Molecular mechanisms of pathogenicity: how do pathogenic microorganisms develop cross-kingdom host jumps?

Abstract

It is common knowledge that pathogenic viruses can change hosts, with avian influenza, the HIV, and the causal agent of variant Creutzfeldt-Jacob encephalitis as well-known examples. Less well known, however, is that host jumps also occur with more complex pathogenic microorganisms such as bacteria and fungi. In extreme cases, these host jumps even cross kingdom of life barriers. A number of requirements need to be met to enable a microorganism to cross such kingdom barriers. Potential cross-kingdom pathogenic microorganisms must be able to come into close and frequent contact with potential hosts, and must be able to overcome or evade host defences. Reproduction on, in, or near the new host will ensure the transmission or release of successful genotypes. An unexpectedly high number of cross-kingdom host shifts of bacterial and fungal pathogens are described in the literature. Interestingly, the molecular mechanisms underlying these shifts show commonalities. The evolution of pathogenicity towards novel hosts may be based on traits that were originally developed to ensure survival in the microorganism's original habitat, including former hosts.

TheCladosporium fulvumVirulence Protein Avr2 Inhibits Host Proteases Required for Basal Defense

“…Several virulence targets of Avr2 were identified both in Arabidopsis and in tomato, while increased susceptibility toward some of the same pathogens was demonstrated. This not only suggests that basal defense responses in different plant species are highly conserved but also that effector targets of different pathogens with diverse hosts may be orthologs (van Baarlen et al, 2007).…”

Pathogenesis of Chagas' Disease: Parasite Persistence and Autoimmunity

“…Parasite latency is an active process regulated by an initiation factor (␣ subunit of eukaryotic initiation factor 2 [eIF2␣]) kinase (IK2), the cell cycle of which is downregulated by a phosphatase. When the eIF2␣ phosphatase removes PO 4 from phosphorylated eIF2␣ (eIF2␣-P), repressed translation then gives rise to latency (434). Thus, latency and long-lasting persistence, which are important requirements for the completion of parasite-host life cycles, may consist of concerted ability to exploit the stress response mechanism in eukaryotic cells.…”

“…However, a clear demonstration of the mechanism of and the part that autoimmunity plays in the development of Chagas' heart disease is essential for the effective delivery of treatment. To demonstrate the important role played independently by autoimmunity in the pathogenesis of Chagas' heart disease, coexisting tissue inflammation with active infection needs to be eliminated (40,203,408,434). An approach to answering this question requires the abrogation of the parasite infection.…”

Immune defence, parasite evasion strategies and their relevance for ‘macroscopic phenomena’ such as virulence

“…Immune evasion is likely to play a major role in many of the cases and should also elucidate problems such as cross-species infections or invasion by novel parasites into a host population (Schmid-Hempel 2008). For example, if successful infection and parasite persistence inside the host critically depends on a particular immune evasion mechanism, this mechanism might only work in host A but be ineffective in host B (van Baarlen et al 2007). As this review shows, immune evasion mechanisms are typically tuned towards interfering with specific host molecules or signalling pathways, which are not necessarily conserved across host species.…”