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Early B-cell activation after West Nile virus infection requires alpha/beta interferon but not antigen receptor signaling.

Publication ,  Journal Article
Purtha, WE; Chachu, KA; Virgin, HW; Diamond, MS
Published in: J Virol
November 2008

The B-cell response against West Nile virus (WNV), an encephalitic Flavivirus of global concern, is critical to controlling central nervous system dissemination and neurological sequelae, including death. Here, using a well-characterized mouse model of WNV infection, we examine the factors that govern early B-cell activation. Subcutaneous inoculation with a low dose of replicating WNV results in extensive B-cell activation in the draining lymph node (LN) within days of infection as judged by upregulation of the surface markers CD69, class II major histocompatibility complex, and CD86 on CD19(+) cells. B-cell activation in the LN but not the spleen was dependent on signals through the type I alpha/beta interferon (IFN-alpha/beta) receptor. Despite significant activation in the draining LN at day 3 after infection, WNV-specific B cells were not detected by immunoglobulin M enzyme-linked immunospot analysis until day 7. Liposome depletion experiments demonstrate that B-cell activation after WNV infection was not affected by the loss of F4/80(+) or CD169(+) subcapsular macrophages. Nonetheless, LN myeloid cells were essential for control of viral replication and survival from infection. Overall, our data suggest that the massive, early polyclonal B-cell activation occurring in the draining LN after WNV infection is immunoglobulin receptor and macrophage independent but requires sustained signals through the type I IFN-alpha/beta receptor.

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Published In

J Virol

DOI

EISSN

1098-5514

Publication Date

November 2008

Volume

82

Issue

22

Start / End Page

10964 / 10974

Location

United States

Related Subject Headings

  • West Nile virus
  • West Nile Fever
  • Virology
  • Up-Regulation
  • Spleen
  • Signal Transduction
  • Receptors, Antigen
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice
 

Citation

APA
Chicago
ICMJE
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Purtha, W. E., Chachu, K. A., Virgin, H. W., & Diamond, M. S. (2008). Early B-cell activation after West Nile virus infection requires alpha/beta interferon but not antigen receptor signaling. J Virol, 82(22), 10964–10974. https://doi.org/10.1128/JVI.01646-08
Purtha, Whitney E., Karen A. Chachu, Herbert W. Virgin, and Michael S. Diamond. “Early B-cell activation after West Nile virus infection requires alpha/beta interferon but not antigen receptor signaling.J Virol 82, no. 22 (November 2008): 10964–74. https://doi.org/10.1128/JVI.01646-08.
Purtha WE, Chachu KA, Virgin HW, Diamond MS. Early B-cell activation after West Nile virus infection requires alpha/beta interferon but not antigen receptor signaling. J Virol. 2008 Nov;82(22):10964–74.
Purtha, Whitney E., et al. “Early B-cell activation after West Nile virus infection requires alpha/beta interferon but not antigen receptor signaling.J Virol, vol. 82, no. 22, Nov. 2008, pp. 10964–74. Pubmed, doi:10.1128/JVI.01646-08.
Purtha WE, Chachu KA, Virgin HW, Diamond MS. Early B-cell activation after West Nile virus infection requires alpha/beta interferon but not antigen receptor signaling. J Virol. 2008 Nov;82(22):10964–10974.

Published In

J Virol

DOI

EISSN

1098-5514

Publication Date

November 2008

Volume

82

Issue

22

Start / End Page

10964 / 10974

Location

United States

Related Subject Headings

  • West Nile virus
  • West Nile Fever
  • Virology
  • Up-Regulation
  • Spleen
  • Signal Transduction
  • Receptors, Antigen
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice