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Identification of the CD163 protein domains involved in infection of the porcine reproductive and respiratory syndrome virus.

Abstract
Scavenger receptor CD163 is a key entry mediator for porcine reproductive and respiratory syndrome virus (PRRSV). To identify the CD163 protein domains involved in PRRSV infection, deletion mutants and chimeric mutants were created. Infection experiments revealed that scavenger receptor cysteine-rich (SRCR) domain 5 (SRCR 5) is essential for PRRSV infection, while the four N-terminal SRCR domains and the cytoplasmic tail are not required. The remaining CD163 protein domains need to be present but can be replaced by corresponding SRCR domains from CD163-L1, resulting in reduced (SRCR 6 and interdomain regions) or unchanged (SRCR 7 to SRCR 9) infection efficiency. In addition, CD163-specific antibodies recognizing SRCR 5 are able to reduce PRRSV infection.
AuthorsHanne Van Gorp, Wander Van Breedam, Jan Van Doorsselaere, Peter L Delputte, Hans J Nauwynck
JournalJournal of virology (J Virol) Vol. 84 Issue 6 Pg. 3101-5 (Mar 2010) ISSN: 1098-5514 [Electronic] United States
PMID20032174 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • CD163 antigen
  • Protein Isoforms
  • Receptors, Cell Surface
  • Recombinant Fusion Proteins
  • Scavenger Receptors, Class B
Topics
  • Animals
  • Antigens, CD (chemistry, genetics, metabolism)
  • Antigens, Differentiation, Myelomonocytic (chemistry, genetics, metabolism)
  • Humans
  • Porcine Reproductive and Respiratory Syndrome (metabolism, virology)
  • Porcine respiratory and reproductive syndrome virus (genetics, metabolism, pathogenicity)
  • Protein Isoforms (chemistry, genetics, metabolism)
  • Protein Structure, Tertiary
  • Receptors, Cell Surface (chemistry, genetics, metabolism)
  • Recombinant Fusion Proteins (chemistry, genetics, metabolism)
  • Scavenger Receptors, Class B (genetics, metabolism)
  • Sequence Deletion
  • Swine
  • Virus Internalization

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