Serving the Society Since 1986
Advanced Search
Volume 36 Issue 4
August 2021
    Citation: Eman Teer, Danzil E. Joseph, Richard H. Glashoff, M.Faadiel Essop. Monocyte/Macrophage-Mediated Innate Immunity in HIV-1 Infection: From Early Response to Late Dysregulation and Links to Cardiovascular Diseases Onset .VIROLOGICA SINICA, 2021, 36(4) : 565-576.  http://dx.doi.org/10.1007/s12250-020-00332-0
    shu

    Monocyte/Macrophage-Mediated Innate Immunity in HIV-1 Infection: From Early Response to Late Dysregulation and Links to Cardiovascular Diseases Onset

    • 1.

      Centre for Cardio-metabolic Research in Africa(CARMA), Department of Physiological Sciences, Stellenbosch University, Stellenbosch 7600, South Africa

    • 2.

      Division of Medical Microbiology & Immunology, Department of Pathology, Stellenbosch University and NHLS, Cape Town 7505, South Africa

    • Corresponding author: M.Faadiel Essop, mfessop@sun.ac.za, ORCID: 0000-0002-8434-4294
    • Received Date: 29 July 2020
      Accepted Date: 26 October 2020
      Published Date: 05 January 2021
      Available online: 01 August 2021
    • Although monocytes and macrophages are key mediators of the innate immune system, the focus has largely been on the role of the adaptive immune system in the context of human immunodeficiency virus (HIV) infection. Thus more attention and research work regarding the innate immune system—especially the role of monocytes and macrophages during early HIV-1 infection—is required. Blood monocytes and tissue macrophages are both susceptible targets of HIV-1 infection, and the early host response can determine whether the nature of the infection becomes pathogenic or not. For example, monocytes and macrophages can contribute to the HIV reservoir and viral persistence, and influence the initiation/extension of immune activation and chronic inflammation. Here the expansion of monocyte subsets (classical, intermediate and non-classical) provide an increased understanding of the crucial role they play in terms of chronic inflammation and also by increasing the risk of coagulation during HIV-1 infection. This review discusses the role of monocytes and macrophages during HIV-1 pathogenesis, starting from the early response to late dysregulation that occurs as a result of persistent immune activation and chronic inflammation. Such changes are also linked to downstream targets such as increased coagulation and the onset of cardiovascular diseases.
    • 加载中

      1. Abreu CM, Veenhuis RT, Avalos CR et al (2019) Myeloid and CD4 T cells comprise the latent reservoir in antiretroviral therapy-suppressed SIVmac251-infected Macaques. MBio 10:e01659-e1719
          doi: 10.1128/mBio.01659-19

      2. Al-Harthi L, Voris J, Patterson BK et al (2004) Evaluation of the impact of highly active antiretroviral therapy on immune recovery in antiretroviral naive patients. HIV Med 5:55–65
          doi: 10.1111/j.1468-1293.2004.00186.x

      3. Anzinger JJ, Butterfield TR, Angelovich TA et al (2014) Monocytes as regulators of inflammation and HIV-related comorbidities during cART. J Immunol Res 2014:569819
          doi: 10.1155/2014/569819

      4. Auld E, Lin J, Chang E et al (2016) HIV infection is associated with shortened Telomere length in Ugandans with Suspected Tuberculosis. PLoS ONE 11:e0163153
          doi: 10.1371/journal.pone.0163153

      5. Ballegaard V, Brændstrup P, Pedersen KK et al (2018) Cytomegalovirus-specific T-cells are associated with immune senescence, but not with systemic inflammation, in people living with HIV. Sci Rep 8:3778
          doi: 10.1038/s41598-018-21347-4

      6. Barsov EV (2011) Telomerase and primary T cells: biology and immortalization for adoptive immunotherapy. Immunotherapy 3:407–421
          doi: 10.2217/imt.10.107

      7. Belge K-U, Dayyani F, Horelt A et al (2002) The proinflammatory CD14 + CD16 + DR ++ monocytes are a major source of TNF. J Immunol 168:3536–3542
          doi: 10.4049/jimmunol.168.7.3536

      8. Bertram KM, Botting RA, Baharlou H et al (2019) Identification of HIV transmitting CD11c+ human epidermal dendritic cells. Nat Commun 10:2759
          doi: 10.1038/s41467-019-10697-w

      9. Blackburn SD, Wherry EJ (2007) IL-10, T cell exhaustion and viral persistence. Trends Microbiol 15:143–146
          doi: 10.1016/j.tim.2007.02.006

      10. Boasso A, Shearer GM, Chougnet C (2009) Immune dysregulation in human immunodeficiency virus infection: know it, fix it, prevent it? J Intern Med 265:78–96
          doi: 10.1111/j.1365-2796.2008.02043.x

      11. Borrow P, Bhardwaj N (2008) Innate immune responses in primary HIV-1 infection. Curr Opin HIV AIDS 3:36–44
          doi: 10.1097/COH.0b013e3282f2bce7

      12. Botting RA, Rana H, Bertram KM et al (2017) Langerhans cells and sexual transmission of HIV and HSV. Rev Med Virol 27:e1923
          doi: 10.1002/rmv.1923

      13. Boyette LB, Macedo C, Hadi K et al (2017) Phenotype, function, and differentiation potential of human monocyte subsets. PLoS ONE 12:e0176460
          doi: 10.1371/journal.pone.0176460

      14. Brenchley JM (2013) Mucosal immunity in human and simian immunodeficiency lentivirus infections. Mucosal Immunol 6:657–665
          doi: 10.1038/mi.2013.15

      15. Brenchley JM, Karandikar NJ, Betts MR et al (2003) Expression of CD57 defines replicative senescence and antigen-induced apoptotic death of CD8+ T cells. Blood 101:2711–2720
          doi: 10.1182/blood-2002-07-2103

      16. Brenchley JM, Price DA, Schacker TW et al (2006) Microbial translocation is a cause of systemic immune activation in chronic HIV infection. Nat Med 12:1365–1371
          doi: 10.1038/nm1511

      17. Brenchley JM, Schacker TW, Ruff LE et al (2004) CD4+ T cell depletion during all stages of HIV disease occurs predominantly in the gastrointestinal tract. J Exp Med 200:749–759
          doi: 10.1084/jem.20040874

      18. Brooks DG, Trifilo MJ, Edelmann KH et al (2006) Interleukin-10 determines viral clearance or persistence in vivo. Nat Med 12:1301–1309
          doi: 10.1038/nm1492

      19. Buscher K, Marcovecchio P, Hedrick CC, Ley K (2017) Patrolling mechanics of non-classical monocytes in vascular inflammation. Front Cardiovasc Med 4:80
          doi: 10.3389/fcvm.2017.00080

      20. Carrington M, Alter G (2012) Innate immune control of HIV. Cold Spring Harb Perspect Med 2:a007070

      21. Cassol E, Malfeld S, Mahasha P et al (2010) Persistent microbial translocation and immune activation in HIV-1-infected South Africans receiving combination antiretroviral therapy. J Infect Dis 202:723–733
          doi: 10.1086/655229

      22. Chang JJ, Altfeld M (2010) Innate immune activation in primary HIV-1 infection. J Infect Dis 202:S297–S301
          doi: 10.1086/655657

      23. Chou JP, Effros RB (2013) T cell replicative senescence in human aging. Curr Pharm Des 19:1680–1698

      24. Christiaansen A, Varga SM, Spencer JV (2015) Viral manipulation of the host immune response. Curr Opin Immunol 36:54–60
          doi: 10.1016/j.coi.2015.06.012

      25. Clerici M, Shearer GM (1993) A TH1–>TH2 switch is a critical step in the etiology of HIV infection. Immunol Today 14:107–111
          doi: 10.1016/0167-5699(93)90208-3

      26. Cohen MS, Shaw GM, McMichael AJ, Haynes BF (2011) Acute HIV-1 infection. N Engl J Med 364:1943–1954
          doi: 10.1056/NEJMra1011874

      27. Cormican S, Griffin MD (2020) Human monocyte subset distinctions and function: insights from gene expression analysis. Front Immunol 11:1070
          doi: 10.3389/fimmu.2020.01070

      28. Creagh EM, O'Neill LAJ (2006) TLRs, NLRs and RLRs: a trinity of pathogen sensors that co-operate in innate immunity. Trends Immunol 27:352–357
          doi: 10.1016/j.it.2006.06.003

      29. De Smedt T, Van Mechelen M, De Becker G et al (1997) Effect of interleukin-10 on dendritic cell maturation and function. Eur J Immunol 27:1229–1235
          doi: 10.1002/eji.1830270526

      30. Deeks SG (2011) HIV infection, inflammation, immunosenescence, and aging. Annu Rev Med 62:141–155
          doi: 10.1146/annurev-med-042909-093756

      31. Duncan CJA, Russell RA, Sattentau QJ (2013) High multiplicity HIV-1 cell-to-cell transmission from macrophages to CD4+ T cells limits antiretroviral efficacy. AIDS 27:2201–2206
          doi: 10.1097/QAD.0b013e3283632ec4

      32. Ellery PJ, Tippett E, Chiu Y-L et al (2007) The CD16+ monocyte subset is more permissive to infection and preferentially harbors HIV-1 in vivo. J Immunol 178:6581–6589
          doi: 10.4049/jimmunol.178.10.6581

      33. Espíndola MS, Soares LS, Galvão-Lima LJ et al (2018) Epigenetic alterations are associated with monocyte immune dysfunctions in HIV-1 infection. Sci Rep 8:5505
          doi: 10.1038/s41598-018-23841-1

      34. Février M, Dorgham K, Rebollo A (2011) CD4+ T cell depletion in human immunodeficiency virus (HIV) infection: role of apoptosis. Viruses 3:586–612
          doi: 10.3390/v3050586

      35. Funderburg NT, Lederman MM (2014) Coagulation and morbidity in treated HIV infection. Thromb Res 133(Suppl 1):S21–S24

      36. Funderburg NT, Mayne E, Sieg SF et al (2010) Increased tissue factor expression on circulating monocytes in chronic HIV infection: relationship to in vivo coagulation and immune activation. Blood 115:161–167.
          doi: 10.1182/blood-2009-03-210179

      37. Funderburg NT, Zidar DA, Shive C et al (2012) Shared monocyte subset phenotypes in HIV-1 infection and in uninfected subjects with acute coronary syndrome. Blood 120:4599–4608.
          doi: 10.1182/blood-2012-05-433946

      38. Geissmann F, Jung S, Littman DR (2003) Blood monocytes consist of two principal subsets with distinct migratory properties. Immunity 19:71–82
          doi: 10.1016/S1074-7613(03)00174-2

      39. Ghattas A, Griffiths HR, Devitt A et al (2013) Monocytes in coronary artery disease and atherosclerosis: where are we now? J Am Coll Cardiol 62:1541–1551
          doi: 10.1016/j.jacc.2013.07.043

      40. Giorgi JV, Liu Z, Hultin LE et al (1993) Elevated levels of CD38+ CD8+ T cells in HIV infection add to the prognostic value of low CD4+ T cell levels: results of 6 years of follow-up. The Los Angeles Center, Multicenter AIDS Cohort Study. J Acquir Immune Defic Syndr 6:904–912
          doi: 10.1016/0928-8244(93)90068-F

      41. Gren ST, Rasmussen TB, Janciauskiene S et al (2015) A single-cell gene-expression profile reveals inter-cellular heterogeneity within human monocyte subsets. PLoS ONE 10:e0144351
          doi: 10.1371/journal.pone.0144351

      42. Hamers AAJ, Dinh HQ, Thomas GD et al (2019) Human monocyte heterogeneity as revealed by high-dimensional mass cytometry. Arterioscler Thromb Vasc Biol 39:25–36
          doi: 10.1161/ATVBAHA.118.311022

      43. Hearps AC, Maisa A, Cheng W-J et al (2012) HIV infection induces age-related changes to monocytes and innate immune activation in young men that persist despite combination antiretroviral therapy. AIDS 26:843–853
          doi: 10.1097/QAD.0b013e328351f756

      44. Hilgendorf I, Swirski FK (2012) Making a difference: monocyte heterogeneity in cardiovascular disease. Curr Atheroscler Rep 14:450–459
          doi: 10.1007/s11883-012-0274-8

      45. Hunt PW (2007) Role of immune activation in HIV pathogenesis. Curr HIV/AIDS Rep 4:42–47
          doi: 10.1007/s11904-007-0007-8

      46. Jaroenpool J, Rogers KA, Pattanapanyasat K et al (2007) Differences in the constitutive and SIV infection induced expression of Siglecs by hematopoietic cells from non-human primates. Cell Immunol 250:91–104
          doi: 10.1016/j.cellimm.2008.01.009

      47. Kedzierska K, Crowe SM (2001) Cytokines and HIV-1: interactions and clinical implications. Antivir Chem Chemother 12:133–150
          doi: 10.1177/095632020101200301

      48. Kedzierska K, Crowe SM, Turville S, Cunningham AL (2003) The influence of cytokines, chemokines and their receptors on HIV-1 replication in monocytes and macrophages. Rev Med Virol 13:39–56
          doi: 10.1002/rmv.369

      49. Kestens L, Vanham G, Vereecken C et al (1994) Selective increase of activation antigens HLA-DR and CD38 on CD4+ CD45RO+ T lymphocytes during HIV-1 infection. Clin Exp Immunol 95:436–441
          doi: 10.1111/j.1365-2249.1994.tb07015.x

      50. Klatt NR, Silvestri G, Hirsch V (2012) Nonpathogenic simian immunodeficiency virus infections. Cold Spring Harb Perspect Med 2:a007153
          doi: 10.1101/cshperspect.a007153

      51. Klein SA, Dobmeyer JM, Dobmeyer TS et al (1997) Demonstration of the Th1 to Th2 cytokine shift during the course of HIV-1 infection using cytoplasmic cytokine detection on single cell level by flow cytometry. AIDS 11:1111–1118
          doi: 10.1097/00002030-199709000-00005

      52. Kruize Z, Kootstra NA (2019) The role of macrophages in HIV-1 persistence and pathogenesis. Front Microbiol 10:2828
          doi: 10.3389/fmicb.2019.02828

      53. Kuller LH, Tracy R, Belloso W et al (2008) Inflammatory and coagulation biomarkers and mortality in patients with HIV infection. PLoS Med 5:e203
          doi: 10.1371/journal.pmed.0050203

      54. Kumar A, Abbas W, Herbein G (2013) TNF and TNF receptor superfamily members in HIV infection: new cellular targets for therapy? Mediators Inflamm 2013:484378
          doi: 10.1155/2013/484378

      55. Kumar H, Kawai T, Akira S (2009) Toll-like receptors and innate immunity. Biochem Biophys Res Commun 388:621–625
          doi: 10.1016/j.bbrc.2009.08.062

      56. Land WG (2015) The role of damage-associated molecular patterns in human diseases: Part Ⅰ - Promoting inflammation and immunity. Sultan Qaboos Univ Med J 15:e9–e21

      57. Lawn SD, Butera ST, Folks TM (2001) Contribution of immune activation to the pathogenesis and transmission of human immunodeficiency virus type 1 infection. Clin Microbiol Rev 14:753–777, table of contents.

      58. Lee SA, Sinclair E, Jain V et al (2014) Low proportions of CD28- CD8+ T cells expressing CD57 can be reversed by early ART initiation and predict mortality in treated HIV infection. J Infect Dis 210:374–382
          doi: 10.1093/infdis/jiu109

      59. Levi M, Keller TT, van Gorp E, ten Cate H (2003) Infection and inflammation and the coagulation system. Cardiovasc Res 60:26–39
          doi: 10.1016/S0008-6363(02)00857-X

      60. Levy E, Xanthou G, Petrakou E et al (2009) Distinct roles of TLR4 and CD14 in LPS-induced inflammatory responses of neonates. Pediatr Res 66:179–184
          doi: 10.1203/PDR.0b013e3181a9f41b

      61. Lindmark E, Tenno T, Chen J, Siegbahn A (1998) IL-10 inhibits LPS-induced human monocyte tissue factor expression in whole blood. Br J Haematol 102:597–604
          doi: 10.1046/j.1365-2141.1998.00808.x

      62. Loo Y-M, Fornek J, Crochet N et al (2008) Distinct RIG-I and MDA5 signaling by RNA viruses in innate immunity. J Virol 82:335–345
          doi: 10.1128/JVI.01080-07

      63. Mascola JR, Haynes BF (2013) HIV-1 neutralizing antibodies: understanding nature's pathways. Immunol Rev 254:225–244
          doi: 10.1111/imr.12075

      64. Meier A, Alter G, Frahm N et al (2007) MyD88-dependent immune activation mediated by human immunodeficiency virus type 1-encoded Toll-like receptor ligands. J Virol 81:8180–8191
          doi: 10.1128/JVI.00421-07

      65. Merino KM, Allers C, Didier ES, Kuroda MJ (2017) Role of Monocyte/Macrophages during HIV/SIV Infection in Adult and Pediatric Acquired Immune Deficiency Syndrome. Front Immunol 8:1693
          doi: 10.3389/fimmu.2017.01693

      66. Miller MM, Petty CS, Tompkins MB, Fogle JE (2014) CD4+CD25+ T regulatory cells activated during feline immunodeficiency virus infection convert T helper cells into functional suppressors through a membrane-bound TGFβ / GARP-mediated mechanism. Virol J 11:7
          doi: 10.1186/1743-422X-11-7

      67. Mogensen T, Melchjorsen J, Larsen C, Paludan S (2010) Innate immune recognition and activation during HIV infection. Retrovirology 7:54
          doi: 10.1186/1742-4690-7-54

      68. Mukherjee R, Kanti Barman P, Kumar Thatoi P et al (2015) Non-classical monocytes display inflammatory features: validation in sepsis and systemic lupus erythematous. Sci Rep 5:13886
          doi: 10.1038/srep13886

      69. Nahrendorf M, Swirski FK, Aikawa E et al (2007) The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions. J Exp Med 204:3037–3047
          doi: 10.1084/jem.20070885

      70. Nakagawa F, May M, Phillips A (2013) Life expectancy living with HIV. Curr Opin Infect Dis 26:17–25
          doi: 10.1097/QCO.0b013e32835ba6b1

      71. Nazli A, Chan O, Dobson-Belaire WN et al (2010) Exposure to HIV-1 directly impairs mucosal epithelial barrier integrity allowing microbial translocation. PLoS Pathog 6:e1000852
          doi: 10.1371/journal.ppat.1000852

      72. Norris PJ, Pappalardo BL, Custer B et al (2006) Elevations in IL-10, TNF-alpha, and IFN-gamma from the earliest point of HIV Type 1 infection. AIDS Res Hum Retroviruses 22:757–762
          doi: 10.1089/aid.2006.22.757

      73. Nyamweya S, Hegedus A, Jaye A et al (2013) Comparing HIV-1 and HIV-2 infection: lessons for viral immunopathogenesis. Rev Med Virol 23:221–240
          doi: 10.1002/rmv.1739

      74. Ong S-M, Hadadi E, Dang T-M et al (2018) The pro-inflammatory phenotype of the human non-classical monocyte subset is attributed to senescence. Cell Death Dis 9:266
          doi: 10.1038/s41419-018-0327-1

      75. Ownby RL, Kumar AM, Benny Fernandez J et al (2009) Tumor necrosis factor-alpha levels in HIV-1 seropositive injecting drug users. J Neuroimmune Pharmacol 4:350–358
          doi: 10.1007/s11481-009-9150-x

      76. Paiardini M, Müller-Trutwin M (2013) HIV-associated chronic immune activation. Immunol Rev 254:78–101
          doi: 10.1111/imr.12079

      77. Palmer S, Wiegand AP, Maldarelli F et al (2003) New real-time reverse transcriptase-initiated PCR assay with single-copy sensitivity for human immunodeficiency virus type 1 RNA in plasma. J Clin Microbiol 41:4531–4536
          doi: 10.1128/JCM.41.10.4531-4536.2003

      78. Pandrea I, Sodora DL, Silvestri G, Apetrei C (2008) Into the wild: simian immunodeficiency virus (SIV) infection in natural hosts. Trends Immunol 29:419–428
          doi: 10.1016/j.it.2008.05.004

      79. Pasquereau S, Kumar A, Herbein G (2017) Targeting TNF and TNF receptor pathway in HIV-1 infection: from immune activation to viral reservoirs. Viruses 9:64
          doi: 10.3390/v9040064

      80. Patel AA, Zhang Y, Fullerton JN et al (2017) The fate and lifespan of human monocyte subsets in steady state and systemic inflammation. J Exp Med 214:1913–1923
          doi: 10.1084/jem.20170355

      81. Pena-Cruz V, Agosto LM, Akiyama H et al (2018) HIV-1 replicates and persists in vaginal epithelial dendritic cells. J Clin Invest 128:3439–3444
          doi: 10.1172/JCI98943

      82. Pinzone MR, Di Rosa M, Cacopardo B, Nunnari G (2012) HIV RNA suppression and immune restoration: can we do better? Clin Dev Immunol 2012:1–12
          doi: 10.1155/2012/515962

      83. Prabhakar B, Banu A, Pavithra HB et al (2011) Immunological failure despite virological suppression in HIV seropositive individuals on antiretroviral therapy. Indian J Sex Transm Dis AIDS 32:94–98
          doi: 10.4103/0253-7184.85412

      84. Prabhu VM, Singh AK, Padwal V et al (2019) Monocyte based correlates of immune activation and Viremia in HIV-infected long-term non-progressors. Front Immunol 10:2849
          doi: 10.3389/fimmu.2019.02849

      85. Pulliam L (2014) Cognitive consequences of a sustained monocyte type 1 IFN response in HIV-1 infection. Curr HIV Res 12:77–84
          doi: 10.2174/1570162X12666140526113544

      86. Reuter MA, Pombo C, Betts MR (2012) Cytokine production and dysregulation in HIV pathogenesis: lessons for development of therapeutics and vaccines. Cytokine Growth Factor Rev 23:181–191
          doi: 10.1016/j.cytogfr.2012.05.005

      87. Roff SR, Noon-Song EN, Yamamoto JK (2014) The significance of interferon-γ in HIV-1 pathogenesis, therapy, and prophylaxis. Front Immunol 4:498
          doi: 10.3389/fimmu.2013.00498

      88. Rogacev KS, Cremers B, Zawada AM et al (2012) CD14++CD16+ monocytes independently predict cardiovascular events: a cohort study of 951 patients referred for elective coronary angiography. J Am Coll Cardiol 60:1512–1520
          doi: 10.1016/j.jacc.2012.07.019

      89. Rogacev KS, Zawada AM, Emrich I et al (2014) Lower Apo A-I and lower HDL-C levels are associated with higher intermediate CD14++CD16+ monocyte counts that predict cardiovascular events in chronic kidney disease. Arterioscler Thromb Vasc Biol 34:2120–2127
          doi: 10.1161/ATVBAHA.114.304172

      90. Rossol M, Heine H, Meusch U et al (2011) LPS-induced cytokine production in human monocytes and macrophages. Crit Rev Immunol 31:379–446
          doi: 10.1615/CritRevImmunol.v31.i5.20

      91. Röszer T (2018) Understanding the biology of self-renewing macrophages. Cells 7:103
          doi: 10.3390/cells7080103

      92. Sabbah A, Chang TH, Harnack R et al (2009) Activation of innate immune antiviral responses by Nod2. Nat Immunol 10:1073–1080
          doi: 10.1038/ni.1782

      93. Sabin CA (2013) Do people with HIV infection have a normal life expectancy in the era of combination antiretroviral therapy? BMC Med 11:251
          doi: 10.1186/1741-7015-11-251

      94. Said EA, Dupuy FP, Trautmann L et al (2010) Programmed death-1-induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection. Nat Med 16:452–459
          doi: 10.1038/nm.2106

      95. Schutte RJ, Parisi-Amon A, Reichert WM (2009) Cytokine profiling using monocytes/macrophages cultured on common biomaterials with a range of surface chemistries. J Biomed Mater Res A 88:128–139
          doi: 10.1002/jbm.a.31863

      96. Semeraro F, Ammollo CT, Semeraro N, Colucci M (2009) Tissue factor-expressing monocytes inhibit fibrinolysis through a TAFI-mediated mechanism, and make clots resistant to heparins. Haematologica 94:819–826
          doi: 10.3324/haematol.2008.000042

      97. Si Y, Tsou C-L, Croft K, Charo IF (2010) CCR2 mediates hematopoietic stem and progenitor cell trafficking to sites of inflammation in mice. J Clin Invest 120:1192–1203
          doi: 10.1172/JCI40310

      98. Sokol CL, Luster AD (2015) The chemokine system in innate immunity. Cold Spring Harb Perspect Biol 7:a016303
          doi: 10.1101/cshperspect.a016303

      99. Sonza S, Mutimer HP, Oelrichs R et al (2001) Monocytes harbour replication-competent, non-latent HIV-1 in patients on highly active antiretroviral therapy. AIDS 15:17–22
          doi: 10.1097/00002030-200101050-00005

      100. Stansfield BK, Ingram DA (2015) Clinical significance of monocyte heterogeneity. Clin Transl Med 4:5
          doi: 10.1186/s40169-014-0040-3

      101. Teer E, Joseph DE, Driescher N et al (2019) HIV and cardiovascular diseases risk: exploring the interplay between T-cell activation, coagulation, monocyte subsets, and lipid subclass alterations. Am J Physiol Heart Circ Physiol 316:H1146–H1157
          doi: 10.1152/ajpheart.00797.2018

      102. Wallet MA, Rodriguez CA, Yin L et al (2010) Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy. AIDS 24:1281–1290
          doi: 10.1097/QAD.0b013e328339e228

      103. Wilson EB, Brooks DG (2011) The role of IL-10 in regulating immunity to persistent viral infections. Curr Top Microbiol Immunol 350:39–65
          doi: 10.1007/82_2010_96

      104. Wilson EMP, Sereti I (2013) Immune restoration after antiretroviral therapy: the pitfalls of hasty or incomplete repairs. Immunol Rev 254:343–354
          doi: 10.1111/imr.12064

      105. Woollard KJ, Geissmann F (2010) Monocytes in atherosclerosis: subsets and functions. Nat Rev Cardiol 7:77–86
          doi: 10.1038/nrcardio.2009.228

      106. Wong KL, Tai JJ-Y, Wong W-C et al (2011) Gene expression profiling reveals the defining features of the classical, intermediate, and nonclassical human monocyte subsets. Blood 118:e16-31
          doi: 10.1182/blood-2010-12-326355

      107. Wong ME, Jaworowski A, Hearps AC (2019) The HIV reservoir in monocytes and macrophages. Front Immunol 10:1435
          doi: 10.3389/fimmu.2019.01435

      108. World Health Organization (WHO) (2020) WHO | Data and statistics. In: WHO HIV/AIDS Data Stat. https://www.who.int/hiv/data/en/. Accessed 7 Jul 2020

      109. Yang J, Zhang L, Yu C et al (2014) Monocyte and macrophage differentiation: circulation inflammatory monocyte as biomarker for inflammatory diseases. Biomark Res 2:1
          doi: 10.1186/2050-7771-2-1

      110. Zawada AM, Rogacev KS, Schirmer SH et al (2012) Monocyte heterogeneity in human cardiovascular disease. Immunobiology 217:1273–1284
          doi: 10.1016/j.imbio.2012.07.001

      111. Zhu T, Muthui D, Holte S et al (2002) Evidence for human immunodeficiency virus type 1 replication in vivo in CD14(+) monocytes and its potential role as a source of virus in patients on highly active antiretroviral therapy. J Virol 76:707–716
          doi: 10.1128/JVI.76.2.707-716.2002

      112. Ziegler-Heitbrock L (2007) The CD14+ CD16+ blood monocytes: their role in infection and inflammation. J Leukoc Biol 81:584–592
          doi: 10.1189/jlb.0806510

      113. Ziegler-Heitbrock L (2015) Blood monocytes and their subsets: established features and open questions. Front Immunol 6:423
          doi: 10.3389/fimmu.2015.00423

      114. Ziegler-Heitbrock L, Ancuta P, Crowe S et al (2010) Nomenclature of monocytes and dendritic cells in blood. Blood 116:e74–e80
          doi: 10.1182/blood-2010-02-258558

    • 加载中

    Figures(1) / Tables(2)

    PDF

    Article Metrics

    Article views(5910) PDF downloads(50) Cited by()

    Related
    Proportional views

      Monocyte/Macrophage-Mediated Innate Immunity in HIV-1 Infection: From Early Response to Late Dysregulation and Links to Cardiovascular Diseases Onset

        Corresponding author: M.Faadiel Essop, mfessop@sun.ac.za
      • 1. Centre for Cardio-metabolic Research in Africa(CARMA), Department of Physiological Sciences, Stellenbosch University, Stellenbosch 7600, South Africa
      • 2. Division of Medical Microbiology & Immunology, Department of Pathology, Stellenbosch University and NHLS, Cape Town 7505, South Africa
      • Received Date: 29 July 2020
      • Accepted Date: 26 October 2020
      • Published Date: 05 January 2021

      Abstract: Although monocytes and macrophages are key mediators of the innate immune system, the focus has largely been on the role of the adaptive immune system in the context of human immunodeficiency virus (HIV) infection. Thus more attention and research work regarding the innate immune system—especially the role of monocytes and macrophages during early HIV-1 infection—is required. Blood monocytes and tissue macrophages are both susceptible targets of HIV-1 infection, and the early host response can determine whether the nature of the infection becomes pathogenic or not. For example, monocytes and macrophages can contribute to the HIV reservoir and viral persistence, and influence the initiation/extension of immune activation and chronic inflammation. Here the expansion of monocyte subsets (classical, intermediate and non-classical) provide an increased understanding of the crucial role they play in terms of chronic inflammation and also by increasing the risk of coagulation during HIV-1 infection. This review discusses the role of monocytes and macrophages during HIV-1 pathogenesis, starting from the early response to late dysregulation that occurs as a result of persistent immune activation and chronic inflammation. Such changes are also linked to downstream targets such as increased coagulation and the onset of cardiovascular diseases.

        HTML

      Introduction