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Mycoplasma genitalium infections are enabled by multiple virulence factors, both intracellular and expressed on the cholesterol-containing phospholipid membrane. Intracellular accessory proteins form the tip structure, which adheres to epithelial cells in vivo via the transmembrane adhesion complex of Nap proteins, P110 and P140. Protein M binds to the Fab region of immunoglobulins with a high affinity to both λ and κ chains, enabling immune system evasion. Membrane lipoproteins and extracellular polymeric substances help in biofilm formation, which is thought to facilitate infection persistence.
Mycoplasma genitalium is characterized by a small genome and a lack of a cell wall, contributing to its unique biology. It is associated with reproductive tract infections, including non-gonococcal urethritis and pelvic inflammatory disease. It is nearly as common as chlamydia in most studies from high-income countries. The emergence of antimicrobial resistance in M. genitalium raises concern about the long-term efficacy of current therapeutic strategies. Understanding its genomic intricacies and pathogenic mechanisms is crucial for developing targeted interventions to address the growing public health impact of this elusive microbe.
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