Norman R, Begon M, Bowers R G
Department of Applied Mathematics and Theoretical Physics, University of Liverpool, England.
Theor Popul Biol. 1994 Aug;46(1):96-119. doi: 10.1006/tpbi.1994.1021.
The models of Anderson and May on the dynamics of vertebrate (1979, Nature 280, 361-367) and invertebrate (1981, Philos, Trans. R. Soc. 291, 451-524) populations and their microparasites have been extended and elaborated. Hence, in a series of models the effects of a range of biological factors have been considered. These models taken together clarify in particular the effects of recovery from the disease back to a state of susceptibility and the additional effects of recovery to a state of immunity. In general recovery increases both the threshold density and the equilibrium density but does not alter the prevalence of infection or the region in parameter space in which the host is regulated. Immunity causes a further increase in the equilibrium density, does not alter either the prevalence of infection or the threshold density, but reduces the region in which there is regulation. In both cases exceptions tend to occur when there is density dependence.
安德森和梅关于脊椎动物（1979年，《自然》280卷，361 - 367页）和无脊椎动物（1981年，《皇家学会哲学学报》291卷，451 - 524页）种群及其微寄生虫动力学的模型已得到扩展和细化。因此，在一系列模型中考虑了一系列生物因素的影响。这些模型共同特别阐明了从疾病恢复到易感性状态的影响以及恢复到免疫状态的额外影响。一般来说，恢复既增加了阈值密度又增加了平衡密度，但不会改变感染率或宿主受到调节的参数空间区域。免疫会使平衡密度进一步增加，既不改变感染率也不改变阈值密度，但会缩小存在调节的区域。在这两种情况下，当存在密度依赖性时往往会出现例外情况。
