Delayed Disease Progression in HIV-2: the Importance of TRIM5α and the Retroviral Capsid

Overview

Journal Clin Exp Immunol

Publisher Oxford University Press

Specialty Allergy & Immunology

Date 2019 Feb 19

PMID 30773620

Citations 5

Authors

M T Boswell

S L Rowland-Jones

Affiliations

Soon will be listed here.

Abstract

HIV-2 is thought to have entered the human population in the 1930s through cross-species transmission of SIV from sooty mangabeys in West Africa. Unlike HIV-1, HIV-2 has not led to a global pandemic, and recent data suggest that HIV-2 prevalence is declining in some West African states where it was formerly endemic. Although many early isolates of HIV-2 were derived from patients presenting with AIDS-defining illnesses, it was noted that a much larger proportion of HIV-2-infected subjects behaved as long-term non-progressors (LTNP) than their HIV-1-infected counterparts. Many HIV-2-infected adults are asymptomatic, maintaining an undetectable viral load for over a decade. However, despite lower viral loads, HIV-2 progresses to clinical AIDS without therapeutic intervention in most patients. In addition, successful treatment with anti-retroviral therapy (ART) is more challenging than for HIV-1. HIV-2 is significantly more sensitive to restriction by host restriction factor tripartite motif TRIM5α than HIV-1, and this difference in sensitivity is linked to differences in capsid structure. In this review we discuss the determinants of HIV-2 disease progression and focus on the important interactions between TRIM5α and HIV-2 capsid in long-term viral control.

Citing Articles

Plasma proteomics analysis of Chinese HIV-1 infected individuals focusing on the immune and inflammatory factors afford insight into the viral control mechanism.

Ni W, Ren L, Liao L, Li D, Luo Z, Zhu M Front Immunol. 2024; 15:1378048.

PMID: 38799426 PMC: 11116669. DOI: 10.3389/fimmu.2024.1378048.

Systematic review and meta-analysis of seroprevalence of human immunodeficiency virus serological markers among pregnant women in Africa, 1984-2020.

Ebogo-Belobo J, Kenmoe S, Andre Mbongue Mikangue C, Tchatchouang S, Robertine L, Takuissu G World J Crit Care Med. 2024; 12(5):264-285.

PMID: 38188451 PMC: 10768416. DOI: 10.5492/wjccm.v12.i5.264.

HIV-Host Cell Interactions.

Masenga S, Mweene B, Luwaya E, Muchaili L, Chona M, Kirabo A Cells. 2023; 12(10.

PMID: 37408185 PMC: 10216808. DOI: 10.3390/cells12101351.

HIV-2-Infected Macrophages Produce and Accumulate Poorly Infectious Viral Particles.

Gea-Mallorqui E, Zablocki-Thomas L, Maurin M, Jouve M, Rodrigues V, Ruffin N Front Microbiol. 2020; 11:1603.

PMID: 32754142 PMC: 7365954. DOI: 10.3389/fmicb.2020.01603.

Performance evaluation of a laboratory developed PCR test for quantitation of HIV-2 viral RNA.

Jagodzinski L, Manak M, Hack H, Liu Y, Peel S PLoS One. 2020; 15(2):e0229424.

PMID: 32109949 PMC: 7048284. DOI: 10.1371/journal.pone.0229424.

References

Sterling T, Vlahov D, Astemborski J, Hoover D, Margolick J, Quinn T . Initial plasma HIV-1 RNA levels and progression to AIDS in women and men. N Engl J Med. 2001; 344(10):720-5. DOI: 10.1056/NEJM200103083441003. View

McMichael A, Rowland-Jones S . Cellular immune responses to HIV. Nature. 2001; 410(6831):980-7. DOI: 10.1038/35073658. View

Grossman Z, Meier-Schellersheim M, Sousa A, Victorino R, Paul W . CD4+ T-cell depletion in HIV infection: are we closer to understanding the cause?. Nat Med. 2002; 8(4):319-23. DOI: 10.1038/nm0402-319. View

Douek D, Brenchley J, Betts M, Ambrozak D, Hill B, Okamoto Y . HIV preferentially infects HIV-specific CD4+ T cells. Nature. 2002; 417(6884):95-8. DOI: 10.1038/417095a. View

Forshey B, von Schwedler U, Sundquist W, Aiken C . Formation of a human immunodeficiency virus type 1 core of optimal stability is crucial for viral replication. J Virol. 2002; 76(11):5667-77. PMC: 137032. DOI: 10.1128/jvi.76.11.5667-5677.2002. View

Sousa A, Carneiro J, Meier-Schellersheim M, Grossman Z, Victorino R . CD4 T cell depletion is linked directly to immune activation in the pathogenesis of HIV-1 and HIV-2 but only indirectly to the viral load. J Immunol. 2002; 169(6):3400-6. DOI: 10.4049/jimmunol.169.6.3400. View

Schim van der Loeff M, Jaffar S, Aveika A, Sabally S, Corrah T, Harding E . Mortality of HIV-1, HIV-2 and HIV-1/HIV-2 dually infected patients in a clinic-based cohort in The Gambia. AIDS. 2002; 16(13):1775-83. DOI: 10.1097/00002030-200209060-00010. View

Diouf K, Sarr A, Eisen G, Popper S, Mboup S, Kanki P . Associations between MHC class I and susceptibility to HIV-2 disease progression. J Hum Virol. 2002; 5(1):1-7. View

Matheron S, Pueyo S, Damond F, Simon F, Lepretre A, Campa P . Factors associated with clinical progression in HIV-2 infected-patients: the French ANRS cohort. AIDS. 2003; 17(18):2593-601. DOI: 10.1097/00002030-200312050-00006. View

10.

Stremlau M, Owens C, Perron M, Kiessling M, Autissier P, Sodroski J . The cytoplasmic body component TRIM5alpha restricts HIV-1 infection in Old World monkeys. Nature. 2004; 427(6977):848-53. DOI: 10.1038/nature02343. View

11.

Jaffar S, Grant A, Whitworth J, Smith P, Whittle H . The natural history of HIV-1 and HIV-2 infections in adults in Africa: a literature review. Bull World Health Organ. 2004; 82(6):462-9. PMC: 2622848. View

12.

Arien K, Abraha A, Quinones-Mateu M, Kestens L, Vanham G, Arts E . The replicative fitness of primary human immunodeficiency virus type 1 (HIV-1) group M, HIV-1 group O, and HIV-2 isolates. J Virol. 2005; 79(14):8979-90. PMC: 1168791. DOI: 10.1128/JVI.79.14.8979-8990.2005. View

13.

Ylinen L, Keckesova Z, Wilson S, Ranasinghe S, Towers G . Differential restriction of human immunodeficiency virus type 2 and simian immunodeficiency virus SIVmac by TRIM5alpha alleles. J Virol. 2005; 79(18):11580-7. PMC: 1212619. DOI: 10.1128/JVI.79.18.11580-11587.2005. View

14.

Alatrakchi N, Damond F, Matheron S, Beretta-Tempelhoff S, Campa P, Carcelain G . Proliferative, IFNgamma and IL-2-producing T-cell responses to HIV-2 in untreated HIV-2 infection. AIDS. 2005; 20(1):29-34. DOI: 10.1097/01.aids.0000198077.30421.bf. View

15.

Duvall M, Jaye A, Dong T, Brenchley J, Alabi A, Jeffries D . Maintenance of HIV-specific CD4+ T cell help distinguishes HIV-2 from HIV-1 infection. J Immunol. 2006; 176(11):6973-81. DOI: 10.4049/jimmunol.176.11.6973. View

16.

Blaak H, van der Ende M, Boers P, Schuitemaker H, Osterhaus A . In vitro replication capacity of HIV-2 variants from long-term aviremic individuals. Virology. 2006; 353(1):144-54. DOI: 10.1016/j.virol.2006.05.029. View

17.

Goldschmidt V, Bleiber G, May M, Martinez R, Ortiz M, Telenti A . Role of common human TRIM5alpha variants in HIV-1 disease progression. Retrovirology. 2006; 3:54. PMC: 1560158. DOI: 10.1186/1742-4690-3-54. View

18.

Brenchley J, Price D, Schacker T, Asher T, Silvestri G, Rao S . Microbial translocation is a cause of systemic immune activation in chronic HIV infection. Nat Med. 2006; 12(12):1365-71. DOI: 10.1038/nm1511. View

19.

Kiepiela P, Ngumbela K, Thobakgale C, Ramduth D, Honeyborne I, Moodley E . CD8+ T-cell responses to different HIV proteins have discordant associations with viral load. Nat Med. 2006; 13(1):46-53. DOI: 10.1038/nm1520. View

20.

Phillips R, Rowland-Jones S, Nixon D, Gotch F, Edwards J, Ogunlesi A . Human immunodeficiency virus genetic variation that can escape cytotoxic T cell recognition. Nature. 1991; 354(6353):453-9. DOI: 10.1038/354453a0. View