By Pooja Toshniwal PahariaApr 10 2024Reviewed by Susha Cheriyedath, M.Sc. In a recent review published in the journal PNAS, researchers examined the germ theory from a non-centric perspective on infection outcome, considering the variables that influence illness severity while drawing on a known understanding of microbial pathogenesis, evolutionary biology, and pathogen-host interactions.
Recent research questions the theory, giving rise to the full-blown host theory, which holds that infectious illnesses are caused by inherited or acquired immunodeficiencies in the host. According to this hypothesis, viruses are passive environmental triggers, and disease development results from pre-existing host immunodeficiencies. These inadequacies can be covert or overt, depending on diagnostic procedures used to identify critical diseases.
Examples demonstrating the evolved ability of S. pyogenes to promote disease in immunocompetent individuals. The surface M protein recruits human C4BP to inhibit complement opsonization of the bacterial surface. Secreted streptokinase binds to human Plg, which causes a conformational change of Plg into a plasmin active state. The secreted endoglycosidase EndoS inactivates effector functions of IgG by cleaving off N-glycans from the Fc-region.
Host-pathogenic microbe interactions and genetic variability Streptococcus pyogenes, a bacterium often present in humans, can cause asymptomatic carriership and symptomatic illnesses such as septic shock and necrotizing infections in soft tissues.
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