A potential robust antiviral defense state in the common vampire bat: Expression, induction and molecular characterization of the three interferon-stimulated genes -OAS1, ADAR1 and PKR

Dev Comp Immunol. 2018 Aug:85:95-107. doi: 10.1016/j.dci.2018.04.006. Epub 2018 Apr 7.

Abstract

Bats are known to harbor many zoonotic viruses, some of which are pathogenic to other mammals while they seem to be harmless in bats. As the interferon (IFN) response represents the first line of defense against viral infections in mammals, it is hypothesized that activation of the IFN system is one of the mechanisms enabling bats to co-exist with viruses. We have previously reported induction of type I IFN in a cell line from the common vampire bat, Desmodus rotundus, upon polyinosinic:polycytidylic acid (poly(I:C)) stimulation. To deepen our knowledge on D. rotundus' IFN-I antiviral response, we molecularly characterized three interferon-stimulated genes (ISGs), OAS1, PKR and ADAR1, closely implicated in the IFN-I antiviral response, and tested their functionality in our cellular model. We first found that D. rotundus encoded two OAS1 paralogs, OAS1a and OAS1b, and that the functional domains of the four ISGs characterized were highly conserved with those of other mammals. Despite their significant transcription level in the absence of stimulation, the transcription of the four ISGs characterized was enhanced by poly(I:C). In addition, the transcription of OAS1a and OAS1b appears to be differentially regulated. These findings demonstrate an active ISG antiviral response in D. rotundus in which OAS1b may play an important role.

Keywords: ADAR1; Desmodus rotundus; ISGs; Innate immunity; OAS1a; OAS1b; PKR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 2',5'-Oligoadenylate Synthetase / genetics*
  • Adenosine Deaminase / genetics*
  • Animals
  • Antiviral Agents / pharmacology*
  • Cell Line
  • Chiroptera / genetics*
  • Interferons / pharmacology*
  • Poly I-C / genetics
  • Transcription, Genetic / drug effects
  • Transcription, Genetic / genetics
  • Virus Diseases / genetics
  • eIF-2 Kinase / genetics*

Substances

  • Antiviral Agents
  • Interferons
  • eIF-2 Kinase
  • 2',5'-Oligoadenylate Synthetase
  • Adenosine Deaminase
  • Poly I-C