The impact of Toxoplasma gondii on the mammalian genome

Abstract

Nobody doubts that infections have imposed specialisations on the mammalian genome. However sufficient information is usually missing to attribute a specific genomic modification to pressure from a specific pathogen. Recent studies on mechanisms of mammalian resistance against the ubiquitous protozoan parasite, Toxoplasma gondii, have shown that the small rodents presumed to be largely responsible for transmission of the parasite to its definitive host, the domestic cat, possess distinctive recognition proteins, and interferon-inducible effector proteins (IRG proteins) that limit the potential virulence of the parasite. The phylogenetic association of the recognition proteins, TLR11 and TLR12, with T. gondii resistance is weak, but there is evidence for reciprocal polymorphism between parasite virulence proteins and host IRG proteins that strongly suggests current or recent coevolution.

Adaptive and genetic evolution of Toxoplasma gondii: a host-parasite interaction

“…The original genetic diversity of T. gondii strains predominant in North America and Europe may have been very wide, although a recent increase in distribution of the domestic cat (an Old World species), since the sixteenth century, may have favored a specific subset of pre-adapted genotypes 10 . In addition, virulence profiles indicate more virulent strains in Central American and South American isolates, corroborating to a more diverse genotypic profile.…”

“…The mammalian genome has clearly been influenced by infection. The da Silva RC et al -Toxoplasma gondii atypical isolates extraordinary genomic complexity of the re-arranging receptors of lymphocytes, and the complex array of immune functions assembled in the mammalian major histocompatibility complex are indications of millions of years of pathogen pressure 10 .…”

“…Therefore, in response to the parasite's manipulation caused by the invasion of lesions sites, or biochemical signals, infected hosts show more active behavior, and reduced neophobic behavior, making the parasite more prone to completing its life cycle. T. gondii is able to determine a delicate balance between parasitism and the host's immune response, which is supported by the mode of infection, strain, immune and cytokine response, as well the interaction of host genes and parasite genes 10,11 , characterizing a behavioral manipulation, and conferring a selective advantage to T. gondii. In other words, T. gondii is an opportunistic parasite for humans and other animals (i.e., cats and dogs), as published before.…”

“…Humans, while abundantly and globally infected by T. gondii at a rate of over 1% per year of age, are inaccessible as prey for domestic cats 10 , as are other mammals or bird species. The parasite needs to control the progress of the infection.…”

“…The adaptive immune system shows little co-adaptation to different pathogens, at the genomic level; it is an anti-pathogenic machine. In this way, the allelic frequencies will depend on the ratio of the intensity of selection pressures of the parasites 10 . In this way, upcoming human and animals should focus on the correlation between the genome (mainly atypical isolates) and corresponding unusual clinical manifestations, emphasizing on longitudinal studies.…”