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Terminal sialic acid linkages determine different cell infectivities of human parainfluenza virus type 1 and type 3.

Abstract
Human parainfluenza virus type 1 (hPIV1) and type 3 (hPIV3) initiate infection by sialic acid binding. Here, we investigated sialic acid linkage specificities for binding and infection of hPIV1 and hPIV3 by using sialic acid linkage-modified cells treated with sialidases or sialyltransferases. The hPIV1 is bound to only α2,3-linked sialic acid residues, whereas hPIV3 is bound to α2,6-linked sialic acid residues in addition to α2,3-linked sialic acid residues in human red blood cells. α2,3 linkage-specific sialidase treatment of LLC-MK2 cells and A549 cells decreased the infectivity of hPIV1 but not that of hPIV3. Treatment of A549 cells with α2,3 linkage-specific sialyltransferase increased infectivities of both hPIV1 and hPIV3, whereas α2,6 linkage-specific sialyltransferase treatment increased only hPIV3 infectivity. Clinical isolates also showed similar sialic acid linkage specificities. We concluded that hPIV1 utilizes only α2,3 sialic acid linkages and that hPIV3 makes use of α2,6 sialic acid linkages in addition to α2,3 sialic acid linkages as viral receptors.
AuthorsKeijo Fukushima, Tadanobu Takahashi, Seigo Ito, Masahiro Takaguchi, Maiko Takano, Yuuki Kurebayashi, Kenta Oishi, Akira Minami, Tatsuya Kato, Enoch Y Park, Hidekazu Nishimura, Toru Takimoto, Takashi Suzuki
JournalVirology (Virology) Vol. 464-465 Pg. 424-431 (Sep 2014) ISSN: 1096-0341 [Electronic] United States
PMID25146600 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2014. Published by Elsevier Inc.
Chemical References
  • Receptors, Virus
  • N-Acetylneuraminic Acid
Topics
  • Cell Line
  • Humans
  • N-Acetylneuraminic Acid (chemistry, metabolism)
  • Parainfluenza Virus 1, Human (genetics, metabolism, pathogenicity)
  • Parainfluenza Virus 3, Human (genetics, metabolism, pathogenicity)
  • Protein Binding
  • Receptors, Virus (chemistry, metabolism)
  • Respirovirus Infections (metabolism, virology)
  • Virulence

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