Role of complement in dengue virus infection: protection or pathogenesis? mBio 3(1): e00003–12–e00003–12 DOI

ABSTRACT Dengue viruses (DENV) cause a spectrum of disease in humans, ranging from dengue fever (DF) to a severe, life-threatening syndrome called dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). Despite the global morbidity and mortality associated with DENV infection, mechanisms of immune control and viral pathogenesis are poorly understood. In a recent article, Avirutnan et al. [mBio 2(6):e00276-11, 2011] demonstrated that DENV can be directly neutralized via the mannose binding lectin (MBL) pathway of the complement system and that deficiency inMBL level or activity due to host polymorphisms in theMBL2 gene correlates with reduced levels of DENV neutralization. These findings implicate a role for the MBL pathway in controlling DENV infections andmodulating DHF/DSSmanifestations. The four serotypes of dengue viruses (DENV) cause 100 to 500million infections each year in over 100 countries, resulting in 40 million clinically apparent cases and 20,000 deaths (1). The clinically apparent cases represent a spectrum of illnesses ranging from an acute febrile disease called dengue fever (DF) to the severe and life-threatening dengue hemorrhagic fever/dengue shock syn-drome (DHF/DSS). Severe disease is preferentially associatedwith secondary infection with a different serotype and with primary infection of infants born to DENV-immune mothers. To explai