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Home / Equine Research Bank / J Med Virol / Different chemokine expression in lethal and non-lethal muri...
Journal of medical virology2004; 74(3); 507-513; doi: 10.1002/jmv.20205

Different chemokine expression in lethal and non-lethal murine West Nile virus infection.

Abstract: West Nile (WN) virus is a mosquito-borne flavivirus that can cause lethal encephalitis in humans and horses. The WN virus endemic in New York City (NY) in 1999 caused large-scale mortality of wild birds that was not evident in endemic areas in other parts of the world, and the pathogenesis of the WN virus strain isolated in NY (NY strain) appears to differ from that of previously isolated strains. However, the pathogenesis of NY strain infection remains unclear. This study examined CC (RANTES/CCL5, MIP-1 alpha/CCL3, MIP-1 beta/CCL4) and CXC (IP-10/CXCL10, B lymphocyte chemoattractant (BLC/CXCL13), and B cell- and monocyte-activating chemokine (BMAC/CXCL14)) chemokine expression during lethal NY strain and non-lethal Eg101 strain infection in mice. We found that the mRNA of the CC chemokines, RANTES, MIP-1 alpha, MIP-1 beta, and IP-10 was highly up-regulated in the brain of NY strain-infected mice. By contrast, BLC mRNA was not detected in either group of mice, and BMAC mRNA was highly up-regulated in late stage of infection with the non-lethal Eg101 strain relative to levels in NY strain-infected mice.
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Publication Date: 2004-09-16 PubMed ID: 15368509DOI: 10.1002/jmv.20205Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The researchers investigated the expression of specific chemokines (signaling proteins) during lethal and non-lethal West Nile virus infections in mice. They found differences in the levels of these chemokines expressed, which may shed light on the pathogenesis of the disease.

Chemokines and West Nile Virus Infection

Chemokines are small proteins that play important roles in directing the movement of white blood cells to infected or damaged tissues and in regulating the immune response to infections. In this experiment, the researchers investigated the expression of two groups of chemokines, known as CC (RANTES/CCL5, MIP-1 alpha/CCL3, MIP-1 beta/CCL4) and CXC (IP-10/CXCL10, B lymphocyte chemoattractant (BLC/CXCL13), and B cell- and monocyte-activating chemokine (BMAC/CXCL14)), during lethal and non-lethal strains of West Nile virus infection in mice. The viral strains used were the West Nile virus NY strain and Eg101 strain.

  • The West Nile Virus (WNV) is commonly transmitted to animals and humans through mosquito bites. Lethal outcomes often include encephalitis, inflammation of the brain.
  • The NY strain is known for causing large-scale mortality of wild birds and distinct pathogenesis in humans, which differs from other West Nile virus strains.
  • Eg101 is a naturally attenuated strain of the West Nile virus that does not cause a severe disease in mice.

Differences in CC and CXC Chemokine expression

The researchers found varied levels of expression for the investigated chemokines during infection with the different strains of the West Nile virus:

  • The mRNA of the CC chemokines RANTES, MIP-1 alpha, MIP-1 beta, and IP-10 was greatly up-regulated in the brains of mice infected with the lethal NY strain. This means that the genes of these chemokines were highly active, leading to their increased production and presence. As these chemokines are associated with immune response, their over-expression could be linked to intense inflammation and neuro-damage associated with lethal West Nile virus infections.
  • Interestingly, the chemokine BLC’s mRNA was not detected in either group of infected mice, indicating that it might not be involved in the mouse’s immune response to West Nile virus infection.
  • Peculiarly, the BMAC mRNA was significantly up-regulated at the late stage of infection with the non-lethal Eg101 strain in comparison to the levels in NY strain-infected mice. This insights that BMAC might have a protective role in non-lethal West Nile virus infections.

Significance of the Study

Understanding differences in the immune response to lethal and non-lethal West Nile virus infection could offer important insights into the pathogenesis of the disease and uncover potential targets for prevention and treatment strategies. More research is necessary to fully understand the role of these chemokines and their implication in the severity and outcome of West Nile virus infections. Additionally, the study’s findings could potentially apply to other viruses in the flavivirus genus, which includes viruses like Zika and Dengue, as they all share similar infection and replication mechanisms.

Cite This Article

APA
Shirato K, Kimura T, Mizutani T, Kariwa H, Takashima I. (2004). Different chemokine expression in lethal and non-lethal murine West Nile virus infection. J Med Virol, 74(3), 507-513. https://doi.org/10.1002/jmv.20205

Publication

Journal of medical virology
ISSN: 0146-6615
NlmUniqueID: 7705876
Country: United States
Language: English
Volume: 74
Issue: 3
Pages: 507-513

Researcher Affiliations

Shirato, Kazuya
  • Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
Kimura, Takashi
    Mizutani, Tetsuya
      Kariwa, Hiroaki
        Takashima, Ikuo

          MeSH Terms

          • Animals
          • Antibodies, Viral / blood
          • Base Sequence
          • Birds / virology
          • Brain / immunology
          • Chemokines / genetics
          • Gene Expression
          • Humans
          • Mice
          • Mice, Inbred BALB C
          • Neutralization Tests
          • New York City
          • RNA, Messenger / genetics
          • RNA, Messenger / metabolism
          • Species Specificity
          • Spleen / immunology
          • West Nile Fever / genetics
          • West Nile Fever / immunology
          • West Nile Fever / virology
          • West Nile virus / immunology
          • West Nile virus / isolation & purification
          • West Nile virus / pathogenicity

          Citations

          This article has been cited 39 times.
          1. Benzarti E, Murray KO, Ronca SE. Interleukins, Chemokines, and Tumor Necrosis Factor Superfamily Ligands in the Pathogenesis of West Nile Virus Infection.. Viruses 2023 Mar 22;15(3).
            doi: 10.3390/v15030806pubmed: 36992514google scholar: lookup
          2. Bengue M, Ferraris P, Barthelemy J, Diagne CT, Hamel R, Liégeois F, Nougairède A, de Lamballerie X, Simonin Y, Pompon J, Salinas S, Missé D. Mayaro Virus Infects Human Brain Cells and Induces a Potent Antiviral Response in Human Astrocytes.. Viruses 2021 Mar 11;13(3).
            doi: 10.3390/v13030465pubmed: 33799906google scholar: lookup
          3. Byas AD, Ebel GD. Comparative Pathology of West Nile Virus in Humans and Non-Human Animals.. Pathogens 2020 Jan 7;9(1).
            doi: 10.3390/pathogens9010048pubmed: 31935992google scholar: lookup
          4. Rothan HA, Arora K, Natekar JP, Strate PG, Brinton MA, Kumar M. Z-DNA-Binding Protein 1 Is Critical for Controlling Virus Replication and Survival in West Nile Virus Encephalitis.. Front Microbiol 2019;10:2089.
            doi: 10.3389/fmicb.2019.02089pubmed: 31572318google scholar: lookup
          5. Chowdhury P, Khan SA. Significance of CCL2, CCL5 and CCR2 polymorphisms for adverse prognosis of Japanese encephalitis from an endemic population of India.. Sci Rep 2017 Oct 20;7(1):13716.
            doi: 10.1038/s41598-017-14091-8pubmed: 29057937google scholar: lookup
          6. Phongphaew W, Kobayashi S, Sasaki M, Carr M, Hall WW, Orba Y, Sawa H. Valosin-containing protein (VCP/p97) plays a role in the replication of West Nile virus.. Virus Res 2017 Jan 15;228:114-123.
            doi: 10.1016/j.virusres.2016.11.029pubmed: 27914931google scholar: lookup
          7. Dahm T, Rudolph H, Schwerk C, Schroten H, Tenenbaum T. Neuroinvasion and Inflammation in Viral Central Nervous System Infections.. Mediators Inflamm 2016;2016:8562805.
            doi: 10.1155/2016/8562805pubmed: 27313404google scholar: lookup
          8. Kobayashi S, Suzuki T, Kawaguchi A, Phongphaew W, Yoshii K, Iwano T, Harada A, Kariwa H, Orba Y, Sawa H. Rab8b Regulates Transport of West Nile Virus Particles from Recycling Endosomes.. J Biol Chem 2016 Mar 18;291(12):6559-68.
            doi: 10.1074/jbc.M115.712760pubmed: 26817838google scholar: lookup
          9. Durrant DM, Daniels BP, Pasieka T, Dorsey D, Klein RS. CCR5 limits cortical viral loads during West Nile virus infection of the central nervous system.. J Neuroinflammation 2015 Dec 15;12:233.
            doi: 10.1186/s12974-015-0447-9pubmed: 26667390google scholar: lookup
          10. Kumar M, Roe K, O'Connell M, Nerurkar VR. Induction of virus-specific effector immune cell response limits virus replication and severe disease in mice infected with non-lethal West Nile virus Eg101 strain.. J Neuroinflammation 2015 Sep 22;12:178.
            doi: 10.1186/s12974-015-0400-ypubmed: 26392176google scholar: lookup
          11. Suen WW, Uddin MJ, Wang W, Brown V, Adney DR, Broad N, Prow NA, Bowen RA, Hall RA, Bielefeldt-Ohmann H. Experimental West Nile Virus Infection in Rabbits: An Alternative Model for Studying Induction of Disease and Virus Control.. Pathogens 2015 Jul 14;4(3):529-58.
            doi: 10.3390/pathogens4030529pubmed: 26184326google scholar: lookup
          12. Erickson AK, Pfeiffer JK. Spectrum of disease outcomes in mice infected with YFV-17D.. J Gen Virol 2015 Jun;96(Pt 6):1328-1339.
            doi: 10.1099/vir.0.000075pubmed: 25646269google scholar: lookup
          13. Peña J, Plante JA, Carillo AC, Roberts KK, Smith JK, Juelich TL, Beasley DW, Freiberg AN, Labute MX, Naraghi-Arani P. Multiplexed digital mRNA profiling of the inflammatory response in the West Nile Swiss Webster mouse model.. PLoS Negl Trop Dis 2014 Oct;8(10):e3216.
            doi: 10.1371/journal.pntd.0003216pubmed: 25340818google scholar: lookup
          14. Michlmayr D, Lim JK. Chemokine receptors as important regulators of pathogenesis during arboviral encephalitis.. Front Cell Neurosci 2014;8:264.
            doi: 10.3389/fncel.2014.00264pubmed: 25324719google scholar: lookup
          15. Quick ED, Leser JS, Clarke P, Tyler KL. Activation of intrinsic immune responses and microglial phagocytosis in an ex vivo spinal cord slice culture model of West Nile virus infection.. J Virol 2014 Nov;88(22):13005-14.
            doi: 10.1128/JVI.01994-14pubmed: 25165111google scholar: lookup
          16. Sabouri AH, Marcondes MC, Flynn C, Berger M, Xiao N, Fox HS, Sarvetnick NE. TLR signaling controls lethal encephalitis in WNV-infected brain.. Brain Res 2014 Jul 29;1574:84-95.
            doi: 10.1016/j.brainres.2014.05.049pubmed: 24928618google scholar: lookup
          17. Kumar M, O'Connell M, Namekar M, Nerurkar VR. Infection with non-lethal West Nile virus Eg101 strain induces immunity that protects mice against the lethal West Nile virus NY99 strain.. Viruses 2014 Jun 6;6(6):2328-39.
            doi: 10.3390/v6062328pubmed: 24915459google scholar: lookup
          18. Hussmann KL, Fredericksen BL. Differential induction of CCL5 by pathogenic and non-pathogenic strains of West Nile virus in brain endothelial cells and astrocytes.. J Gen Virol 2014 Apr;95(Pt 4):862-867.
            doi: 10.1099/vir.0.060558-0pubmed: 24413421google scholar: lookup
          19. Graham JB, Da Costa A, Lund JM. Regulatory T cells shape the resident memory T cell response to virus infection in the tissues.. J Immunol 2014 Jan 15;192(2):683-90.
            doi: 10.4049/jimmunol.1202153pubmed: 24337378google scholar: lookup
          20. Qian F, Chung L, Zheng W, Bruno V, Alexander RP, Wang Z, Wang X, Kurscheid S, Zhao H, Fikrig E, Gerstein M, Snyder M, Montgomery RR. Identification of genes critical for resistance to infection by West Nile virus using RNA-Seq analysis.. Viruses 2013 Jul 8;5(7):1664-81.
            doi: 10.3390/v5071664pubmed: 23881275google scholar: lookup
          21. Fredericksen BL. The neuroimmune response to West Nile virus.. J Neurovirol 2014 Apr;20(2):113-21.
            doi: 10.1007/s13365-013-0180-zpubmed: 23843081google scholar: lookup
          22. Palus M, Vojtíšková J, Salát J, Kopecký J, Grubhoffer L, Lipoldová M, Demant P, Růžek D. Mice with different susceptibility to tick-borne encephalitis virus infection show selective neutralizing antibody response and inflammatory reaction in the central nervous system.. J Neuroinflammation 2013 Jun 27;10:77.
            doi: 10.1186/1742-2094-10-77pubmed: 23805778google scholar: lookup
          23. Cho H, Diamond MS. Immune responses to West Nile virus infection in the central nervous system.. Viruses 2012 Dec 17;4(12):3812-30.
            doi: 10.3390/v4123812pubmed: 23247502google scholar: lookup
          24. Jiang J, Karimi O, Ouburg S, Champion CI, Khurana A, Liu G, Freed A, Pleijster J, Rozengurt N, Land JA, Surcel HM, Tiitinen A, Paavonen J, Kronenberg M, Morré SA, Kelly KA. Interruption of CXCL13-CXCR5 axis increases upper genital tract pathology and activation of NKT cells following chlamydial genital infection.. PLoS One 2012;7(11):e47487.
            doi: 10.1371/journal.pone.0047487pubmed: 23189125google scholar: lookup
          25. Bardina SV, Lim JK. The role of chemokines in the pathogenesis of neurotropic flaviviruses.. Immunol Res 2012 Dec;54(1-3):121-32.
            doi: 10.1007/s12026-012-8333-3pubmed: 22547394google scholar: lookup
          26. Munoz-Erazo L, Natoli R, Provis JM, Madigan MC, King NJ. Microarray analysis of gene expression in West Nile virus-infected human retinal pigment epithelium.. Mol Vis 2012;18:730-43.
            pubmed: 22509103
          27. Wang K, Deubel V. Mice with different susceptibility to Japanese encephalitis virus infection show selective neutralizing antibody response and myeloid cell infectivity.. PLoS One 2011;6(9):e24744.
            doi: 10.1371/journal.pone.0024744pubmed: 21949747google scholar: lookup
          28. Hasebe R, Suzuki T, Makino Y, Igarashi M, Yamanouchi S, Maeda A, Horiuchi M, Sawa H, Kimura T. Transcellular transport of West Nile virus-like particles across human endothelial cells depends on residues 156 and 159 of envelope protein.. BMC Microbiol 2010 Jun 8;10:165.
            doi: 10.1186/1471-2180-10-165pubmed: 20529314google scholar: lookup
          29. Rogers KM, Heise M. Modulation of cellular tropism and innate antiviral response by viral glycans.. J Innate Immun 2009;1(5):405-12.
            doi: 10.1159/000226422pubmed: 20375598google scholar: lookup
          30. King M, Poya H, Rao J, Natarajan S, Butch AW, Aziz N, Kok S, Chang MH, Lyons JM, Ault K, Kelly KA. CXCL13 expression in Chlamydia trachomatis infection of the female reproductive tract.. Drugs Today (Barc) 2009 Nov;45 Suppl B(Suppl B):125-34.
            pubmed: 20011704
          31. Pulendran B. Learning immunology from the yellow fever vaccine: innate immunity to systems vaccinology.. Nat Rev Immunol 2009 Oct;9(10):741-7.
            doi: 10.1038/nri2629pubmed: 19763148google scholar: lookup
          32. Querec TD, Akondy RS, Lee EK, Cao W, Nakaya HI, Teuwen D, Pirani A, Gernert K, Deng J, Marzolf B, Kennedy K, Wu H, Bennouna S, Oluoch H, Miller J, Vencio RZ, Mulligan M, Aderem A, Ahmed R, Pulendran B. Systems biology approach predicts immunogenicity of the yellow fever vaccine in humans.. Nat Immunol 2009 Jan;10(1):116-125.
            doi: 10.1038/ni.1688pubmed: 19029902google scholar: lookup
          33. Scott EP, Branigan PJ, Del Vecchio AM, Weiss SR. Chemokine expression during mouse-hepatitis-virus-induced encephalitis: contributions of the spike and background genes.. J Neurovirol 2008 Jan;14(1):5-16.
            doi: 10.1080/13550280701750635pubmed: 18300071google scholar: lookup
          34. Garcia-Tapia D, Hassett DE, Mitchell WJ Jr, Johnson GC, Kleiboeker SB. West Nile virus encephalitis: sequential histopathological and immunological events in a murine model of infection.. J Neurovirol 2007 Apr;13(2):130-8.
            doi: 10.1080/13550280601187185pubmed: 17505981google scholar: lookup
          35. Zhou J, Law HK, Cheung CY, Ng IH, Peiris JS, Lau YL. Differential expression of chemokines and their receptors in adult and neonatal macrophages infected with human or avian influenza viruses.. J Infect Dis 2006 Jul 1;194(1):61-70.
            doi: 10.1086/504690pubmed: 16741883google scholar: lookup
          36. Glass WG, McDermott DH, Lim JK, Lekhong S, Yu SF, Frank WA, Pape J, Cheshier RC, Murphy PM. CCR5 deficiency increases risk of symptomatic West Nile virus infection.. J Exp Med 2006 Jan 23;203(1):35-40.
            doi: 10.1084/jem.20051970pubmed: 16418398google scholar: lookup
          37. Cheeran MC, Hu S, Sheng WS, Rashid A, Peterson PK, Lokensgard JR. Differential responses of human brain cells to West Nile virus infection.. J Neurovirol 2005 Dec;11(6):512-24.
            doi: 10.1080/13550280500384982pubmed: 16338745google scholar: lookup
          38. Glass WG, Lim JK, Cholera R, Pletnev AG, Gao JL, Murphy PM. Chemokine receptor CCR5 promotes leukocyte trafficking to the brain and survival in West Nile virus infection.. J Exp Med 2005 Oct 17;202(8):1087-98.
            doi: 10.1084/jem.20042530pubmed: 16230476google scholar: lookup
          39. Klein RS, Lin E, Zhang B, Luster AD, Tollett J, Samuel MA, Engle M, Diamond MS. Neuronal CXCL10 directs CD8+ T-cell recruitment and control of West Nile virus encephalitis.. J Virol 2005 Sep;79(17):11457-66.
            doi: 10.1128/JVI.79.17.11457-11466.2005pubmed: 16103196google scholar: lookup
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