HIV and HCV Activate the Inflammasome in Monocytes and Macrophages via Endosomal Toll-Like Receptors without Induction of Type 1 Interferon
Pathogens are detected by the immune system in multiple ways that initiate responses to control infection. Two systems of first line defense against viruses are 1) the production of Type I interferons and 2) production of the cytokines IL-1β and IL-18 by the inflammasome. Type I interferons promote an antiviral state in the infected host. Inflammasome cytokines induce inflammation, modulate adaptive immune responses, and have direct antiviral effects. While both are produced in response to the chronic human viral infections HIV and HCV, we demonstrate here that inflammasome activation does not require cell infection and that the mechanisms for viral sensing as well as cell types in which sensing occurs are distinct between the two viruses and between the type I interferon vs. inflammasome systems. The relative amount of sensing via these different mechanisms may affect the balance between antiviral and inflammatory responses to chronic infection.
Vyšlo v časopise:
HIV and HCV Activate the Inflammasome in Monocytes and Macrophages via Endosomal Toll-Like Receptors without Induction of Type 1 Interferon. PLoS Pathog 10(5): e32767. doi:10.1371/journal.ppat.1004082
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.ppat.1004082
Souhrn
Pathogens are detected by the immune system in multiple ways that initiate responses to control infection. Two systems of first line defense against viruses are 1) the production of Type I interferons and 2) production of the cytokines IL-1β and IL-18 by the inflammasome. Type I interferons promote an antiviral state in the infected host. Inflammasome cytokines induce inflammation, modulate adaptive immune responses, and have direct antiviral effects. While both are produced in response to the chronic human viral infections HIV and HCV, we demonstrate here that inflammasome activation does not require cell infection and that the mechanisms for viral sensing as well as cell types in which sensing occurs are distinct between the two viruses and between the type I interferon vs. inflammasome systems. The relative amount of sensing via these different mechanisms may affect the balance between antiviral and inflammatory responses to chronic infection.
Zdroje
1. UNAIDS (2011) UNAIDS 2011 World AIDS Day report. http://www.unaids.org/en/resources/publications/2011/name,63525,en.asp
2. WHO (1997) World Health Organization Hepatitis C: global prevalance. Wkly Epidemiol Rec 341–348.
3. StetsonDB, MedzhitovR (2006) Type I interferons in host defense. Immunity 25: 373–381.
4. BeignonAS, McKennaK, SkoberneM, ManchesO, DaSilvaI, et al. (2005) Endocytosis of HIV-1 activates plasmacytoid dendritic cells via Toll-like receptor-viral RNA interactions. J Clin Invest 115: 3265–3275.
5. LepelleyA, LouisS, SourisseauM, LawHK, PothlichetJ, et al. (2011) Innate sensing of HIV-infected cells. PLoS Pathog 7: e1001284.
6. O'BrienM, ManchesO, SabadoRL, BarandaSJ, WangY, et al. (2011) Spatiotemporal trafficking of HIV in human plasmacytoid dendritic cells defines a persistently IFN-alpha-producing and partially matured phenotype. J Clin Invest 121: 1088–1101.
7. DreuxM, GaraigortaU, BoydB, DecembreE, ChungJ, et al. (2012) Short-range exosomal transfer of viral RNA from infected cells to plasmacytoid dendritic cells triggers innate immunity. Cell Host Microbe 12: 558–570.
8. RobertsL, PassmoreJA, WilliamsonC, LittleF, BebellLM, et al. (2010) Plasma cytokine levels during acute HIV-1 infection predict HIV disease progression. AIDS 24: 819–831.
9. ChattergoonMA, LevineJS, LatanichR, OsburnWO, ThomasDL, et al. (2011) High plasma interleukin-18 levels mark the acute phase of hepatitis C virus infection. The Journal of infectious diseases 204: 1730–1740.
10. LamkanfiM, KannegantiTD, FranchiL, NunezG (2007) Caspase-1 inflammasomes in infection and inflammation. Journal of leukocyte biology 82: 220–225.
11. YearleyJH, XiaD, PearsonCB, CarvilleA, ShannonRP, et al. (2009) Interleukin-18 predicts atherosclerosis progression in SIV-infected and uninfected rhesus monkeys (Macaca mulatta) on a high-fat/high-cholesterol diet. Laboratory investigation; a journal of technical methods and pathology 89: 657–667.
12. MallatZ, CorbazA, ScoazecA, BesnardS, LesecheG, et al. (2001) Expression of interleukin-18 in human atherosclerotic plaques and relation to plaque instability. Circulation 104: 1598–1603.
13. PirhonenJ, SarenevaT, KurimotoM, JulkunenI, MatikainenS (1999) Virus infection activates IL-1 beta and IL-18 production in human macrophages by a caspase-1-dependent pathway. Journal of immunology 162: 7322–7329.
14. SharmaA, ChakrabortiA, DasA, DhimanRK, ChawlaY (2009) Elevation of interleukin-18 in chronic hepatitis C: implications for hepatitis C virus pathogenesis. Immunology 128: e514–522.
15. WatanabeD, UehiraT, YonemotoH, BandoH, OgawaY, et al. (2010) Sustained high levels of serum interferon-gamma during HIV-1 infection: a specific trend different from other cytokines. Viral immunology 23: 619–625.
16. IannelloA, BoulasselMR, SamaraniS, TremblayC, TomaE, et al. (2010) HIV-1 causes an imbalance in the production of interleukin-18 and its natural antagonist in HIV-infected individuals: implications for enhanced viral replication. The Journal of infectious diseases 201: 608–617.
17. BurdetteD, HaskettA, PresserL, McRaeS, IqbalJ, et al. (2012) Hepatitis C virus activates interleukin-1beta via caspase-1-inflammasome complex. J Gen Virol 93: 235–246.
18. ShrivastavaS, MukherjeeA, RayR, RayRB (2013) Hepatitis C Virus Induces Il-1beta/Il-18 In Circulatory And Resident Liver Macrophages. J Virol [epub ahead of print].
19. NegashAA, RamosHJ, CrochetN, LauDT, DoehleB, et al. (2013) IL-1beta production through the NLRP3 inflammasome by hepatic macrophages links hepatitis C virus infection with liver inflammation and disease. PLoS Pathog 9: e1003330.
20. DoitshG, GallowayNL, GengX, YangZ, MonroeKM, et al. (2013) Cell death by pyroptosis drives CD4 T-cell depletion in HIV-1 infection. Nature 505(7484): 509–14.
21. DoitshG, CavroisM, LassenKG, ZepedaO, YangZ, et al. (2010) Abortive HIV infection mediates CD4 T cell depletion and inflammation in human lymphoid tissue. Cell 143: 789–801.
22. ShrivastavaS, MukherjeeA, RayR, RayRB (2013) Hepatitis C virus induces interleukin-1beta (IL-1beta)/IL-18 in circulatory and resident liver macrophages. J Virol 87: 12284–12290.
23. YiM, VillanuevaRA, ThomasDL, WakitaT, LemonSM (2006) Production of infectious genotype 1a hepatitis C virus (Hutchinson strain) in cultured human hepatoma cells. Proceedings of the National Academy of Sciences of the United States of America 103: 2310–2315.
24. MonroeKM, YangZ, JohnsonJR, GengX, DoitshG, et al. (2013) IFI16 DNA Sensor Is Required for Death of Lymphoid CD4 T Cells Abortively Infected with HIV. Science 343: 428–432.
25. RasaiyaahJ, TanCP, FletcherAJ, PriceAJ, BlondeauC, et al. (2013) HIV-1 evades innate immune recognition through specific cofactor recruitment. Nature 503: 402–405.
26. CervantesJL, WeinermanB, BasoleC, SalazarJC (2012) TLR8: the forgotten relative revindicated. Cell Mol Immunol 9: 434–438.
27. HeilF, HemmiH, HochreinH, AmpenbergerF, KirschningC, et al. (2004) Species-specific recognition of single-stranded RNA via toll-like receptor 7 and 8. Science 303: 1526–1529.
28. GringhuisSI, van der VlistM, van den BergLM, den DunnenJ, LitjensM, et al. (2010) HIV-1 exploits innate signaling by TLR8 and DC-SIGN for productive infection of dendritic cells. Nat Immunol 11: 419–426.
29. KannegantiTD (2010) Central roles of NLRs and inflammasomes in viral infection. Nature reviews Immunology 10: 688–698.
30. SaitoT, OwenDM, JiangF, MarcotrigianoJ, GaleMJr (2008) Innate immunity induced by composition-dependent RIG-I recognition of hepatitis C virus RNA. Nature 454: 523–527.
31. ZhongJ, GastaminzaP, ChengG, KapadiaS, KatoT, et al. (2005) Robust hepatitis C virus infection in vitro. Proceedings of the National Academy of Sciences of the United States of America 102: 9294–9299.
32. OttoMJ, GarberS, WinslowDL, ReidCD, AldrichP, et al. (1993) In vitro isolation and identification of human immunodeficiency virus (HIV) variants with reduced sensitivity to C-2 symmetrical inhibitors of HIV type 1 protease. Proceedings of the National Academy of Sciences of the United States of America 90: 7543–7547.
33. GalloRC, SalahuddinSZ, PopovicM, ShearerGM, KaplanM, et al. (1984) Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS. Science 224: 500–503.
34. GartnerS, MarkovitsP, MarkovitzDM, KaplanMH, GalloRC, et al. (1986) The role of mononuclear phagocytes in HTLV-III/LAV infection. Science 233: 215–219.
35. DelgrangeD, PillezA, CastelainS, CocquerelL, RouilleY, et al. (2007) Robust production of infectious viral particles in Huh-7 cells by introducing mutations in hepatitis C virus structural proteins. The Journal of general virology 88: 2495–2503.
36. HellerT, SaitoS, AuerbachJ, WilliamsT, MoreenTR, et al. (2005) An in vitro model of hepatitis C virion production. Proceedings of the National Academy of Sciences of the United States of America 102: 2579–2583.
Štítky
Hygiena a epidemiológia Infekčné lekárstvo LaboratóriumČlánok vyšiel v časopise
PLOS Pathogens
2014 Číslo 5
- Očkování proti virové hemoragické horečce Ebola experimentální vakcínou rVSVDG-ZEBOV-GP
- Parazitičtí červi v terapii Crohnovy choroby a dalších zánětlivých autoimunitních onemocnění
- Koronavirus hýbe světem: Víte jak se chránit a jak postupovat v případě podezření?
Najčítanejšie v tomto čísle
- Venus Kinase Receptors Control Reproduction in the Platyhelminth Parasite
- Dual-Site Phosphorylation of the Control of Virulence Regulator Impacts Group A Streptococcal Global Gene Expression and Pathogenesis
- Severe Acute Respiratory Syndrome Coronavirus Envelope Protein Ion Channel Activity Promotes Virus Fitness and Pathogenesis
- High-Efficiency Targeted Editing of Large Viral Genomes by RNA-Guided Nucleases