作者: Peifang Sun , Karolis Bauza , Subhamoy Pal , Zhaodong Liang , Shuenn-jue Wu
DOI: 10.1016/J.VIROL.2011.08.026
关键词:
摘要: Human monocytes are susceptible to dengue virus (DV) infection through an FcR-dependent pathway known as antibody-dependent enhancement (ADE). In this study, was observed when purified were infected with DV serotypes in the presence of serially diluted immune serum antibodies. Analyzing binding DV-antibody complexes by quantifying amount viruses attached monocytes, we found that did not correlate input antibodies; rather, it peaked at suboptimal antibody concentrations, correlating enhancement. These results suggested involved hindering from FcR-bearing cells; such a protective feature is weakened, viral attachment and ADE observed. Further, increased cytokine production (TNF-alpha IFN-alpha), costimulatory marker expression (CD86 CD40), be associated enhancement, suggesting pathological role ADE-affected hemorrhagic diseases.