Frontiers in Immunology (May 2024)

Apolipoprotein D facilitates rabies virus propagation by interacting with G protein and upregulating cholesterol

  • Hongyan Zhang,
  • Hongyan Zhang,
  • Xingxue Liang,
  • Xingxue Liang,
  • Duoduo Li,
  • Duoduo Li,
  • Chuanliang Zhang,
  • Chuanliang Zhang,
  • Wenfeng Wang,
  • Wenfeng Wang,
  • Rongze Tang,
  • Rongze Tang,
  • Hongyun Zhang,
  • Hongyun Zhang,
  • Abraha Bahlbi Kiflu,
  • Abraha Bahlbi Kiflu,
  • Cheng Liu,
  • Cheng Liu,
  • Cheng Liu,
  • Cheng Liu,
  • Jingjing Liang,
  • Jingjing Liang,
  • Jingjing Liang,
  • Jingjing Liang,
  • Xiaoning Li,
  • Xiaoning Li,
  • Xiaoning Li,
  • Xiaoning Li,
  • Ting Rong Luo,
  • Ting Rong Luo,
  • Ting Rong Luo,
  • Ting Rong Luo

DOI
https://doi.org/10.3389/fimmu.2024.1392804
Journal volume & issue
Vol. 15

Abstract

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Rabies virus (RABV) causes a fatal neurological disease, consisting of unsegmented negative-strand RNA, which encodes five structural proteins (3′-N-P-M-G-L-5′). Apolipoprotein D (ApoD), a lipocalin, is upregulated in the nervous system after injury or pathological changes. Few studies have focused on the role of ApoD during virus infection so far. This study demonstrated that ApoD is upregulated in the mouse brain (in vivo) and C8-D1A cells (in vitro) after RABV infection. By upregulating ApoD expression in C8-D1A cells, we found that ApoD facilitated RABV replication. Additionally, Co-immunoprecipitation demonstrated that ApoD interacted with RABV glycoprotein (G protein). The interaction could promote RABV replication by upregulating the cholesterol level. These findings revealed a novel role of ApoD in promoting RABV replication and provided a potential therapeutic target for rabies.

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