Abstract
Acyl-coenzyme A binding domain containing 3 (ACBD3) is a multifunctional protein residing in the Golgi apparatus and is involved in several signaling pathways. The current knowledge on ACBD3 has been extended to virology. ACBD3 has recently emerged as a key factor subverted by viruses, including kobuvirus, enterovirus, and hepatitis C virus. The ACBD3-PI4KB complex is critical for the role of ACBD3 in viral replication. In most cases, ACBD3 plays a positive role in viral infection. ACBD3 associates with viral 3A proteins from a variety of Picornaviridae family members at membrane contact sites (MCSs), which are used by diverse viruses to ensure lipid transfer to replication organelles (ROs). In this review, we discuss the mechanisms underlying the involvement of ACBD3 in viral infection at MCSs. Our review will highlight the current research and reveal potential avenues for future research.
Highlights
Ten years ago, PI4KB and PI4KA were identified as host factors to produce phosphatidylinositol-4-phosphate (PI4P) for virus replication (Hsu et al, 2010; Reiss et al, 2011)
Researchers demonstrated that the non-structural proteins 2B, 2BC, 2C, 3A, and 3AB from Aichi virus interacted with ACBD3 and PI4KB to form a protein complex at replication organelles (ROs) to promote PI4P synthesis (Greninger et al, 2012; Sasaki et al, 2012; Klima et al, 2017; McPhail et al, 2017; Chalupska et al, 2019)
ACBD3 interacts with many 3A proteins from Picornaviridae family to affect viral replication (Table 1)
Summary
PI4KB (for enterovirus) and PI4KA (for hepatitis C virus, HCV) were identified as host factors to produce phosphatidylinositol-4-phosphate (PI4P) for virus replication (Hsu et al, 2010; Reiss et al, 2011). Those viruses hijack the ACBD3 protein to recruit PI4KB to the viral ROs to produce PI4P (Hsu et al, 2010; Ronnberg et al, 2012; Nchoutmboube et al, 2013). Researchers demonstrated that the non-structural proteins 2B, 2BC, 2C, 3A, and 3AB from Aichi virus interacted with ACBD3 and PI4KB to form a protein complex at ROs to promote PI4P synthesis (Greninger et al, 2012; Sasaki et al, 2012; Klima et al, 2017; McPhail et al, 2017; Chalupska et al, 2019).
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