How Streptococcus suis serotype 2 attempts to avoid attack by host immune defenses

Abstract

Streptococcus suis (S. suis) type 2 (SS2) is an important zoonotic pathogen that causes swine streptococcosis, a widespread infectious disease that occurs in pig production areas worldwide and causes serious economic losses in the pork industry. Hosts recognize pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) to activate both innate and acquired immune responses. However, S. suis has evolved multiple mechanisms to escape host defenses. Pathogenic proteins, such as enolase, double-component regulatory systems, factor H-combining proteins and other pathogenic and virulence factors, contribute to immune escape by evading host phagocytosis, reactive oxygen species (ROS), complement-mediated immune destruction, etc. SS2 can prevent neutrophil extracellular trap (NET) formation to avoid being trapped by porcine neutrophils and disintegrate host immunoglobulins via IgA1 hydrolases and IgM proteases. Currently, the pathogenesis of arthritis and meningitis caused by SS2 infection remains unclear, and further studies are necessary to elucidate it. Understanding immune evasion mechanisms after SS2 infection is important for developing high-efficiency vaccines and targeted drugs.

Keywords: Immune escape; Pathogenesis; Streptococcus suis serotype 2; Virulence factor.