The regulation of type I interferon production by paramyxoviruses - PubMed
Review
The regulation of type I interferon production by paramyxoviruses
Stephen Goodbourn et al. J Interferon Cytokine Res. 2009 Sep.
Abstract
Experimentally, paramyxoviruses are conventionally considered good inducers of type I interferons (IFN-alpha/beta), and have been used as agents in the commercial production of human IFN-alpha. However, in the last few years it has become clear that viruses in general mount a major challenge to the IFN system, and paramyxoviruses are no exception. Indeed, most paramyxoviruses encode mechanisms to inhibit both the production of, and response to, type I IFN. Here we review our knowledge of the type I IFN-inducing signals (by so-called pathogen-associated molecular patterns, or PAMPs) produced during paramyxovirus infections, and discuss how paramyxoviruses limit the production of PAMPs and inhibit the cellular responses to PAMPs by interfering with the activities of the pattern recognition receptors (PRRs), mda-5, and RIG-I, as well as downstream components in the type I IFN induction cascades.
Figures

Classification of paramyxoviruses. The Paramyxoviridae family is divided into Paramyxovirinae and the Pneumovirinae subfamilies. The Paramyxovirinae subfamily contains five genera: respiroviruses, rubulaviruses, henipaviruses, morbilliviruses, and avulaviruses. The Pneumovirinae subfamily contains 2 genera: pneumoviruses and metapneumoviruses. This classification is based predominantly on sequence homology and genome organization. Abbreviations: SeV, Sendai virus; HPIV, human parainfluenza viruses; BPIV3, bovine parainfluenza virus 3; MuV, mumps virus; SV5, simian virus 5; HeV, Hendra virus; NiV, Nipah virus; MeV, measles virus; CDV, canine distemper virus; RPV, rinderpest virus; PDV, phocine distemper virus; NDV, Newcastle disease virus; APMVs, avian paramyxoviruses; HRSV, human respiratory syncytial virus; BRSV, bovine respiratory syncytial virus; HMPV, human metapneumovirus; TRTV, turkey rhinotrachetis virus.

Organization of the P/V/C genes of Paramyxovirinae and their relationship to their accessory proteins. (A) The P proteins of morbilliviruses, respiroviruses, and henipaviruses are translated from mRNAs produced as faithful copies of their P/V/C genes (green bar). Insertion of a single G at the RNA-editing site generates a transcript that encodes the V protein, and insertion of 2 G residues generates a transcript that encodes the W proteins and D proteins (HPIV3). The P, V, W, and D proteins share a common N-terminus (blue bar), but distinct C-termini (P = pink bar, V = light green bar, W and D = yellow bar). The C protein(s) (lilac bars) are generated by translation of the P/V/W/D mRNAs using alternative initiation codons. Translation of the prototypical C protein begins at an AUG that resides downstream of P protein initiation codon, and the Y1 and Y2 proteins of Sendai virus are translated from AUGs that reside even further downstream. The C′ protein made by Sendai virus is translated from an ACG codon that resides 5′ to the AUG of the P protein. (B) The P proteins of avulaviruses are also translated from mRNAs produced as faithful copies of their P/V genes (green bar). Insertion of a single G at the RNA-editing site generates a transcript that encodes the V protein, and insertion of 2 G residues generates a transcript that encodes the I protein. (C) In contrast, the V proteins of rubulaviruses are translated from mRNAs produced as faithful copies of their P/V genes (green bar). Insertion of 1 or 4 G residues at the RNA-editing site generates a transcript that encodes the I protein, and insertion of 2 G residues generates a transcript that encodes the P protein.

Paramyxovirus accessory proteins target the intracellular viral pathogen-associated molecular patterns (PAMP) signaling pathways. The signaling pathways leading from the RNA helicases mda-5 and RIG-I to IFN-β induction are shown (reviewed in Randall and Goodbourn (2008), Gale and Sen (2009)). As discussed in the text, paramyxovirus V proteins interact with mda-5 and prevent its activation. Sendai virus (SeV) C protein targets RIG-I, although a specific molecular interaction has yet to be shown. The NS2 protein of human respiratory syncytial virus (HRSV) directly binds to RIG-I and inhibits its activity. The V proteins of human parainfluenza virus 2 (HPIV2), simian virus 5 (PIV5, formerly SV5), and mumps virus (MuV) interact with and inhibit TBK1 and IKK-ɛ, and NiV V inhibits IKK-ɛ (although not TBK1). The C protein of rinderpest virus (RPV) and the W protein of Nipah virus (NiV) have uncharacterized nuclear targets that act downstream of transcription factors.
Similar articles
-
Paramyxovirus activation and inhibition of innate immune responses.
Parks GD, Alexander-Miller MA. Parks GD, et al. J Mol Biol. 2013 Dec 13;425(24):4872-92. doi: 10.1016/j.jmb.2013.09.015. Epub 2013 Sep 20. J Mol Biol. 2013. PMID: 24056173 Free PMC article. Review.
-
Yoshida A, Kawabata R, Honda T, Sakai K, Ami Y, Sakaguchi T, Irie T. Yoshida A, et al. J Virol. 2018 Feb 12;92(5):e02094-17. doi: 10.1128/JVI.02094-17. Print 2018 Mar 1. J Virol. 2018. PMID: 29237838 Free PMC article.
-
Ikegame S, Takeda M, Ohno S, Nakatsu Y, Nakanishi Y, Yanagi Y. Ikegame S, et al. J Virol. 2010 Jan;84(1):372-9. doi: 10.1128/JVI.01690-09. J Virol. 2010. PMID: 19846522 Free PMC article.
-
Audsley MD, Marsh GA, Lieu KG, Tachedjian M, Joubert DA, Wang LF, Jans DA, Moseley GW. Audsley MD, et al. J Gen Virol. 2016 Mar;97(3):581-592. doi: 10.1099/jgv.0.000388. Epub 2015 Dec 24. J Gen Virol. 2016. PMID: 26703878
-
Paramyxovirus disruption of interferon signal transduction: STATus report.
Ramachandran A, Horvath CM. Ramachandran A, et al. J Interferon Cytokine Res. 2009 Sep;29(9):531-7. doi: 10.1089/jir.2009.0070. J Interferon Cytokine Res. 2009. PMID: 19694544 Free PMC article. Review.
Cited by
-
LGP2 plays a critical role in sensitizing mda-5 to activation by double-stranded RNA.
Childs KS, Randall RE, Goodbourn S. Childs KS, et al. PLoS One. 2013 May 9;8(5):e64202. doi: 10.1371/journal.pone.0064202. Print 2013. PLoS One. 2013. PMID: 23671710 Free PMC article.
-
African swine fever: A re-emerging viral disease threatening the global pig industry.
Sánchez-Cordón PJ, Montoya M, Reis AL, Dixon LK. Sánchez-Cordón PJ, et al. Vet J. 2018 Mar;233:41-48. doi: 10.1016/j.tvjl.2017.12.025. Epub 2018 Jan 3. Vet J. 2018. PMID: 29486878 Free PMC article. Review.
-
Sánchez-Aparicio MT, Feinman LJ, García-Sastre A, Shaw ML. Sánchez-Aparicio MT, et al. J Virol. 2018 Feb 26;92(6):e01960-17. doi: 10.1128/JVI.01960-17. Print 2018 Mar 15. J Virol. 2018. PMID: 29321315 Free PMC article.
-
Ku D, Yang Y, Park Y, Jang D, Lee N, Lee YK, Lee K, Lee J, Han YB, Jang S, Choi SR, Ha YJ, Choi YS, Jeong WJ, Lee YJ, Lee KJ, Cha S, Kim Y. Ku D, et al. bioRxiv [Preprint]. 2024 Jun 10:2024.03.28.587146. doi: 10.1101/2024.03.28.587146. bioRxiv. 2024. PMID: 38915695 Free PMC article. Preprint.
-
Aggregated Hendra virus C-protein activates the NLRP3 inflammasome to induce inflammation.
Barry K, Harpur C, Lam M, Tate MD, Mansell A. Barry K, et al. J Inflamm (Lond). 2023 Nov 10;20(1):38. doi: 10.1186/s12950-023-00365-8. J Inflamm (Lond). 2023. PMID: 37950278 Free PMC article.
References
-
- Bankamp B. Wilson J. Bellini WJ. Rota PA. Identification of naturally occurring amino acid variations that affect the ability of the measles virus C protein to regulate genome replication and transcription. Virology. 2005;336:120–129. - PubMed
-
- Berghall H. Siren J. Sarkar D. Julkunen I. Fisher PB. Vainionpaa R. Matikainen S. The interferon-inducible RNA helicase, mda-5, is involved in measles virus-induced expression of antiviral cytokines. Microbes Infect. 2006;8:2138–2144. - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Research Materials