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The lectin pathway of complement activation contributes to protection from West Nile virus infection

Anja Fuchs1, Amelia K Pinto, Wilhelm J Schwaeble

  • 1Department of Medicine, Washington University School of Medicine, 660 South Euclid Ave., St. Louis, MO 63110, USA.

Virology
|January 29, 2011
PubMed

Insights

The lectin pathway, involving mannose binding lectin (MBL) and MASP-2, plays a role in West Nile virus (WNV) defense. However, its absence did not significantly alter viral spread or adaptive immunity.

Area of Science:

  • Immunology
  • Virology
  • Complement System

Background:

  • The lectin pathway's role in antiviral defense, specifically against West Nile virus (WNV), remains unclear.
  • Mannose binding lectin (MBL) and mannan-binding lectin-associated serine protease-2 (MASP-2) are key components of this pathway.

Purpose of the Study:

  • To define the in vivo function of the lectin pathway in WNV infection.
  • To investigate the impact of deficiencies in MBL-A, MBL-C, and MASP-2 on WNV pathogenesis.

Main Methods:

  • Utilized gene-deficient mouse models lacking MBL-A/MBL-C or MASP-2.
  • Assessed WNV susceptibility and disease severity in these models compared to wild-type mice.
  • Monitored viral spread to the central nervous system (CNS) and adaptive immune responses (B and T cells).

Main Results:

  • Mice deficient in lectin pathway components (MBL-A/MBL-C or MASP-2) exhibited increased vulnerability to WNV infection.
  • However, these deficiencies resulted in a less severe disease course compared to deficiencies in classical or alternative complement pathways.
  • Lectin pathway deficiency did not significantly impact viral CNS dissemination or adaptive immune responses.

Conclusions:

  • Mannose binding lectin (MBL)-mediated recognition and lectin pathway activation are important, but subordinate, in WNV protection.
  • The lectin pathway contributes to host defense against WNV but is not essential for controlling viral spread or adaptive immunity.

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