Share This Article:

HIV-1 Primarily Targets the Innate Immune System and Only Secondarily Modulates Adaptive Immune Cell Depletion

Abstract Full-Text HTML Download Download as PDF (Size:80KB) PP. 226-231
DOI: 10.4236/wja.2012.23029    3,814 Downloads   5,474 Views  

ABSTRACT

Persistence of HIV-1 infection allows for permissive microenvironmental conditioning in terms of contextual innate immune participation. The progression of host cell injury constitutes an additional parametric formulation in self-amplifying modulation of the adaptive immune response in a manner that inclusively promotes the emergence of a final stage of AIDS that is both depletive and permissive for opportunistic infections and various forms of neoplasia. It is within contextual indices of promotion of depleted T-helper lymphocytes and of augmented viremic loads that manifestations of classic lesions emerge as the AIDS phenomenon. It is further to be realized that an apoptotic response of multiple cell subtypes including T-lymphocytes includes host-cell participation within formulated settings of further persistence of the retroviral infection. An all-inclusive phenomenon of dendritic cell-lymphocyte synapse formulation corresponds to the establishment of HIV-1 infection that specifically conditions all subsequent stages in depletion of the injured host cells regardless of the dynamics or kinetics of the retroviral replicative infectious process itself.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

L. M. Agius, "HIV-1 Primarily Targets the Innate Immune System and Only Secondarily Modulates Adaptive Immune Cell Depletion," World Journal of AIDS, Vol. 2 No. 3, 2012, pp. 226-231. doi: 10.4236/wja.2012.23029.

References

[1] M. Q. Liu, D. J. Zhou , X. Wang , W. Zhou , L. Ye and J. L. Li, “IFN-Lambda3 Inhibits HIV Infection of Macrophages through the JAK-STAT Pathway,” PloS One, Vol. 7, No. 4, 2012, Article ID: e35902.
[2] M. L. Gougeon and J. P. Herbeuval, “IFN-ALPHA and TRAIL: A Double Edge Sword in HIV-1 Disease?” Experimental Cell Research, Vol. 318, No. 11, 2012, pp. 1260-1268. doi:10.1016/j.yexcr.2012.03.012
[3] L. Cassetta, E. Cassol and G. Poli, “Macrophage Polarization in Health and Disease,” Scientific World Journal, Vol. 11, 2011, pp. 2391-2402. doi:10.1100/2011/213962
[4] A. Nath and J. R. Berger, “Complications of Immunosupressive/Immunomodulatory Therapy in Neurological Diseases,” Current Treatment Options in Neurology, Vol. 14, No. 3, 2012, pp. 241-255. doi:10.1007/s11940-012-0172-y
[5] M. Fogil, C. Toiti, F. Malacarne, S. Florentini, M. Albani and I. Izzo, “Emergence of Exhausted B Cells in Asymptomatic HIV-1 Infected Patients Naive for HAART Is Related to Reduced Immune Surveillance,” Clinical and Developmental Immunology, 2012. doi:10.1155/2012/829584
[6] A. Benecke, M. Gale Jr. and M. G. Katze, “Dynamics of Innate Immunity Are Key to Chronic Immune Activation in AIDS,” Current Opinion in HIV and AIDS, Vol. 7, No. 1, 2012, pp. 79-85. doi:10.1097/COH.0b013e32834dde31
[7] C. St. Gelais, C. M. Coleman, J. H. Wang and L. Wu, “HIV-1 Nef Enhances Dendritic Cell-Mediated Viral Transmission to CD4(+) T Cells and Promotes T-Cell Activation,” PLoS One, Vol. 7, No. 3, 2012, Article ID: e34521. doi:10.1371/journal.pone.0034521
[8] J. K. Sandberg, S. K. Andersson, S. M. Bachle, D. F. Nixon and M. Moll, “HIV-1 Vpu Interference with Innate Cell-Mediated Immune Mechanisms,” Current HIV Research, 2012.
[9] L. Vassena, H. Miao, R. Cibro, M. S. Mainati, G. Cassina and M. A. Proschan, “Treatment with IL-7 Prevents the Decline of Circulating CD4 (+) T Cells during the Acute Phase of SIV Infection in Rhesus Macaques,” PLoS Pathogens, Vol. 8, No. 4, 2012, Article ID: e1002636. doi:10.1371/journal.ppat.1002636
[10] J. E. Hazleton, J. W. Berman and E. A. Eugenin, “Purinergic Receptors Are Required for HIV-1 Infection of Primary Human Macrophages,” Journal of Immunology, 2012.
[11] C. Guerra, K. Johal, D. Morris, S. Moreno, O. Alvarado and D. Gray, “Control of Mycobacterium Tuberculosis Growth by Activated Natural Killer Cells,” Clinical & Experimental Immunology, Vol. 168, No. 1, 2012, pp. 142-152. doi:10.1111/j.1365-2249.2011.04552.x
[12] K. Sato, P. Gee and Y. Koyanagi, “Vpu and BST2: Still Not There Yet?” Frontiers in Microbiology, Vol. 3, No. 131, 2012.
[13] A. C. Hearps, T. A. Angelovich, A. Jaworowski, J. Mills, A. L. Landay and S. M. Crowe, “HIV Infection and Aging of the Innate Immune System,” Sex Health, Vol. 8, No. 4, 2011, pp. 453-464. doi:10.1071/SH11028
[14] J. Bertin, C. Baret, D. Belanger and M. J. Tremblay, “Leukotrienes Inhibit Early Stages of HIV-1 Infection in Monocyte-Derived Microglia-Like Cells,” Journal of Neuroinflammation, Vol. 9, No. 1, 2012, p. 55. doi:10.1186/1742-2094-9-55
[15] R. Hughes, G. Towers and M. Noursadeghi, “Innate Immune Interferon Responses to Human Immunodeficiency Virus-1 Infection,” Reviews in Medical Virology, Vol. 22, No. 4, 2012, pp. 257-266. doi:10.1002/rmv.1708
[16] J. L. Reading, A. F. Meyers and A. Vyakarnam, “Whey Acidic Proteins (WAPs): Novel Modulators of Innate Immunity to HIV Infection,” Current Opinion in HIV and AIDS, Vol. 7, No. 2, 2012, pp. 172-179. doi:10.1097/COH.0b013e32835005d9
[17] D. S. Kwon, M. Augin, T. Hongo, K. M. Law, J. Johnson and F. Porichis “CD4+ CD25+ Regulatory T Cells Impair HIV-Specific CD4 T Cell Responses by Upregulating IL-10 Production in Monocytes,” Journal of Virology, 2012. doi:10.1128/JVI.06251-11
[18] K. Machmach, M. Leal, C. Gras, P. Viciana, M. Geneba and E. Franco, “Plasmacytoid Dendritic Cells Reduce HIV Production in Elite Controllers,” Journal of Virology, Vol. 86, No. 8, 2012, pp. 4245-4252. doi:10.1128/JVI.07114-11
[19] W. Royal III, L. Zhang, M. Guo, O. Jones, H. Davis and J. L. Bryant, “Immune Activation, Viral Gene Product Expression and Neurotoxicity in the HIV-1 Transgenic Rat,” Journal of Neuroimmunology, Vol. 247, No. 1, 2012, pp. 16-24. doi:10.1016/j.jneuroim.2012.03.015
[20] N. Yan and Z. J. Chen, “Intrinsic Antiviral Immunity,” Nature Immunology, Vol. 13, No. 3, 2012, pp. 214-222. doi:10.1038/ni.2229
[21] J. C. Hernandez, M. Stevenson, E. Latz and S. Urcuqui-Inchima, “HIV Type 1 Infection Up-Regulates TLR-2 and TLR-4 Expression and Function in Vivo and in Vitro,” AIDS Research and Human Retroviruses, 2012.
[22] L. Zhang and L. Su, “HIV-1 Immunopathogenesis in Humanized Mouse Models,” Cellular & Molecular Immunology, 2012. doi:10.1038/cmi.2012.7
[23] R. Freguja, K. Glanesin, P. Del Bianco, S. Malacrida, O. Rampon and M. Zanchetta, “Polymorphisms of Innate Immunity Genes Influence Disease Progression in HIV-1 Infected Children,” AIDS, Vol. 26, No. 6, 2012, pp. 765-768. doi:10.1097/QAD.0b013e3283514350
[24] I. A. Abela, L. Berlinger, M. Schanz, L. Reynell, H. F. Gunthard and P. Rusert, “Cell-Cell Transmission Enables HIV-1 to Evade Inhibition by Potent CD4bs Directed Antibodies,” PLoS Pathogens, Vol. 8, No. 4, 2012, Article ID: e1002634. doi:10.1371/journal.ppat.1002634
[25] M. E. Ackerman, A. S. Dugast and G. Alter, “Emerging Concepts on the Role of Innate Immunity in the Prevention and Control of HIV Infection,” Annual Review of Medicine, Vol. 63, 2012, pp. 113-130. doi:10.1146/annurev-med-050310-085221
[26] J. Vani, S. V. Kaveri and J. Bayry, “Myeloid Dendritic Cell Dysfunction during Primary HIV-1 Infection Is Independent of Interaction with gp120,” Journal of Infectious Diseases, 2012. doi:10.1093/infdis/jis292
[27] V. Deretic, “Autophagy as an Innate Immunity Paradigm: Expanding the Scope and Repertoire of Pattern Recognition Receptors,” Current Opinion in Immunology, Vol. 24, No. 1, 2012, pp. 21-31. doi:10.1016/j.coi.2011.10.006
[28] M. G. Grutter and J. Luban, “TRIM5 Structure, HIV-1 Capsid Recognition, and Innate Immune Signalling,” Current Opinion in Virology, Vol. 2, No. 2, 2012, pp. 142-150. doi:10.1016/j.coviro.2012.02.003
[29] Y. Ghiglione and G. Turk, “Nef Performance in Macrophages: The Master Orchestrator of Viral Persistence and Spread,” Current HIV Research, Vol. 9, No. 7, 2011, pp. 505-513. doi:10.2174/157016211798842080
[30] B. K. Chen, “T Cell Virological Synapses and HIV-1 Pathogenesis,” Immunology Research, 2012, in Press. doi:10.1007/s12026-012-8320-8
[31] A. Pontillo, T. M. Oshiro, M. Girardelli, A. J. Kamada, S. Crovella and A. J. Duarte, “Polymorphisms in Inflammasome Genes and Susceptibility to HIV-1 Infection,” Journal of Acquired Immune Deficiency Syndromes, Vol. 59, No. 2, 2012, pp. 121-125. doi:10.1097/QAI.0b013e3182392ebe
[32] C. F. Thobakgale, L. Fadda, K. Lane, I. Toth, F. Pereyra and S. Bazner, “Frequent and Strong Antibody-Mediated Natural Killer C Activation to HIV Env in Individuals with Chronic HIV-1 Infection,” Journal of Virology, 2012. doi:10.1128/JVI.00569-12
[33] K. D. Jayappa, Z. Ao and X. Yao, “The HIV-1 Passage from Cytoplasm to Nucleus: The Process Involving a Complex Exchange between the Components of HIV-1 and Cellular Machinery to Access Nuclear and Successful Integration,” International Journal of Biochemistry and Molecular Biology, Vol. 3, No. 1, 2012, pp. 70-85.

  
comments powered by Disqus

Copyright © 2018 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.