Effect of Bovine Alpha-1-Interferon On Bovine Herpesvirus Type-1-Induced Respiratory-Disease

Babiuk, LA, Ohmann, HB, Gifford, G, Czarniecki, CW, Scialli, VT and Hamilton, EB (1985) Effect of Bovine Alpha-1-Interferon On Bovine Herpesvirus Type-1-Induced Respiratory-Disease. Journal of General Virology, 66 NOV: 2383-2394. doi:10.1099/0022-1317-66-11-2383

Author Babiuk, LA
Ohmann, HB
Gifford, G
Czarniecki, CW
Scialli, VT
Hamilton, EB
Title Effect of Bovine Alpha-1-Interferon On Bovine Herpesvirus Type-1-Induced Respiratory-Disease
Journal name Journal of General Virology   Check publisher's open access policy
ISSN 0022-1317
Publication date 1985-01-01
Year available 1985
Sub-type Article (original research)
DOI 10.1099/0022-1317-66-11-2383
Open Access Status Not Open Access
Volume 66
Issue NOV
Start page 2383
End page 2394
Total pages 12
Language eng
Abstract Murid Herpesvirus-4 (MuHV-4) is a B cell-tropic gamma-herpesvirus that can be studied in vivo Despite viral evasion, type 1 interferons (IFN-I) limit its spread. After MuHV-4 inoculation into footpads, IFN-I protect lymph node subcapsular sinus macrophages (SSM) against productive infection; after peritoneal inoculation, they protect splenic marginal zone macrophages; and they limit MuHV-4 replication in the lungs. While invasive infections can test specific aspects of host colonization, it is important also to understand natural infection. MuHV-4 taken up spontaneously by alert mice enters them via olfactory neurons. We determined how IFN-I act in this context. Blocking IFN-I signalling did not increase neuronal infection, but allowed its spread to the adjacent respiratory epithelium. In lymph nodes a complete IFN-I signalling block increased MuHV-4 lytic infection in SSM and increased the number of dendritic cells (DC) expressing viral GFP independently of lytic infection. A CD11c(+) cell-directed signalling block increased only DC infection. However this was sufficient to increase down-stream infection, consistent with DC providing the main viral route to B cells. The capacity of IFN-I to limit DC infection indicated that viral IFN-I evasion was only partly effective. Therefore DC are a possible target for IFN-I-based interventions to reduce host colonization.IMPORTANCE Human gamma-herpesviruses infect B cells and cause B cell cancers. Interventions to block virus binding to B cells have not stopped their infection. Therefore we must identify other control points that are relevant to natural infection. Human infections are difficult to analyse. However gamma-herpesviruses colonize all mammals. A related gamma-herpesvirus of mice reaches B cells not directly but via infected dendritic cells. We show that type 1 interferons, an important general anti-viral defence, limit gamma-herpesvirus B cell infection by acting on dendritic cells. Therefore dendritic cell infection is a potential point of interferon-based therapeutic intervention.
Keyword Biotechnology & Applied Microbiology
Biotechnology & Applied Microbiology
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: ResearcherID Downloads - Archived
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 62 times in Thomson Reuters Web of Science Article | Citations
Google Scholar Search Google Scholar
Created: Sat, 25 Feb 2012, 00:48:26 EST by System User on behalf of Library - Information Access Service