Interferon production and signaling pathways are antagonized during henipavirus infection of fruit bat cell lines.

Bats are natural reservoirs for a spectrum of infectious zoonotic diseases including the recently emerged henipaviruses (Hendra and Nipah viruses). Henipaviruses have been observed both naturally and experimentally to cause serious and often fatal disease in many different mammal species, including humans. Interestingly, infection of the flying fox with henipaviruses occurs in the absence of clinical disease. The extreme variation in the disease pattern between humans and bats has led to an investigation into the effects of henipavirus infection on the innate immune response in bat cell lines. We report that henipavirus infection does not result in the induction of interferon expression, and the viruses also inhibit interferon signaling. We also confirm that the interferon production and signaling block in bat cells is not due to differing viral protein expression levels between human and bat hosts. This information, in addition to the known lack of clinical signs in bats following henipavirus infection, suggests that bats control henipavirus infection by an as yet unidentified mechanism, not via the interferon response. This is the first report of henipavirus infection in bat cells specifically investigating aspects of the innate immune system.
AuthorsElena R Virtue, Glenn A Marsh, Michelle L Baker, Lin-Fa Wang
JournalPloS one (PLoS One) Vol. 6 Issue 7 Pg. e22488 ( 2011) ISSN: 1932-6203 [Electronic] United States
PMID21811620 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Interferon Type I
  • Viral Proteins
  • Interferons
  • Animals
  • Cell Line
  • Chiroptera (virology)
  • Genes, Viral (genetics)
  • Henipavirus (drug effects, genetics, immunology)
  • Henipavirus Infections (immunology, virology)
  • Humans
  • Interferon Type I (biosynthesis)
  • Interferons (biosynthesis, pharmacology)
  • Signal Transduction (drug effects, immunology)
  • Viral Proteins (metabolism)

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