- Top of page
- Do Archaea possess the ability to cause disease?
- Could Archaea contribute to disease caused by other organisms?
- Hypothesis: Lack of transduction by relevant bacterial phages prevents Archaea from becoming pathogens
- Phages: The source of many pathogen-associated genes
- Archaeal viruses differ from bacterial phages in many respects
- Gene-based phylogeny of archaeal viruses and bacterial phages – no evidence of recent gene exchange
- Bacteriophage receptors in Bacteria, and their structures, are largely absent from Archaea
- The archaeal virus and bacterial phage gene pools are likely independent
- Why have Archaea not developed virulence independently of Bacteria?
- Toward a better understanding of pathogen evolution
- Implications and conclusions
Although Archaea inhabit the human body and possess some characteristics of pathogens, there is a notable lack of pathogenic archaeal species identified to date. We hypothesize that the scarcity of disease-causing Archaea is due, in part, to mutually-exclusive phage and virus populations infecting Bacteria and Archaea, coupled with an association of bacterial virulence factors with phages or mobile elements. The ability of bacterial phages to infect Bacteria and then use them as a vehicle to infect eukaryotes may be difficult for archaeal viruses to evolve independently. Differences in extracellular structures between Bacteria and Archaea would make adsorption of bacterial phage particles onto Archaea (i.e. horizontal transfer of virulence) exceedingly hard. If phage and virus populations are indeed exclusive to their respective host Domains, this has important implications for both the evolution of pathogens and approaches to infectious disease control.