Skip to main content

5. Conclusions

Although viruses from all genera within the Paramyxoviridae family antagonize the IFN response, there are a wide variety of mechanisms by which this antagonism occurs. It appears that viruses from both sub-families suppress the production of IFN via the V protein for members of the Paramyxovirinae and the NS proteins for members of the Pneumovirinae. Members of the Paramyxovirinae also use the V protein and/or other products of the viral P gene, such as C and W, to antagonize IFN signaling. Some of these viruses block both IFN-α/β and IFN-γ signaling pathways, whilst others block only IFN-α/β signaling by various mechanisms including interactions with the IFN receptor complex, targeted degradation of components of the signaling pathway and sequestration of signaling molecules in high molecular weight complexes.

Several viruses encode multiple proteins that act as IFN antagonists and it is likely that these proteins are multifunctional and have other, as of yet undefined roles in the viral life cycle that may or may not be concerned with immune evasion. For example, it remains to be ascertained why the V proteins of Henipaviruses are significantly bigger than the V proteins of other paramyxoviruses, and what if any are the additional functions associated with these larger proteins. As discussed, studies designed to tell us more about how paramyxoviruses evade cellular antiviral responses may shed further light in such diverse areas as the molecular pathogenesis of virus infections, virus host range and virus persistence, as well as potentially having implications for the development of novel approaches to creating attenuated viruses or antiviral drugs.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 129.00
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 169.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Wang, L.-F. & Eaton, B. Emerging Paramyxoviruses. The Infectious Disease Review-microbes of man, animals and the environment 3:52–69

    Google Scholar 

  2. Lamb, R. A. & Kolakofsky, D. in Fields’ Virology (eds. Fields, B. N., Knipe, D. M., Howley, P. M. & Griffin, D. E.) 1305–1340 (Lippincott Williams and Wilkins, Philadelphia, 2001)

    Google Scholar 

  3. Stark, G. R., Kerr, I. M., Williams, B. R., Silverman, R. H. & Schreiber, R. D. How cells respond to interferons. Annu Rev Biochem 67: 227–64

    Google Scholar 

  4. Goodbourn, S., Didcock, L. & Randall, R. E. Interferons: cell signaling, immune modulation, antiviral response and virus countermeasures. J Gen Virol 81:2341–64

    Google Scholar 

  5. Sen, G. C. Viruses and interferons. Annu Rev Microbiol 55:255–81

    Google Scholar 

  6. Levy, D. E. & Garcia-Sastre, A. The virus battles: IFN induction of the antiviral state and mechanisms of viral evasion. Cytokine Growth Factor Rev 12:143–56

    Google Scholar 

  7. Guidotti, L. G. & Chisari, F. V. Noncytolytic control of viral infections by the innate and adaptive immune response. Annu Rev Immunol 19:65–91

    Google Scholar 

  8. Grandvaux, N., tenOever, B. R., Servant, M. J. & Hiscott, J. The interferon antiviral response: from viral invasion to evasion. Curr Opin Infect Dis 15:259–67

    Google Scholar 

  9. Garcia-Sastre, A. Mechanisms of inhibition of the host interferon alpha/beta-mediated antiviral responses by viruses. Microbes Infect 4:647–55

    Google Scholar 

  10. Katze, M. G., He, Y. & Gale, M., Jr. Viruses and interferon: a fight for supremacy. Nat Rev Immunol 2:675–87

    Google Scholar 

  11. Biron, C. A. & Sen, G. C. in Fields’ Virology (eds. Fields, B. N., Knipe, D. M., Howley, P. M. & Griffin, D. E.) 321–349 (Lippincott Williams and Wilkins, Philadelphia, 2001)

    Google Scholar 

  12. Gotoh, B., Komatsu, T., Takeuchi, K. & Yokoo, J. Paramyxovirus accessory proteins as interferon antagonists. Microbiol Immunol 45:787–800

    Google Scholar 

  13. Horvath, C. M. Silencing STATs: lessons from paramyxovirus interferon evasion. Cytokine Growth Factor Rev 15:117–27

    Google Scholar 

  14. Andrejeva, J., Young, D. F., Goodbourn, S. & Randall, R. E. Degradation of STAT1 and STAT2 by the V proteins of simian virus 5 and human parainfluenza virus type 2, respectively: consequences for virus replication in the presence of alpha/beta and gamma interferons. J Virol 76:2159–67

    Google Scholar 

  15. Poole, E., He, B., Lamb, R. A., Randall, R. E. & Goodbourn, S. The V proteins of simian virus 5 and other paramyxoviruses inhibit induction of interferon-beta. Virology 303:33–46

    Google Scholar 

  16. Atreya, P. L. & Kulkarni, S. Respiratory syncytial virus strain A2 is resistant to the antiviral effects of type I interferons and human MxA. Virology 261:227–41 (1999).

    Article  PubMed  CAS  Google Scholar 

  17. Bender, I. B. Paget’s disease. J Endod 29:720–3

    Google Scholar 

  18. Rall, G. F. Measles virus 1998–2002: progress and controversy. Annu Rev Microbiol 57:343–67

    Google Scholar 

  19. Rima, B. K., Gassen, U., Helfrich, M. H. & Ralston, S. H. The pro and con of measles virus in Paget’s disease: con. J Bone Miner Res 17:2290–2; author reply 2293

    Google Scholar 

  20. Takayanagi, H., Kim, S. & Taniguchi, T. Signaling crosstalk between RANKL and interferons in osteoclast differentiation. Arthritis Res 4Suppl 3:S227–32

    Google Scholar 

  21. Bossert, B. & Conzelmann, K. K. Respiratory syncytial virus (RSV) nonstructural (NS) proteins as host range determinants: a chimeric bovine RSV with NS genes from human RSV is attenuated in interferon-competent bovine cells. J Virol 76:4287–93

    Google Scholar 

  22. Parisien, J. P., Lau, J. F. & Horvath, C. M. STAT2 acts as a host range determinant for species-specific paramyxovirus interferon antagonism and simian virus 5 replication. J Virol 76:6435–41

    Google Scholar 

  23. Park, M. S., Garcia-Sastre, A., Cros, J. F., Basler, C. F. & Palese, P. Newcastle disease virus V protein is a determinant of host range restriction. J Virol 77:9522–32

    Google Scholar 

  24. Young, D. F. et al. Single amino acid substitution in the V protein of simian virus 5 differentiates its ability to block interferon signaling in human and murine cells. J Virol 75:3363–70

    Google Scholar 

  25. Didcock, L., Young, D. F., Goodbourn, S. & Randall, R. E. Sendai virus and simian virus 5 block activation of interferon-responsive genes: importance for virus pathogenesis. J Virol 73:3125–33

    Google Scholar 

  26. Young, D. F. et al. Virus replication in engineered human cells that do not respond to interferons. J Virol 77:2174–81

    Google Scholar 

  27. Garcia-Sastre, A. et al. Influenza A virus lacking the NS1 gene replicates in interferon-deficient systems. Virology 252:324–30

    Google Scholar 

  28. Levy, D. E. & Darnell, J. E., Jr. Stats: transcriptional control and biological impact. Nat Rev Mol Cell Biol 3:651–62

    Google Scholar 

  29. Ulane, C. M., Rodriguez, J. J., Parisien, J. P. & Horvath, C. M. STAT3 ubiquitylation and degradation by mumps virus suppress cytokine and oncogene signaling. J Virol 77:6385–93

    Google Scholar 

  30. Didcock, L., Young, D. F., Goodbourn, S. & Randall, R. E. The V protein of simian virus 5 inhibits interferon signaling by targeting STAT1 for proteasome-mediated degradation. J Virol 73:9928–33

    Google Scholar 

  31. He, B. et al. Recovery of paramyxovirus simian virus 5 with a V protein lacking the conserved cysteine-rich domain: the multifunctional V protein blocks both interferon-beta induction and interferon signaling. Virology 303:15–32

    Google Scholar 

  32. Wansley, E. K. & Parks, G. D. Naturally occurring substitutions in the P/V gene convert the noncytopathic paramyxovirus simian virus 5 into a virus that induces alpha/beta interferon synthesis and cell death. J Virol 76:10109–21

    Google Scholar 

  33. Weissman, A. M. Themes and variations on ubiquitylation. Nat Rev Mol Cell Biol 2:169–78

    Google Scholar 

  34. Jackson, P. K. et al. The lore of the RINGs: substrate recognition and catalysis by ubiquitin ligases. Trends Cell Biol 10:429–39

    Google Scholar 

  35. Ulane, C. M. & Horvath, C. M. Paramyxoviruses SV5 and HPIV2 Assemble STAT Protein Ubiquitin Ligase Complexes from Cellular Components. Virology 304:160–6

    Google Scholar 

  36. Hariya, Y., Yokosawa, N., Yonekura, N., Kohama, G. & Fuji, N. Mumps virus can suppress the effective augmentation of HPC-induced apoptosis by IFN-gamma through disruption of IFN signaling in U937 cells. Microbiol Immunol 44:537–41

    Google Scholar 

  37. Kubota, T., Yokosawa, N., Yokota, S. & Fujii, N. C terminal CYS-RICH region of mumps virus structural V protein correlates with block of interferon alpha and gamma signal transduction pathway through decrease of STAT 1-alpha. Biochem Biophys Res Commun 283:255–9

    Google Scholar 

  38. Nishio, M. et al. High resistance of human parainfluenza type 2 virus protein-expressing cells to the antiviral and anti-cell proliferative activities of alpha/beta interferons: cysteine-rich V-specific domain is required for high resistance to the interferons. J Virol 75:9165–76

    Google Scholar 

  39. Young, D. F., Didcock, L., Goodbourn, S. & Randall, R. E. Paramyxoviridae use distinct virus-specific mechanisms to circumvent the interferon response. Virology 269:383–90

    Google Scholar 

  40. Parisien, J. P. et al. The V protein of human parainfluenza virus 2 antagonizes type I interferon responses by destabilizing signal transducer and activator of transcription 2. Virology 283:230–9

    Google Scholar 

  41. Huang, Z., Krishnamurthy, S., Panda, A. & Samal, S. K. Newcastle disease virus V protein is associated with viral pathogenesis and functions as an alpha interferon antagonist. J Virol 77:8676–85

    Google Scholar 

  42. Young, V. A. & Parks, G. D. Simian virus 5 is a poor inducer of chemokine secretion from human lung epithelial cells: identification of viral mutants that activate interleukin-8 secretion by distinct mechanisms. J Virol 77:7124–30

    Google Scholar 

  43. Parisien, J. P., Lau, J. F., Rodriguez, J. J., Ulane, C. M. & Horvath, C. M. Selective STAT protein degradation induced by paramyxoviruses requires both STAT1 and STAT2 but is independent of alpha/beta interferon signal transduction. J Virol 76:4190–8

    Google Scholar 

  44. Andrejeva, J., Poole, E., Young, D. F., Goodbourn, S. & Randall, R. E. The p127 subunit (DDB1) of the UV-DNA damage repair binding protein is essential for the targeted degradation of STAT1 by the V protein of the paramyxovirus simian virus 5. J Virol 76:11379–86

    Google Scholar 

  45. Young, D. F., Didcock, L. & Randall, R. E. Isolation of highly fusogenic variants of simian virus 5 from persistently infected cells that produce and respond to interferon. J Virol 71:9333–42

    Google Scholar 

  46. Nishio, M., Garcin, D., Simonet, V. & Kolakofsky, D. The carboxyl segment of the mumps virus V protein associates with Stat proteins in vitro via a tryptophan-rich motif. Virology 300:92–9

    Google Scholar 

  47. Yokosawa, N., Yokota, S., Kubota, T. & Fujii, N. C-terminal region of STAT-1alpha is not necessary for its ubiquitination and degradation caused by mumps virus V protein. J Virol 76:12683–90

    Google Scholar 

  48. Randall, R. E. & Bermingham, A. NP:P and NP:V interactions of the paramyxovirus simian virus 5 examined using a novel protein: protein capture assay. Virology 224:121–9

    Google Scholar 

  49. Paterson, R. G., Leser, G. P., Shaughnessy, M. A. & Lamb, R. A. The paramyxovirus SV5 V protein binds two atoms of zinc and is a structural component of virions. Virology 208:121–31

    Google Scholar 

  50. Lin, G. Y., Paterson, R. G. & Lamb, R. A. The RNA binding region of the paramyxovirus SV5 V and P proteins. Virology 238:460–9

    Google Scholar 

  51. Lin, G. Y., Paterson, R. G., Richardson, C. D. & Lamb, R. A. The V protein of the paramyxovirus SV5 interacts with damage-specific DNA binding protein. Virology 249:189–200

    Google Scholar 

  52. Lin, G. Y. & Lamb, R. A. The paramyxovirus simian virus 5 V protein slows progression of the cell cycle. J Virol 74:9152–66

    Google Scholar 

  53. Leupin, O., Bontron, S. & Strubin, M. Hepatitis B virus X protein and simian virus 5 V protein exhibit similar UV-DDB1 binding properties to mediate distinct activities. J Virol 77:6274–83

    Google Scholar 

  54. Pintard, L., Willems, A. & Peter, M. Cullin-based ubiquitin ligases: Cul3-BTB complexes join the family. Embo J 23:1681–7

    Google Scholar 

  55. Wertz, I. E. et al. Human De-etiolated-1 regulates c-Jun by assembling a CUL4A ubiquitin ligase. Science 303:1371–4

    Google Scholar 

  56. Croze, E. et al. Receptor for activated C-kinase (RACK-1), a WD motif-containing protein, specifically associates with the human type I IFN receptor. J Immunol 165:5127–32

    Google Scholar 

  57. Usacheva, A. et al. The WD motif-containing protein receptor for activated protein kinase C (RACK1) is required for recruitment and activation of signal transducer and activator of transcription 1 through the type I interferon receptor. J Biol Chem 276:22948–53

    Google Scholar 

  58. Kubota, T., Yokosawa, N., Yokota, S. & Fujii, N. Association of mumps virus V protein with RACK1 results in dissociation of STAT-1 from the alpha interferon receptor complex. J Virol 76:12676–82

    Google Scholar 

  59. Kato, A., Kiyotani, K., Sakai, Y., Yoshida, T. & Nagai, Y. The paramyxovirus, Sendai virus, V protein encodes a luxury function required for viral pathogenesis. Embo J 16:578–87

    Google Scholar 

  60. Kato, A. et al. Importance of the cysteine-rich carboxyl-terminal half of V protein for Sendai virus pathogenesis. J Virol 71:7266–72

    Google Scholar 

  61. Delenda, C., Hausmann, S., Garcin, D. & Kolakofsky, D. Normal cellular replication of Sendai virus without the trans-frame, nonstructural V protein. Virology 228:55–62

    Google Scholar 

  62. Delenda, C., Taylor, G., Hausmann, S., Garcin, D. & Kolakofsky, D. Sendai viruses with altered P, V, and W protein expression. Virology 242:327–37

    Google Scholar 

  63. Kurotani, A. et al. Sendai virus C proteins are categorically nonessential gene products but silencing their expression severely impairs viral replication and pathogenesis. Genes Cells 3:111–24

    Google Scholar 

  64. Hasan, M. K. et al. Versatility of the accessory C proteins of Sendai virus: contribution to virus assembly as an additional role. J Virol 74:5619–28

    Google Scholar 

  65. Komatsu, T., Takeuchi, K., Yokoo, J., Tanaka, Y. & Gotoh, B. Sendai virus blocks alpha interferon signaling to signal transducers and activators of transcription. J Virol 74:2477–80

    Google Scholar 

  66. Garcin, D., Curran, J., Itoh, M. & Kolakofsky, D. Longer and shorter forms of Sendai virus C proteins play different roles in modulating the cellular antiviral response. J Virol 75:6800–7

    Google Scholar 

  67. Takeuchi, K. et al. Sendai virus C protein physically associates with Stat1. Genes Cells 6:545–57

    Google Scholar 

  68. Komatsu, T., Takeuchi, K., Yokoo, J. & Gotoh, B. Sendai virus C protein impairs both phosphorylation and dephosphorylation processes of Stat1. FEBS Lett 511:139–44

    Google Scholar 

  69. Saito, S., Ogino, T., Miyajima, N., Kato, A. & Kohase, M. Dephosphorylation failure of tyrosine-phosphorylated STAT1 in IFN-stimulated Sendai virus C protein-expressing cells. Virology 293:205–9

    Google Scholar 

  70. Gotoh, B., Komatsu, T., Takeuchi, K. & Yokoo, J. The C-terminal half-fragment of the Sendai virus C protein prevents the gamma-activated factor from binding to a gamma-activated sequence site. Virology 316:29–40

    Google Scholar 

  71. Garcin, D., Marq, J. B., Goodbourn, S. & Kolakofsky, D. The amino-terminal extensions of the longer Sendai virus C proteins modulate pY701-Stat1 and bulk Stat1 levels independently of interferon signaling. J Virol 77:2321–9

    Google Scholar 

  72. Garcin, D., Marq, J. B., Strahle, L., le Mercier, P. & Kolakofsky, D. All four Sendai Virus C proteins bind Stat1, but only the larger forms also induce its mono-ubiquitination and degradation. Virology 295:256–65

    Google Scholar 

  73. Garcin, D., Latorre, P. & Kolakofsky, D. Sendai virus C proteins counteract the interferon-mediated induction of an antiviral state. J Virol 73:6559–65

    Google Scholar 

  74. Gotoh, B. et al. Knockout of the Sendai virus C gene eliminates the viral ability to prevent the interferon-alpha/beta-mediated responses. FEBS Lett 459:205–10

    Google Scholar 

  75. Kato, A. et al. Y2, the smallest of the Sendai virus C proteins, is fully capable of both counteracting the antiviral action of interferons and inhibiting viral RNA synthesis. J Virol 75:3802–10

    Google Scholar 

  76. Garcin, D., Curran, J. & Kolakofsky, D. Sendai virus C proteins must interact directly with cellular components to interfere with interferon action. J Virol 74:8823–30

    Google Scholar 

  77. Strahle, L., Garcin, D., Le Mercier, P., Schlaak, J. F. & Kolakofsky, D. Sendai virus targets inflammatory responses, as well as the interferon-induced antiviral state, in a multifaceted manner. J Virol 77:7903–13

    Google Scholar 

  78. Durbin, A. P. et al. Recovery of infectious human parainfluenza virus type 3 from cDNA. Virology 235:323–32

    Google Scholar 

  79. Durbin, A. P., McAuliffe, J. M., Collins, P. L. & Murphy, B. R. Mutations in the C, D, and V open reading frames of human parainfluenza virus type 3 attenuate replication in rodents and primates. Virology 261:319–30

    Google Scholar 

  80. Smallwood, S. & Moyer, S. A. The L polymerase protein of parainfluenza virus 3 forms an oligomer and can interact with the heterologous Sendai virus L, P and C proteins. Virology 318:439–50

    Google Scholar 

  81. Malur, A. G., Hoffman, M. A. & Banerjee, A. K. The human parainfluenza virus type 3 (HPIV 3) C protein inhibits viral transcription. Virus Res 99:199–204

    Google Scholar 

  82. Valsamakis, A. et al. Recombinant measles viruses with mutations in the C, V, or F gene have altered growth phenotypes in vivo. J Virol 72:7754–61

    Google Scholar 

  83. Tober, C. et al. Expression of measles virus V protein is associated with pathogenicity and control of viral RNA synthesis. J Virol 72:8124–32

    Google Scholar 

  84. Patterson, J. B., Thomas, D., Lewicki, H., Billeter, M. A. & Oldstone, M. B. V and C proteins of measles virus function as virulence factors in vivo. Virology 267:80–9

    Google Scholar 

  85. Radecke, F. & Billeter, M. A. The nonstructural C protein is not essential for multiplication of Edmonston B strain measles virus in cultured cells. Virology 217:418–21

    Google Scholar 

  86. Schneider, H., Kaelin, K. & Billeter, M. A. Recombinant measles viruses defective for RNA editing and V protein synthesis are viable in cultured cells. Virology 227:314–22

    Google Scholar 

  87. Fujii, N. et al. Oligo-2′,5′-adenylate synthetase activity in K562 cell lines persistently infected with measles or mumps virus. J Gen Virol 69 (Pt 8):085–91

    Google Scholar 

  88. Yokota, S. et al. Measles virus suppresses interferon-alpha signaling pathway: suppression of Jak1 phosphorylation and association of viral accessory proteins, C and V, with interferon-alpha receptor complex. Virology 306:135–46

    Google Scholar 

  89. Takeuchi, K., Kadota, S. I., Takeda, M., Miyajima, N. & Nagata, K. Measles virus V protein blocks interferon (IFN)-alpha/beta but not IFN-gamma signaling by inhibiting STAT1 and STAT2 phosphorylation. FEBS Lett 545:177–82

    Google Scholar 

  90. Rodriguez, J. J., Parisien, J. P. & Horvath, C. M. Nipah virus V protein evades alpha and gamma interferons by preventing STAT1 and STAT2 activation and nuclear accumulation. J Virol 76:11476–83

    Google Scholar 

  91. Rodriguez, J. J., Wang, L. F. & Horvath, C. M. Hendra virus V protein inhibits interferon signaling by preventing STAT1 and STAT2 nuclear accumulation. J Virol 77:11842–5

    Google Scholar 

  92. Rodriguez, J. J., Cruz, C. D. & Horvath, C. M. Identification of the nuclear export signal and STAT-binding domains of the Nipah virus V protein reveals mechanisms underlying interferon evasion. J Virol 78:5358–67

    Google Scholar 

  93. Shaw, M. L., Garcia-Sastre, A., Palese, P. & Basler, C. F. Nipah virus V and W proteins have a common STAT1-binding domain yet inhibit STAT1 activation from the cytoplasmic and nuclear compartments, respectively. J Virol 78:5633–41

    Google Scholar 

  94. Park, M. S. et al. Newcastle disease virus (NDV)-based assay demonstrates interferon antagonist activity for the NDV V protein and the Nipah virus V, W, and C proteins. J Virol 77:1501–11

    Google Scholar 

  95. Bossert, B., Marozin, S. & Conzelmann, K. K. Nonstructural proteins NS1 and NS2 of bovine respiratory syncytial virus block activation of interferon regulatory factor 3. J Virol 77:8661–8

    Google Scholar 

  96. Ramaswamy, M., Shi, L., Monick, M. M., Hunninghake, G. W. & Look, D. C. Specific Inhibition of Type I Interferon Signal Transduction by Respiratory Syncytial Virus. Am J Respir Cell Mol Biol 30:893–900

    Google Scholar 

  97. Teng, M. N. & Collins, P. L. Altered growth characteristics of recombinant respiratory syncytial viruses which do not produce NS2 protein. J Virol 73:466–73

    Google Scholar 

  98. Teng, M. N. et al. Recombinant respiratory syncytial virus that does not express the NS1 or M2-2 protein is highly attenuated and immunogenic in chimpanzees. J Virol 74:9317–21

    Google Scholar 

  99. Whitehead, S. S. et al. Recombinant respiratory syncytial virus bearing a deletion of either the NS2 or SH gene is attenuated in chimpanzees. J Virol 73:3438–42

    Google Scholar 

  100. Schlender, J., Bossert, B., Buchholz, U. & Conzelmann, K. K. Bovine respiratory syncytial virus nonstructural proteins NS1 and NS2 cooperatively antagonize alpha/beta interferon-induced antiviral response. J Virol 74:8234–42

    Google Scholar 

  101. Jin, H. et al. Evaluation of recombinant respiratory syncytial virus gene deletion mutants in African green monkeys for their potential as live attenuated vaccine candidates. Vaccine 21:3647–52

    Google Scholar 

  102. Jin, H. et al. Recombinant respiratory syncytial viruses with deletions in the NS1, NS2, SH, and M2-2 genes are attenuated in vitro and in vivo. Virology 273:210–8

    Google Scholar 

  103. Valarcher, J. F. et al. Role of alpha/beta interferons in the attenuation and immunogenicity of recombinant bovine respiratory syncytial viruses lacking NS proteins. J Virol 77:8426–39

    Google Scholar 

  104. Hall, C. B., Douglas, R. G., Jr., Simons, R. L. & Geiman, J. M. Interferon production in children with respiratory syncytial, influenza, and parainfluenza virus infections. J Pediatr 93:28–32

    Google Scholar 

  105. Krilov, L. R., Hendry, R. M., Godfrey, E. & McIntosh, K. Respiratory virus infection of peripheral blood monocytes: correlation with ageing of cells and interferon production in vitro. J Gen Virol 68 (Pt 6):1749–53

    Google Scholar 

  106. Loveys, D. A., Kulkarni, S. & Atreya, P. L. Role of type I IFNs in the in vitro attenuation of live, temperature-sensitive vaccine strains of human respiratory syncytial virus. Virology 271:390–400

    Google Scholar 

  107. McIntosh, K. Interferon in nasal secretions from infants with viral respiratory tract infections. J Pediatr 93:33–6

    Google Scholar 

  108. Garofalo, R. et al. Respiratory syncytial virus infection of human respiratory epithelial cells up-regulates class I MHC expression through the induction of IFN-beta and IL-1 alpha. J Immunol 157:2506–13

    Google Scholar 

  109. Chonmaitree, T., Roberts, N. J., Jr., Douglas, R. G., Jr., Hall, C. B. & Simons, R. L. Interferon production by human mononuclear leukocytes: differences between respiratory syncytial virus and influenza viruses. Infect Immun 32:300–3

    Google Scholar 

  110. Roberts, N. J., Jr., Hiscott, J. & Signs, D. J. The limited role of the human interferon system response to respiratory syncytial virus challenge: analysis and comparison to influenza virus challenge. Microb Pathog 12:409–14

    Google Scholar 

  111. Hall, C. B., Douglas, R. G., Jr. & Simons, R. L. Interferon production in adults with respiratory syncytial viral infection. Ann Intern Med 94:53–5

    Google Scholar 

  112. Bell, D. M., Roberts, N. J., Jr. & Hall, C. B. Different antiviral spectra of human macrophage interferon activities. Nature 305:319–21

    Google Scholar 

  113. Spann, K. M., Tran, K. C., Chi, B., Rabin, R. L. & Collins, P. L. Suppression of the Induction of Alpha, Beta, and Gamma Interferons by the NS1 and NS2 Proteins of Human Respiratory Syncytial Virus in Human Epithelial Cells and Macrophages. J Virol 78:4363–9

    Google Scholar 

  114. Hanada, N., Morishima, T., Nishikawa, K., Isomura, S. & Nagai, Y. Interferon-mediated self-limiting growth of respiratory syncytial virus in mouse embryo cells. J Med Virol 20:363–70

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2005 Springer

About this chapter

Cite this chapter

Stock, N., Goodbourn, S., Randall, R.E. (2005). The Anti-Interferon Mechanisms of Paramyxoviruses. In: Palese, P. (eds) Modulation of Host Gene Expression and Innate Immunity by Viruses. Springer, Dordrecht. https://doi.org/10.1007/1-4020-3242-0_6

Download citation

Publish with us

Policies and ethics