Titlebook: Infection, Polymorphism and Evolution; W. D. Hamilton,J. C. Howard Book 1997 The Royal Society 1997 behavior.evolution.immunity.immunology

蓋他為秘密

Recognition and polymorphism in host-parasite genetics,y this method may be a poor guide to the actual polymorphism and to the underlying biochemistry of host-parasite recognition. The problem of using detectable polymorphism to infer the true nature of recognition and polymorphism is exacerbated by non-equilibrium fluctuations in allele frequencies tha

冥想后

osteopath

衍生

環(huán)形

Infectious diseases, reproductive effort and the cost of reproduction in birds,und between secondary sexual characters and infection parameters. For brood-size-manipulated birds there was a significant interaction between experimentally increased reproductive effort and parasitic infection rate with regard to both current and future fecundity. It seems possible that the intera

慟哭

Evolution of mutation rate and virulence among human retroviruses,ion. Because rapid replication and high mutation rate probably contribute to rapid progression of infections to aids, the interplay of sexual activity, replication rate, and mutation rate helps explain why HIV-1 has only recently caused a lethal pandemic, even though molecular data suggest that it m

一瞥

,Gene-for-gene recognition in plant—pathogen interactions,metimes comprising genes involved in the recognition of more than one taxonomically unrelated pathogen. For some genes, alleles with different recognition capabilities have been identified while there is also evidence for the existence of genes expressing identical recognition capability present at

誘使

MHC polymorphism and parasites,d became very virulent have had little effect. The latter category includes micro- and macroparasites responsible for the major human infectious diseases. This hypothesis explains why no convincing association between human leucocyte antigen (.) alleles and resistance to infectious disease can thus

Dysplasia

Natural selection at the class II major histocompatibility complex loci of mammals,ample, diverged before all other known mammalian class II loci, possibly before the divergence of tetrapods from bony fishes. Analysis of the patterns of sharing of polymorphic residues at class II MHC loci by mammals of different species revealed that extensive convergent evolution has occurred at

ETCH

The role of infectious disease, inbreeding and mating preferences in maintaining MHC genetic diversypotheses we measured the fitness consequences of both experimentally manipulated levels of inbreeding and MHC homozygosity and heterozygosity in semi-natural populations of wild-derived house mice. We were able to measure a fitness decline associated with inbreeding, but were unable to detect fitne