Host-pathogen interactions in Streptococcus pyogenes infections, with special reference to puerperal fever and a comment on vaccine development.

Thomas Areschoug, Fredric Carlsson, Margaretha Stålhammar-Carlemalm, Gunnar Lindahl

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskriftPeer review

31 Citeringar (SciVal)
301 Nedladdningar (Pure)

Sammanfattning

Streptococcus pyogenes (group A streptococcus) causes a variety of diseases, including acute pharyngitis, impetigo, rheumatic fever and the streptococcal toxic shock syndrome. Moreover, S. pyogenes was responsible for the classical example of a nosocomial infection, the epidemics of puerperal fever (childbed fever) that caused the death of numerous women in earlier centuries. The most extensively studied virulence factor of S. pyogenes is the surface M protein, which inhibits phagocytosis and shows antigenic variation. Recent data indicate that many M proteins confer phagocytosis resistance because the variable N-terminal region has non-overlapping sites that specifically bind two components of the human immune system, the complement inhibitor C4b-binding protein (C4BP) and IgA-Fc. Concerning puerperal fever, molecular and epidemiological analysis suggests that the S. pyogenes surface protein R28 may have played a pathogenetic role in these epidemics. This article summarizes the properties of M protein and the R28 protein and considers a potential problem encountered in connection with the use of animal models for vaccine development.
Originalspråkengelska
Sidor (från-till)S9-S14
TidskriftVaccine
Volym22 Suppl 1
UtgåvaSuppl 1
DOI
StatusPublished - 2004

Ämnesklassifikation (UKÄ)

  • Mikrobiologi inom det medicinska området

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