性的影响; 3)不同遗传多样性测度对生态系统功能的影响不明确; 4)缺少长期的和多空间尺度结合的GD-EF实验; 5)遗传多样性效应相对于其他因子的作用不清楚。     

When are pathogen dynamics likely to reflect host population genetic structure?

Does the structure and connectivity of host populations influence the dynamics and evolution of their pathogens? This topical question is the essence of research investigating the ecology of a Pteropus fruit bat and its zoonotic Nipah virus (NiV) published by Olival et al. in this issue of Molecular Ecology. Questioned less overtly, but nonetheless implicit to the study, is “what are the mechanisms underpinning intraspecific host–pathogen congruence (IHPC) of genetic structure?”. Olival et al. investigated the phylogeographical structure of Pteropus medius and NiV isolates across Bangladesh, from areas inside and outside of the Nipah belt—an area where most human spillover events occur. A high degree of host panmixia was discovered, with some population differentiation east of the Nipah belt. NiV genetic structure was congruent with the host. The authors attributed the panmixia and structuring, respectively, to (a) the highly vagile nature of P. medius, and (b) possible differences between bioregions within and outside the Nipah belt. Other potential explanatory mechanisms were acknowledged, including hybridization and transmission mode. This study makes a valuable contribution to a growing body of literature examining IHPC. This has implications not only for pathogen spillover to humans and domestic animals, but more generally for thinking about the mechanisms that underlie patterns of host and pathogen genetic associations.     

Host community structure and the maintenance of pathogen diversity

Community structure has been widely identified as a feature of many real-world networks. It has been shown that the antigenic diversity of a pathogen population can be significantly affected by the contact network of its hosts; however, the effects of community structure have not yet been explored. Here, we examine the congruence between patterns of antigenic diversity in pathogen populations in neighbouring communities, using both a deterministic metapopulation model and individual-based formulations. We show that the spatial differentiation of the pathogen population can only be maintained at levels of coupling far lower than that necessary for the host populations to remain distinct. Therefore, identifiable community structure in host networks may not reflect differentiation of the processes occurring upon them and, conversely, a lack of genetic differentiation between pathogens from different host communities may not reflect strong mixing between them.