دورية أكاديمية
أعرض في EDS

Higher HIV-1 evolutionary rate is associated with cytotoxic T lymphocyte escape mutations in infants.

التفاصيل البيبلوغرافية
العنوان: Higher HIV-1 evolutionary rate is associated with cytotoxic T lymphocyte escape mutations in infants.
المؤلفون: Nazziwa J; Department of Translational Medicine, Lund University, Lund, Sweden.; Lund University Virus Centre, Lund University, Lund, Sweden., Andrews SM; Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom., Hou MM; Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom., Bruhn CAW; Department of Translational Medicine, Lund University, Lund, Sweden., Garcia-Knight MA; Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom.; Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California, USA., Slyker J; Department of Global Health, University of Washington, Seattle, Washington, USA.; Department of Epidemiology, University of Washington, Seattle, Washington, USA., Hill S; Department of Pathobiology and Population Sciences, Royal Veterinary College, London, United Kingdom., Lohman Payne B; Department of Paediatrics and Child Health, University of Nairobi, Nairobi, Kenya.; Department of Medicine, University of Washington, Seattle, Washington, USA., Moringas D; Department of Paediatrics and Child Health, University of Nairobi, Nairobi, Kenya., Lemey P; Department of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, Leuven, Belgium., John-Stewart G; Department of Global Health, University of Washington, Seattle, Washington, USA.; Department of Epidemiology, University of Washington, Seattle, Washington, USA.; Department of Medicine, University of Washington, Seattle, Washington, USA.; Department of Pediatrics, University of Washington, Seattle, Washington, USA.; Global Center for Integrated Health of Women, Adolescents and Children (Global WACh), University of Washington, Seattle, Washington, USA., Rowland-Jones SL; Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom., Esbjörnsson J; Department of Translational Medicine, Lund University, Lund, Sweden.; Lund University Virus Centre, Lund University, Lund, Sweden.; Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom.
المصدر: Journal of virology [J Virol] 2024 Jul 23; Vol. 98 (7), pp. e0007224. Date of Electronic Publication: 2024 May 30.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: American Society For Microbiology Country of Publication: United States NLM ID: 0113724 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1098-5514 (Electronic) Linking ISSN: 0022538X NLM ISO Abbreviation: J Virol Subsets: MEDLINE
أسماء مطبوعة: Publication: Washington Dc : American Society For Microbiology
Original Publication: Baltimore, American Society for Microbiology.
مواضيع طبية MeSH: HIV-1*/genetics , HIV-1*/immunology , T-Lymphocytes, Cytotoxic*/immunology , HIV Infections*/virology , HIV Infections*/immunology , HIV Infections*/transmission , gag Gene Products, Human Immunodeficiency Virus*/genetics , gag Gene Products, Human Immunodeficiency Virus*/immunology , Mutation* , Evolution, Molecular* , Infectious Disease Transmission, Vertical* , nef Gene Products, Human Immunodeficiency Virus*/genetics , nef Gene Products, Human Immunodeficiency Virus*/immunology, Humans ; Infant ; Female ; Immune Evasion/genetics ; Infant, Newborn ; Phylogeny ; Male ; Longitudinal Studies ; Pregnancy ; Adult
مستخلص: Escape from cytotoxic T lymphocyte (CTL) responses toward HIV-1 Gag and Nef has been associated with reduced control of HIV-1 replication in adults. However, less is known about CTL-driven immune selection in infants as longitudinal studies of infants are limited. Here, 1,210 gag and 1,264 nef sequences longitudinally collected within 15 months after birth from 14 HIV-1 perinatally infected infants and their mothers were analyzed. The number of transmitted founder (T/F) viruses and associations between virus evolution, selection, CTL escape, and disease progression were determined. The analyses indicated that a paraphyletic-monophyletic relationship between the mother-infant sequences was common (80%), and that the HIV-1 infection was established by a single T/F virus in 10 of the 12 analyzed infants (83%). Furthermore, most HIV-1 CTL escape mutations among infants were transmitted from the mothers and did not revert during the first year of infection. Still, immune-driven selection was observed at approximately 3 months after HIV-1 infection in infants. Moreover, virus populations with CTL escape mutations in gag evolved faster than those without, independently of disease progression rate. These findings expand the current knowledge of HIV-1 transmission, evolution, and CTL escape in infant HIV-1 infection and are relevant for the development of immune-directed interventions in infants.IMPORTANCEDespite increased coverage in antiretroviral therapy for the prevention of perinatal transmission, paediatric HIV-1 infection remains a significant public health concern, especially in areas of high HIV-1 prevalence. Understanding HIV-1 transmission and the subsequent virus adaptation from the mother to the infant's host environment, as well as the viral factors that affect disease outcome, is important for the development of early immune-directed interventions for infants. This study advances our understanding of vertical HIV-1 transmission, and how infant immune selection pressure is shaping the intra-host evolutionary dynamics of HIV-1.
Competing Interests: The authors declare no conflict of interest.
References: N Engl J Med. 2012 Jul 19;367(3):224-32. (PMID: 22808957)
Syst Biol. 2011 Oct;60(5):685-99. (PMID: 21540409)
PLoS Pathog. 2019 Dec 10;15(12):e1008177. (PMID: 31821379)
J Acquir Immune Defic Syndr. 2009 Jun 1;51(2):209-15. (PMID: 19504753)
PLoS One. 2015 Mar 17;10(3):e0119886. (PMID: 25781986)
J Immunol. 2005 Nov 15;175(10):6976-86. (PMID: 16272358)
Cell Rep Med. 2021 Jun 16;2(7):100315. (PMID: 34337555)
Nucleic Acids Res. 1994 Nov 11;22(22):4673-80. (PMID: 7984417)
Syst Biol. 2010 May;59(3):307-21. (PMID: 20525638)
J Infect Dis. 2007 Jan 15;195(2):220-9. (PMID: 17191167)
Nat Rev Immunol. 2016 Apr;16(4):259-71. (PMID: 26972723)
J Infect Dis. 2008 Sep 15;198(6):868-76. (PMID: 18700833)
J Virol. 2003 Jun;77(12):7120-3. (PMID: 12768032)
J Virol. 2005 Jul;79(13):8121-30. (PMID: 15956557)
Microb Genom. 2016 Jun 24;2(6):e000057. (PMID: 28348854)
Virus Evol. 2018 Jun 08;4(1):vey016. (PMID: 29942656)
Retrovirology. 2016 Sep 08;13(1):65. (PMID: 27608713)
Mol Biol Evol. 2011 May;28(5):1605-16. (PMID: 21135151)
Nat Rev Immunol. 2012 Sep;12(9):636-48. (PMID: 22918466)
AIDS. 2011 Jan 14;25(2):143-52. (PMID: 21173592)
J Mol Evol. 1985;22(2):160-74. (PMID: 3934395)
J Virol. 2017 Aug 10;91(17):. (PMID: 28637761)
PLoS One. 2010 Feb 18;5(2):e9294. (PMID: 20174636)
Sci Transl Med. 2016 Sep 28;8(358):358ra125. (PMID: 27683550)
Sci Rep. 2014 May 28;4:5079. (PMID: 24866155)
Syst Biol. 2003 Oct;52(5):649-64. (PMID: 14530132)
Proc Natl Acad Sci U S A. 2016 Mar 8;113(10):2690-5. (PMID: 26903617)
J Acquir Immune Defic Syndr. 2014 Sep 1;67(1):15-21. (PMID: 24872130)
Nat Microbiol. 2018 Sep;3(9):983-988. (PMID: 30061758)
Sci Rep. 2016 Jul 12;6:29536. (PMID: 27403940)
J Infect Dis. 2009 May 1;199(9):1292-300. (PMID: 19317628)
Lancet Microbe. 2023 Feb;4(2):e102-e112. (PMID: 36642083)
PLoS One. 2017 Oct 18;12(10):e0182443. (PMID: 29045410)
Science. 2014 Jul 11;345(6193):1254031. (PMID: 25013080)
Immunol Rev. 2013 Jul;254(1):143-69. (PMID: 23772619)
PLoS Pathog. 2012;8(11):e1003041. (PMID: 23209412)
AIDS Res Hum Retroviruses. 2002 Dec 10;18(18):1415-23. (PMID: 12512513)
Bioinformatics. 2012 Dec 15;28(24):3248-56. (PMID: 23064000)
BMC Bioinformatics. 2010 Oct 25;11:532. (PMID: 20973976)
Retrovirology. 2015 Nov 16;12:96. (PMID: 26573574)
J Virol. 2011 Aug;85(16):8253-62. (PMID: 21593171)
J Virol. 2005 Sep;79(18):12100-5. (PMID: 16140787)
PLoS Comput Biol. 2007 Feb 16;3(2):e29. (PMID: 17305421)
Genetics. 2006 Apr;172(4):2665-81. (PMID: 16489234)
Proc Natl Acad Sci U S A. 2008 May 27;105(21):7552-7. (PMID: 18490657)
Science. 2020 Jul 3;369(6499):103-108. (PMID: 32631894)
Virus Evol. 2016 Apr 09;2(1):vew007. (PMID: 27774300)
Nature. 2001 Jul 19;412(6844):334-8. (PMID: 11460164)
J Virol. 2003 Mar;77(5):3050-7. (PMID: 12584330)
PLoS Pathog. 2018 Apr 19;14(4):e1006944. (PMID: 29672607)
PLoS One. 2015 Mar 20;10(3):e0120389. (PMID: 25793402)
معلومات مُعتمدة: M403 Rosetrees Trust (Rosetrees); 2016-01417 Vetenskapsrådet (VR); K24 HD054314 United States HD NICHD NIH HHS; R01 HD023412 United States HD NICHD NIH HHS; P30 AI027757 United States AI NIAID NIH HHS; 089567/Z/09/Z Wellcome Trust (WT); R01-HD023412 K24-HD054314 HHS | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD); United Kingdom WT_ Wellcome Trust; BH14 British HIV Association (BHIVA)
فهرسة مساهمة: Keywords: CTL responses; HIV-1; disease progression; infant; intra-host evolution; vertical transmission
المشرفين على المادة: 0 (gag Gene Products, Human Immunodeficiency Virus)
0 (nef Gene Products, Human Immunodeficiency Virus)
تواريخ الأحداث: Date Created: 20240530 Date Completed: 20240723 Latest Revision: 20240725
رمز التحديث: 20240726
مُعرف محوري في PubMed: PMC11265422
DOI: 10.1128/jvi.00072-24
PMID: 38814066
قاعدة البيانات: MEDLINE
الوصف
تدمد:1098-5514
DOI:10.1128/jvi.00072-24