Most of the pathogens that drive chronic inflammatory disease persist as members of our microbiome communities. The survival mechanisms employed by these pathogens (to remain alive in the face of the host immune response) have been studied for decades. But in 2018, research teams characterized even more novel mechanisms of pathogen persistence (several tied to bacteriophage activity):
Lead author: Daniel Wozniak, The Ohio State University
The team used a burn wound model of chronic infection to study how mixed strains of P. aeruginosa adapt and evolve. They found that certain strains of chronic P. aeruginosa acquired genetic elements that altered their CRISPER-Cas (immune) systems. These mutations allowed these strains to better resist attack from specific bacteriophages. Certain P. auruginosa strains were also capable of surviving as “rugose small-colony variants” (RSCVs): small colonies with an elevated capacity to form biofilms.
Lead author: Timothy Nice, Oregon Health and Science University
The team studied a mouse norovirus. They found that the norovirus capsid (the protein shell of the virus) helped regulate cell lysis and inflammatory cytokine release. The capsid also-triggered inflammation that recruited immune cells like monocytes and neutrophils to sites of replication. This promoted the viruses’ chronic persistence.
Paper highlight: “Infection of continuously recruited inflammatory cells may be a mechanism of persistence broadly utilized by lytic viruses incapable of establishing latency”