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Differential Reliance on Autophagy for Protection from HSV Encephalitis between Newborns and Adults
Disease after infection with a pathogen results from an intersection between the infectious agent and the host. Newborns are particularly susceptible to infectious illness compared to adults, and HSV infection commonly results in devastating encephalitis. We studied the interaction of HSV with the type I interferon pathway and found that a specific activity of the viral protein γ34.5, which counters host autophagy to promote encephalitis in adults, was not required to cause disease in newborns. Furthermore, autophagy was not inhibited by HSV in the neonate and was not activated by type I interferon signaling, unlike in the adult. Activated autophagy was associated with increased apoptosis, which may contribute to the increased pathology in newborns. Our findings reveal development-specific differences in the pathogenesis of HSV encephalitis, including a distinct role for autophagy in the neonatal brain.
Vyšlo v časopise: Differential Reliance on Autophagy for Protection from HSV Encephalitis between Newborns and Adults. PLoS Pathog 11(1): e32767. doi:10.1371/journal.ppat.1004580
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004580Souhrn
Disease after infection with a pathogen results from an intersection between the infectious agent and the host. Newborns are particularly susceptible to infectious illness compared to adults, and HSV infection commonly results in devastating encephalitis. We studied the interaction of HSV with the type I interferon pathway and found that a specific activity of the viral protein γ34.5, which counters host autophagy to promote encephalitis in adults, was not required to cause disease in newborns. Furthermore, autophagy was not inhibited by HSV in the neonate and was not activated by type I interferon signaling, unlike in the adult. Activated autophagy was associated with increased apoptosis, which may contribute to the increased pathology in newborns. Our findings reveal development-specific differences in the pathogenesis of HSV encephalitis, including a distinct role for autophagy in the neonatal brain.
Zdroje
1. PinnintiSG, KimberlinDW (2013) Neonatal herpes simplex virus infections. Pediatr Clin North Am 60 : 351–365.
2. KimberlinDW, LinCY, JacobsRF, PowellDA, FrenkelLM, et al. (2001) Natural history of neonatal herpes simplex virus infections in the acyclovir era. Pediatrics 108 : 223–229.
3. LangenbergA, CoreyL, AshleyR, LeongW, StrausS (1999) A prospective study of new infections with herpes simplex virus type 1 and type 2. Chiron HSV Vaccine Study Group. N Engl J Med 341 : 1432–1438.
4. BernsteinDI, BellamyAR, HookEW3rd, LevinMJ, WaldA, et al. (2013) Epidemiology, clinical presentation, and antibody response to primary infection with herpes simplex virus type 1 and type 2 in young women. Clin Infect Dis 56 : 344–351.
5. JonesCA, Raynes-GreenowC, IsaacsD, on behalf of the NeonatalHSVSI, Contributors to the Australian Paediatric SurveillanceU (2014) Population-Based Surveillance of Neonatal Herpes Simplex Virus Infection in Australia, 1997-2011. Clin Infect Dis 59 : 525–531.
6. KroppRY, WongT, CormierL, RingroseA, BurtonS, et al. (2006) Neonatal herpes simplex virus infections in Canada: results of a 3-year national prospective study. Pediatrics 117 : 1955–1962.
7. GanttS, MullerWJ (2013) The immunologic basis for severe neonatal herpes disease and potential strategies for therapeutic intervention. Clin Dev Immunol 2013 : 369172.
8. MelchjorsenJ, MatikainenS, PaludanSR (2009) Activation and evasion of innate antiviral immunity by herpes simplex virus. Viruses 1 : 737–759.
9. ChouJ, KernER, WhitleyRJ, RoizmanB (1990) Mapping of herpes simplex virus-1 neurovirulence to gamma 134.5, a gene nonessential for growth in culture. Science 250 : 1262–1266.
10. BolovanCA, SawtellNM, ThompsonRL (1994) ICP34.5 mutants of herpes simplex virus type 1 strain 17syn+ are attenuated for neurovirulence in mice and for replication in confluent primary mouse embryo cell cultures. J Virol 68 : 48–55.
11. ChengG, GrossM, BrettME, HeB (2001) AlaArg motif in the carboxyl terminus of the gamma(1)34.5 protein of herpes simplex virus type 1 is required for the formation of a high-molecular-weight complex that dephosphorylates eIF-2alpha. J Virol 75 : 3666–3674.
12. HeB, GrossM, RoizmanB (1997) The gamma(1)34.5 protein of herpes simplex virus 1 complexes with protein phosphatase 1alpha to dephosphorylate the alpha subunit of the eukaryotic translation initiation factor 2 and preclude the shutoff of protein synthesis by double-stranded RNA-activated protein kinase. Proc Natl Acad Sci U S A 94 : 843–848.
13. VerpootenD, MaY, HouS, YanZ, HeB (2009) Control of TANK-binding kinase 1-mediated signaling by the gamma(1)34.5 protein of herpes simplex virus 1. J Biol Chem 284 : 1097–1105.
14. MaY, JinH, Valyi-NagyT, CaoY, YanZ, et al. (2012) Inhibition of TANK binding kinase 1 by herpes simplex virus 1 facilitates productive infection. J Virol 86 : 2188–2196.
15. TalloczyZ, JiangW, VirginHWt, LeibDA, ScheunerD, et al. (2002) Regulation of starvation - and virus-induced autophagy by the eIF2alpha kinase signaling pathway. Proc Natl Acad Sci U S A 99 : 190–195.
16. OrvedahlA, AlexanderD, TalloczyZ, SunQ, WeiY, et al. (2007) HSV-1 ICP34.5 confers neurovirulence by targeting the Beclin 1 autophagy protein. Cell Host Microbe 1 : 23–35.
17. OrvedahlA, MacPhersonS, SumpterRJr, TalloczyZ, ZouZ, et al. (2010) Autophagy protects against Sindbis virus infection of the central nervous system. Cell Host Microbe 7 : 115–127.
18. LiangXH, KleemanLK, JiangHH, GordonG, GoldmanJE, et al. (1998) Protection against fatal Sindbis virus encephalitis by beclin, a novel Bcl-2-interacting protein. J Virol 72 : 8586–8596.
19. YordyB, IijimaN, HuttnerA, LeibD, IwasakiA (2012) A neuron-specific role for autophagy in antiviral defense against herpes simplex virus. Cell Host Microbe 12 : 334–345.
20. KumaA, HatanoM, MatsuiM, YamamotoA, NakayaH, et al. (2004) The role of autophagy during the early neonatal starvation period. Nature 432 : 1032–1036.
21. FimiaGM, StoykovaA, RomagnoliA, GiuntaL, Di BartolomeoS, et al. (2007) Ambra1 regulates autophagy and development of the nervous system. Nature 447 : 1121–1125.
22. LundbergP, RamakrishnaC, BrownJ, TyszkaJM, HamamuraM, et al. (2008) The immune response to herpes simplex virus type 1 infection in susceptible mice is a major cause of central nervous system pathology resulting in fatal encephalitis. J Virol 82 : 7078–7088.
23. KoppSJ, KarabaAH, CohenLK, BanisadrG, MillerRJ, et al. (2013) Pathogenesis of neonatal herpes simplex 2 disease in a mouse model is dependent on entry receptor expression and route of inoculation. J Virol 87 : 474–481.
24. RamakrishnaC, NewoAN, ShenYW, CantinE (2011) Passively administered pooled human immunoglobulins exert IL-10 dependent anti-inflammatory effects that protect against fatal HSV encephalitis. PLoS Pathog 7: e1002071.
25. WangJP, BowenGN, ZhouS, CernyA, ZachariaA, et al. (2012) Role of specific innate immune responses in herpes simplex virus infection of the central nervous system. J Virol 86 : 2273–2281.
26. EjercitoPM, KieffED, RoizmanB (1968) Characterization of herpes simplex virus strains differing in their effects on social behaviour of infected cells. J Gen Virol 2 : 357–364.
27. KabeyaY, MizushimaN, UenoT, YamamotoA, KirisakoT, et al. (2000) LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing. EMBO J 19 : 5720–5728.
28. KabeyaY, MizushimaN, YamamotoA, Oshitani-OkamotoS, OhsumiY, et al. (2004) LC3, GABARAP and GATE16 localize to autophagosomal membrane depending on form-II formation. J Cell Sci 117 : 2805–2812.
29. KlionskyDJ, AbdallaFC, AbeliovichH, AbrahamRT, Acevedo-ArozenaA, et al. (2012) Guidelines for the use and interpretation of assays for monitoring autophagy. Autophagy 8 : 445–544.
30. UchiyamaY, KoikeM, ShibataM (2008) Autophagic neuron death in neonatal brain ischemia/hypoxia. Autophagy 4 : 404–408.
31. BlattNB, GlickGD (2001) Signaling pathways and effector mechanisms pre-programmed cell death. Bioorg Med Chem 9 : 1371–1384.
32. KollmannTR, LevyO, MontgomeryRR, GorielyS (2012) Innate immune function by Toll-like receptors: distinct responses in newborns and the elderly. Immunity 37 : 771–783.
33. ChengG, BrettME, HeB (2001) Val193 and Phe195 of the gamma 1 34.5 protein of herpes simplex virus 1 are required for viral resistance to interferon-alpha/beta. Virology 290 : 115–120.
34. HeB, GrossM, RoizmanB (1998) The gamma134.5 protein of herpes simplex virus 1 has the structural and functional attributes of a protein phosphatase 1 regulatory subunit and is present in a high molecular weight complex with the enzyme in infected cells. J Biol Chem 273 : 20737–20743.
35. LeibDA, HarrisonTE, LasloKM, MachalekMA, MoormanNJ, et al. (1999) Interferons regulate the phenotype of wild-type and mutant herpes simplex viruses in vivo. J Exp Med 189 : 663–672.
36. LeibDA, MachalekMA, WilliamsBR, SilvermanRH, VirginHW (2000) Specific phenotypic restoration of an attenuated virus by knockout of a host resistance gene. Proc Natl Acad Sci U S A 97 : 6097–6101.
37. PindelA, SadlerA (2011) The role of protein kinase R in the interferon response. J Interferon Cytokine Res 31 : 59–70.
38. KangR, TangD (2012) PKR-dependent inflammatory signals. Sci Signal 5: pe47.
39. GrishchukY, GinetV, TruttmannAC, ClarkePG, PuyalJ (2011) Beclin 1-independent autophagy contributes to apoptosis in cortical neurons. Autophagy 7 : 1115–1131.
40. ScarlattiF, MaffeiR, BeauI, CodognoP, GhidoniR (2008) Role of non-canonical Beclin 1-independent autophagy in cell death induced by resveratrol in human breast cancer cells. Cell Death Differ 15 : 1318–1329.
41. KoromM, WylieKM, WangH, DavisKL, SangabathulaMS, et al. (2013) A proautophagic antiviral role for the cellular prion protein identified by infection with a herpes simplex virus 1 ICP34.5 mutant. J Virol 87 : 5882–5894.
42. McKinleyMP, HayB, LingappaVR, LieberburgI, PrusinerSB (1987) Developmental expression of prion protein gene in brain. Developmental Biology 121 : 105–110.
43. SatohJ, KuroharaK, YukitakeM, KurodaY (1998) Constitutive and cytokine-inducible expression of prion protein gene in human neural cell lines. Journal of Neuropathology & Experimental Neurology 57 : 131–139.
44. MaiuriMC, ZalckvarE, KimchiA, KroemerG (2007) Self-eating and self-killing: crosstalk between autophagy and apoptosis. Nat Rev Mol Cell Biol 8 : 741–752.
45. Eisenberg-LernerA, BialikS, SimonHU, KimchiA (2009) Life and death partners: apoptosis, autophagy and the cross-talk between them. Cell Death Differ 16 : 966–975.
46. ScarlattiF, GranataR, MeijerAJ, CodognoP (2009) Does autophagy have a license to kill mammalian cells? Cell Death Differ 16 : 12–20.
47. KroemerG, LevineB (2008) Autophagic cell death: the story of a misnomer. Nat Rev Mol Cell Biol 9 : 1004–1010.
48. AkersKG, Martinez-CanabalA, RestivoL, YiuAP, De CristofaroA, et al. (2014) Hippocampal neurogenesis regulates forgetting during adulthood and infancy. Science 344 : 598–602.
49. YuanJ, YanknerBA (2000) Apoptosis in the nervous system. Nature 407 : 802–809.
50. UnderwoodE (2013) Mysteries of development. Why do so many neurons commit suicide during brain development? Science 340 : 1157–1158.
51. LevyO (2007) Innate immunity of the newborn: basic mechanisms and clinical correlates. Nat Rev Immunol 7 : 379–390.
52. Shoji-KawataS, SumpterR, LevenoM, CampbellGR, ZouZ, et al. (2013) Identification of a candidate therapeutic autophagy-inducing peptide. Nature 494 : 201–206.
53. AlexanderDE, WardSL, MizushimaN, LevineB, LeibDA (2007) Analysis of the role of autophagy in replication of herpes simplex virus in cell culture. J Virol 81 : 12128–12134.
54. TanakaM, KodairaH, NishiyamaY, SataT, KawaguchiY (2004) Construction of recombinant herpes simplex virus type I expressing green fluorescent protein without loss of any viral genes. Microbes Infect 6 : 485–493.
55. MullerU, SteinhoffU, ReisLF, HemmiS, PavlovicJ, et al. (1994) Functional role of type I and type II interferons in antiviral defense. Science 264 : 1918–1921.
56. AdkinsB, LeclercC, Marshall-ClarkeS (2004) Neonatal adaptive immunity comes of age. Nat Rev Immunol 4 : 553–564.
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