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Alphaherpesvirus-induced activation of plasmacytoid dendritic cells depends on the viral glycoprotein gD and is inhibited by non-infectious light particles.
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- Additional Information
- Source:
Publisher: Public Library of Science Country of Publication: United States NLM ID: 101238921 Publication Model: eCollection Cited Medium: Internet ISSN: 1553-7374 (Electronic) Linking ISSN: 15537366 NLM ISO Abbreviation: PLoS Pathog Subsets: MEDLINE
- Publication Information:
Original Publication: San Francisco, CA : Public Library of Science, c2005-
- Subject Terms:
- Abstract:
Plasmacytoid dendritic cells (pDC) are important innate immune cells during the onset of viral infections as they are specialized in the production of massive amounts of antiviral type I interferon (IFN). Alphaherpesviruses such as herpes simplex virus (HSV) or pseudorabies virus (PRV) are double stranded DNA viruses and potent stimulators of pDC. Detailed information on how PRV activates porcine pDC is lacking. Using PRV and porcine primary pDC, we report here that PRV virions, so-called heavy (H-)particles, trigger IFNα production by pDC, whereas light (L-) particles that lack viral DNA and capsid do not. Activation of pDC requires endosomal acidification and, importantly, depends on the PRV gD envelope glycoprotein and O-glycosylations. Intriguingly, both for PRV and HSV-1, we found that L-particles suppress H-particle-mediated activation of pDC, a process which again depends on viral gD. This is the first report describing that gD plays a critical role in alphaherpesvirus-induced pDC activation and that L-particles directly interfere with alphaherpesvirus-induced IFNα production by pDC.
Competing Interests: The authors have declared that no competing interests exist.
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- Accession Number:
0 (Interferon Type I)
0 (Viral Envelope Proteins)
0 (glycoprotein gD, herpes simplex virus type 1)
- Publication Date:
Date Created: 20211129 Date Completed: 20211231 Latest Revision: 20211231
- Publication Date:
20240829
- Accession Number:
PMC8659615
- Accession Number:
10.1371/journal.ppat.1010117
- Accession Number:
34843605
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