Pneumococcal surface protein A contributes to secondary Streptococcus pneumoniae infection after influenza virus

Quinton O King1, Benfang Lei, Allen G Harmsen

  • 1Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717-3610, USA. quinton_king@hotmail.com

Insights

Pneumococcal surface protein A (PspA) is crucial for Streptococcus pneumoniae growth after influenza infection in mice. PspA deficiency severely limits bacterial growth, and PspA immunization protects against secondary lung infections.

Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Influenza virus infection predisposes individuals to secondary bacterial pneumonia.
  • Streptococcus pneumoniae is a common cause of secondary bacterial pneumonia.
  • Pneumococcal surface protein A (PspA) is a major virulence factor of S. pneumoniae.

Purpose of the Study:

  • To investigate the role of PspA, NanA, and Hyl in S. pneumoniae pathogenesis following influenza virus infection.
  • To evaluate the efficacy of PspA immunization in preventing secondary pneumococcal infections.

Main Methods:

  • Competitive growth model in mice with and without prior influenza virus infection.
  • Comparison of wild-type D39 strain with PspA-, NanA-, and Hyl- mutants.
  • Assessment of bacterial burden and lung damage markers post-infection.
  • Evaluation of PspA immunization efficacy.

Main Results:

  • Influenza virus infection significantly increased S. pneumoniae recovery.
  • PspA- mutant showed severe attenuation in both non-infected and influenza-infected mice, with 1800-fold lower growth in the latter.
  • NanA- and Hyl- mutants did not exhibit significant attenuation.
  • PspA immunization reduced bacterial lung burden and lung damage markers.

Conclusions:

  • PspA is essential for S. pneumoniae virulence, particularly during secondary infections following influenza.
  • PspA contributes significantly to S. pneumoniae pathogenesis after viral respiratory infections.
  • PspA-based immunization is a promising strategy to prevent secondary pneumococcal lung infections.

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