Siglec-7 mediates varicella-zoster virus infection by associating with glycoprotein B
Tadahiro Suenaga1, Yasuko Mori2, Tatsuo Suzutani3
1Department of Microbiology, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima, Fukushima, 960-1295, Japan; Department of Immunochemistry, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0081, Japan; WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamadaoka, Suita, Osaka, 565-0081, Japan.
Abstract:
Sialic acid immunoglobulin-like lectin (Siglec) family molecules are immune regulatory receptors that bind to specific molecules containing sialic acids. Varicella-zoster virus (VZV), a member of the herpesvirus family, infects hematopoietic cells and spreads throughout the body, causing chickenpox, shingles, and, sometimes fatal encephalomyelitis. However, the cellular entry receptors that are required for VZV to infect hematopoietic cells have remained unclear. Here, we found that Siglec-7, mainly expressed on hematopoietic cells, binds to VZV envelope glycoprotein B in a sialic acid-dependent manner. Furthermore, Siglec-7 mediated VZV infection by inducing membrane fusion. Our findings provide the first evidence for a molecular mechanism by which VZV infects hematopoietic cells.
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