#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

JC Polyomavirus Infection Is Strongly Controlled by Human Leucocyte Antigen Class II Variants


JC virus infection can lead to progressive multifocal leukoencephalopathy in individuals with a compromised immune system, such as during HIV infections or when treated with immunosuppressive or immunomodulating therapies. Progressive multifocal leukoencephalopathy is a rare but potentially fatal disease characterized by progressive damage of the brain white matter at multiple locations. It is therefore of importance to understand the host genetic control of response to JC virus in order to identify patients that can be treated with immunomodulating therapies, common treatments for autoimmune diseases, without increased risk for progressive multifocal leukoencephalopathy. This may also lead to development of preventative or curative anti-JC virus therapies. We here identify genetic variants being associated with JC virus antibody development; a negative association with the human leucocyte antigen DRB1*15-DQA1*01:02-DQB1*06:02 haplotype and a positive association with the DRB1*13-DQA1*01:03-DQB1*06:03 haplotype among controls and patients with multiple sclerosis from Scandinavia. We confirmed the associations in patients with multiple sclerosis from Germany. These associations between JC virus antibody response and human leucocyte antigens imply that CD4+ T cells are crucial in the immune defence and lay the ground for development of therapy and prevention.


Vyšlo v časopise: JC Polyomavirus Infection Is Strongly Controlled by Human Leucocyte Antigen Class II Variants. PLoS Pathog 10(4): e32767. doi:10.1371/journal.ppat.1004084
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004084

Souhrn

JC virus infection can lead to progressive multifocal leukoencephalopathy in individuals with a compromised immune system, such as during HIV infections or when treated with immunosuppressive or immunomodulating therapies. Progressive multifocal leukoencephalopathy is a rare but potentially fatal disease characterized by progressive damage of the brain white matter at multiple locations. It is therefore of importance to understand the host genetic control of response to JC virus in order to identify patients that can be treated with immunomodulating therapies, common treatments for autoimmune diseases, without increased risk for progressive multifocal leukoencephalopathy. This may also lead to development of preventative or curative anti-JC virus therapies. We here identify genetic variants being associated with JC virus antibody development; a negative association with the human leucocyte antigen DRB1*15-DQA1*01:02-DQB1*06:02 haplotype and a positive association with the DRB1*13-DQA1*01:03-DQB1*06:03 haplotype among controls and patients with multiple sclerosis from Scandinavia. We confirmed the associations in patients with multiple sclerosis from Germany. These associations between JC virus antibody response and human leucocyte antigens imply that CD4+ T cells are crucial in the immune defence and lay the ground for development of therapy and prevention.


Zdroje

1. AstromKE, MancallEL, RichardsonEPJr (1958) Progressive multifocal leuko-encephalopathy; a hitherto unrecognized complication of chronic lymphatic leukaemia and Hodgkin's disease. Brain 81: 93–111.

2. PadgettBL, WalkerDL, ZuRheinGM, EckroadeRJ, DesselBH (1971) Cultivation of papova-like virus from human brain with progressive multifocal leucoencephalopathy. Lancet 1: 1257–1260.

3. CarsonKR, FocosiD, MajorEO, PetriniM, RicheyEA, et al. (2009) Monoclonal antibody-associated progressive multifocal leucoencephalopathy in patients treated with rituximab, natalizumab, and efalizumab: a Review from the Research on Adverse Drug Events and Reports (RADAR) Project. Lancet Oncol 10: 816–824.

4. ErmisU, WeisJ, SchulzJB (2013) PML in a patient treated with fumaric acid. N Engl J Med 368: 1657–1658.

5. PiccinniC, SacripantiC, PoluzziE, De PontiF (2013) Disproportionality signal of progressive multifocal leukoencephalopathy: monoclonal antibodies versus other immunosuppressants. Pharmacoepidemiol Drug Saf 22: 443–445.

6. SchmedtN, AndersohnF, GarbeE (2012) Signals of progressive multifocal leukoencephalopathy for immunosuppressants: a disproportionality analysis of spontaneous reports within the US Adverse Event Reporting System (AERS). Pharmacoepidemiol Drug Saf 21: 1216–1220.

7. van OostenBW, KillesteinJ, BarkhofF, PolmanCH, WattjesMP (2013) PML in a patient treated with dimethyl fumarate from a compounding pharmacy. N Engl J Med 368: 1658–1659.

8. BloomgrenG, RichmanS, HotermansC, SubramanyamM, GoelzS, et al. (2012) Risk of natalizumab-associated progressive multifocal leukoencephalopathy. N Engl J Med 366: 1870–1880.

9. GorelikL, LernerM, BixlerS, CrossmanM, SchlainB, et al. (2010) Anti-JC virus antibodies: implications for PML risk stratification. Ann Neurol 68: 295–303.

10. PlavinaT, BermanM, NjengaM, CrossmanM, LernerM, et al. (2012) Multi-site analytical validation of an assay to detect anti-JCV antibodies in human serum and plasma. J Clin Virol 53: 65–71.

11. BozicC, RichmanS, PlavinaT, NatarajanA, ScanlonJV, et al. (2011) Anti-John Cunnigham virus antibody prevalence in multiple sclerosis patients: baseline results of STRATIFY-1. Ann Neurol 70: 742–750.

12. SorensenPS, BertolottoA, EdanG, GiovannoniG, GoldR, et al. (2012) Risk stratification for progressive multifocal leukoencephalopathy in patients treated with natalizumab. Mult Scler 18: 143–152.

13. WarnkeC, RamanujamR, PlavinaT, BergstromT, GoelzS, et al. (2013) Changes to anti-JCV antibody levels in a Swedish national MS cohort. J Neurol Neurosurg Psychiatry 84: 1199–205.

14. TrampeAK, HemmelmannC, StroetA, HaghikiaA, HellwigK, et al. (2012) Anti-JC virus antibodies in a large German natalizumab-treated multiple sclerosis cohort. Neurology 78: 1736–1742.

15. OutteryckO, OngagnaJC, DuhamelA, ZephirH, CollonguesN, et al. (2012) Anti-JCV antibody prevalence in a French cohort of MS patients under natalizumab therapy. J Neurol 259: 2293–2298.

16. CalguaB, BarardiCR, Bofill-MasS, Rodriguez-ManzanoJ, GironesR (2011) Detection and quantitation of infectious human adenoviruses and JC polyomaviruses in water by immunofluorescence assay. J Virol Methods 171: 1–7.

17. WarnkeC, PawlitaM, DehmelT, Posevitz-FejfarA, HartungHP, et al. (2013) An assay to quantify species-specific anti-JC virus antibody levels in MS patients. Mult Scler 19: 1137–44.

18. BergerJR, HouffSA, GurwellJ, VegaN, MillerCS, et al. (2013) JC virus antibody status underestimates infection rates. Ann Neurol 74: 84–90.

19. AskarM, DaghstaniJ, ThomasD, LeahyN, DunnP, et al. (2013) 16(th) IHIW: global distribution of extended HLA haplotypes. Int J Immunogenet 40: 31–38.

20. BettensF, Nicoloso de FaveriG, TiercyJM (2009) HLA-B51 and haplotypic diversity of B-Cw associations: implications for matching in unrelated hematopoietic stem cell transplantation. Tissue Antigens 73: 316–325.

21. AlperCA, LarsenCE, DubeyDP, AwdehZL, FiciDA, et al. (2006) The haplotype structure of the human major histocompatibility complex. Hum Immunol 67: 73–84.

22. JelcicI, AlyL, BinderTM, Bofill-MasS, PlanasR, et al. (2013) T cell epitope mapping of JC polyoma virus-encoded proteome reveals reduced T cell responses in HLA-DRB1*04:01+ donors. J Virol 87: 3393–3408.

23. BergerJR, HouffSA, GurwellJ, VegaN, MillerCS, et al. (2013) JC virus antibody status underestimates infection rates. Ann Neurol 74: 84–90.

24. MajorEO, FrohmanE, DouekD (2013) JC viremia in natalizumab-treated patients with multiple sclerosis. N Engl J Med 368: 2240–2241.

25. WhitmireJK (2011) Induction and function of virus-specific CD4+ T cell responses. Virology 411: 216–228.

26. Plavina T, Subramanyam M, Bloomgren G, Richman S, Pace A, et al. (2013) JCV Antibody Index Stratifies PML Risk in Natalizumab-Treated MS Patients. In: The 27th Annual Meeting of the Consortium of Multiple Sclerosis Centers. Orlando, Florida, United States. pp. Paper1642.

27. GorelikL, ReidC, TestaM, BrickelmaierM, BossolascoS, et al. (2011) Progressive multifocal leukoencephalopathy (PML) development is associated with mutations in JC virus capsid protein VP1 that change its receptor specificity. J Infect Dis 204: 103–114.

28. ReidCE, LiH, SurG, CarmilloP, BushnellS, et al. (2011) Sequencing and analysis of JC virus DNA from natalizumab-treated PML patients. J Infect Dis 204: 237–244.

29. GheuensS, FellayJ, GoldsteinDB, KoralnikIJ (2010) Role of human leukocyte antigen class I alleles in progressive multifocal leukoencephalopathy. J Neurovirol 16: 41–47.

30. RubiczR, YolkenR, DrigalenkoE, CarlessMA, DyerTD, et al. (2013) A Genome-Wide Integrative Genomic Study Localizes Genetic Factors Influencing Antibodies against Epstein-Barr Virus Nuclear Antigen 1 (EBNA-1). PLoS Genet 9: e1003147.

31. CangussuLO, TeixeiraR, CamposEF, RampimGF, MingotiSA, et al. (2011) HLA class II alleles and chronic hepatitis C virus infection. Scand J Immunol 74: 282–287.

32. ChenD, McKayJD, CliffordG, GaborieauV, ChabrierA, et al. (2011) Genome-wide association study of HPV seropositivity. Hum Mol Genet 20: 4714–4723.

33. KamataniY, WattanapokayakitS, OchiH, KawaguchiT, TakahashiA, et al. (2009) A genome-wide association study identifies variants in the HLA-DP locus associated with chronic hepatitis B in Asians. Nat Genet 41: 591–595.

34. DavilaS, FroelingFE, TanA, BonnardC, BolandGJ, et al. (2010) New genetic associations detected in a host response study to hepatitis B vaccine. Genes Immun 11: 232–238.

35. PngE, ThalamuthuA, OngRT, SnippeH, BolandGJ, et al. (2011) A genome-wide association study of hepatitis B vaccine response in an Indonesian population reveals multiple independent risk variants in the HLA region. Hum Mol Genet 20: 3893–3898.

36. KhorCC, ChauTN, PangJ, DavilaS, LongHT, et al. (2011) Genome-wide association study identifies susceptibility loci for dengue shock syndrome at MICB and PLCE1. Nat Genet 43: 1139–1141.

37. FellayJ, ShiannaKV, GeD, ColomboS, LedergerberB, et al. (2007) A whole-genome association study of major determinants for host control of HIV-1. Science 317: 944–947.

38. KumarV, KatoN, UrabeY, TakahashiA, MuroyamaR, et al. (2011) Genome-wide association study identifies a susceptibility locus for HCV-induced hepatocellular carcinoma. Nat Genet 43: 455–458.

39. LinkJ, KockumI, LorentzenAR, LieBA, CeliusEG, et al. (2012) Importance of human leukocyte antigen (HLA) class I and II alleles on the risk of multiple sclerosis. PLoS One 7: e36779.

40. HedstromAK, BaarnhielmM, OlssonT, AlfredssonL (2009) Tobacco smoking, but not Swedish snuff use, increases the risk of multiple sclerosis. Neurology 73: 696–701.

41. HolmenC, PiehlF, HillertJ, Fogdell-HahnA, LundkvistM, et al. (2011) A Swedish national post-marketing surveillance study of natalizumab treatment in multiple sclerosis. Mult Scler 17: 708–719.

42. OlerupO, ZetterquistH (1992) HLA-DR typing by PCR amplification with sequence-specific primers (PCR-SSP) in 2 hours: an alternative to serological DR typing in clinical practice including donor-recipient matching in cadaveric transplantation. Tissue Antigens 39: 225–235.

43. DiltheyAT, MoutsianasL, LeslieS, McVeanG (2011) HLA*IMP–an integrated framework for imputing classical HLA alleles from SNP genotypes. Bioinformatics 27: 968–972.

44. SawcerS, HellenthalG, PirinenM, SpencerCC, PatsopoulosNA, et al. (2011) Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature 476: 214–219.

45. DiltheyA, LeslieS, MoutsianasL, ShenJ, CoxC, et al. (2013) Multi-Population Classical HLA Type Imputation. PLoS Comput Biol 9: e1002877.

46. BeechamAH, PatsopoulosNA, XifaraDK, DavisMF, KemppinenA, et al. (2013) Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis. Nat Genet 45: 1353–60.

47. AulchenkoYS, RipkeS, IsaacsA, van DuijnCM (2007) GenABEL: an R library for genome-wide association analysis. Bioinformatics 23: 1294–1296.

48. PriceAL, PattersonNJ, PlengeRM, WeinblattME, ShadickNA, et al. (2006) Principal components analysis corrects for stratification in genome-wide association studies. Nat Genet 38: 904–909.

49. PurcellS, NealeB, Todd-BrownK, ThomasL, FerreiraMA, et al. (2007) PLINK: a tool set for whole-genome association and population-based linkage analyses. Am J Hum Genet 81: 559–575.

50. R Development Core Team (2008) R: A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing.

Štítky
Hygiena a epidemiológia Infekčné lekárstvo Laboratórium

Článok vyšiel v časopise

PLOS Pathogens


2014 Číslo 4
Najčítanejšie tento týždeň
Najčítanejšie v tomto čísle
Kurzy

Zvýšte si kvalifikáciu online z pohodlia domova

Získaná hemofilie - Povědomí o nemoci a její diagnostika
nový kurz

Eozinofilní granulomatóza s polyangiitidou
Autori: doc. MUDr. Martina Doubková, Ph.D.

Všetky kurzy
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#