Relaxation of Adaptive Evolution during the HIV-1 Infection Owing to Reduction of CD4+T Cell Counts

Carregando...
Imagem de Miniatura
Citações na Scopus
2
Tipo de produção
article
Data de publicação
2012
Editora
PUBLIC LIBRARY SCIENCE
Indexadores
Título da Revista
ISSN da Revista
Título do Volume
Autores
LEAL, Elcio
HENDRY, Michael
BUSCH, Michael P.
DIAZ, Ricardo Sobhie
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
PLOS ONE, v.7, n.6, article ID e39776, 10p, 2012
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: The first stages of HIV-1 infection are essential to establish the diversity of virus population within host. It has been suggested that adaptation to host cells and antibody evasion are the leading forces driving HIV evolution at the initial stages of AIDS infection. In order to gain more insights on adaptive HIV-1 evolution, the genetic diversity was evaluated during the infection time in individuals contaminated by the same viral source in an epidemic cluster. Multiple sequences of V3 loop region of the HIV-1 were serially sampled from four individuals: comprising a single blood donor, two blood recipients, and another sexually infected by one of the blood recipients. The diversity of the viral population within each host was analyzed independently in distinct time points during HIV-1 infection. Results: Phylogenetic analysis identified multiple HIV-1 variants transmitted through blood transfusion but the establishing of new infections was initiated by a limited number of viruses. Positive selection (d(N)/d(S)>1) was detected in the viruses within each host in all time points. In the intra-host viruses of the blood donor and of one blood recipient, X4 variants appeared respectively in 1993 and 1989. In both patients X4 variants never reached high frequencies during infection time. The recipient, who X4 variants appeared, developed AIDS but kept narrow and constant immune response against HIV-1 during the infection time. Conclusion: Slowing rates of adaptive evolution and increasing diversity in HIV-1 are consequences of the CD4+ T cells depletion. The dynamic of R5 to X4 shift is not associated with the initial amplitude of humoral immune response or intensity of positive selection.
Palavras-chave
Referências
  1. Berkowitz RD, 1998, J VIROL, V72, P10108
  2. Bielawski JP, 2004, J MOL EVOL, V59, P121, DOI 10.1007/s00239-004-2597-8
  3. Blaak H, 2000, P NATL ACAD SCI USA, V97, P1269, DOI 10.1073/pnas.97.3.1269
  4. Bleul CC, 1997, P NATL ACAD SCI USA, V94, P1925, DOI 10.1073/pnas.94.5.1925
  5. BOYD MT, 1993, J VIROL, V67, P3649
  6. Bunnik EM, 2008, J VIROL, V82, P7932, DOI 10.1128/JVI.00757-08
  7. Bunnik EM, 2007, J VIROL, V81, P525, DOI 10.1128/JVI.01983-06
  8. Cicala C, 2006, P NATL ACAD SCI USA, V103, P3746, DOI 10.1073/pnas.0511237103
  9. Dacheux L, 2004, J VIROL, V78, P12625, DOI 10.1128/JVI.78.22.12625-12637.2004
  10. Davenport MP, 2002, TRENDS MICROBIOL, V10, P275, DOI 10.1016/S0966-842X(02)02370-3
  11. DEJONG JJ, 1992, J VIROL, V66, P6777
  12. Diaz RS, 1997, AIDS, V11, P415, DOI 10.1097/00002030-199704000-00003
  13. Diaz RS, 2008, VIROLOGY, V381, P184, DOI 10.1016/j.virol.2008.08.014
  14. English S, 2011, RETROVIROLOGY, V8, DOI 10.1186/1742-4690-8-54
  15. FOUCHIER RAM, 1992, J VIROL, V66, P3183
  16. Frost SDW, 2005, P NATL ACAD SCI USA, V102, P18514, DOI 10.1073/pnas.0504658102
  17. Herbeck JT, 2006, J VIROL, V80, P1637, DOI 10.1128/JVI.80.4.1637-1644.2006
  18. Huelsenbeck JP, 2001, BIOINFORMATICS, V17, P754, DOI 10.1093/bioinformatics/17.8.754
  19. Jensen MA, 2003, J VIROL, V77, P13376, DOI 10.1128/JVI.77.24.13376-13388.2003
  20. KOOT M, 1993, J INFECT DIS, V168, P733
  21. Leal E, 2008, VIROLOGY, V381, P222, DOI 10.1016/j.virol.2008.08.029
  22. Leal E, 2007, INFECT GENET EVOL, V7, P694, DOI 10.1016/j.meegid.2007.07.008
  23. Leal ED, 2004, VIROLOGY, V325, P181, DOI 10.1016/j.virol.2004.04.004
  24. Lemey P, 2007, PLOS COMPUT BIOL, V3, P282, DOI 10.1371/journal.pcbi.0030029
  25. Lemey P, 2005, J VIROL, V79, P11981, DOI 10.1128/JVI.79.18.11981-11989.2005
  26. Li B, 2007, J VIROL, V81, P193, DOI 10.1128/JVI.01231-06
  27. Lusso P, 2005, J VIROL, V79, P6957, DOI 10.1128/JVI.79.11.6957-6968.2005
  28. Milne I, 2004, BIOINFORMATICS, V20, P1806, DOI 10.1093/bioinformatics/bth155
  29. Ribeiro RM, 2006, J VIROL, V80, P802, DOI 10.1128/JVI.80.2.802-809.2006
  30. Scarlatti G, 1997, NAT MED, V3, P1259, DOI 10.1038/nm1197-1259
  31. SCHUITEMAKER H, 1992, J VIROL, V66, P1354
  32. Shankarappa R, 1999, J VIROL, V73, P10489
  33. SHIODA T, 1991, NATURE, V349, P167, DOI 10.1038/349167a0
  34. Tamura K, 2007, MOL BIOL EVOL, V24, P1596, DOI 10.1093/molbev/msm092
  35. Thompson JD, 1997, NUCLEIC ACIDS RES, V25, P4876, DOI 10.1093/nar/25.24.4876
  36. van Rij RP, 2003, VIROLOGY, V314, P451, DOI 10.1016/S0042-6822(03)00454-9
  37. Wei XP, 2003, NATURE, V422, P307, DOI 10.1038/nature01470
  38. Williamson S, 2003, MOL BIOL EVOL, V20, P1318, DOI 10.1093/molbev/msg144
  39. Yang ZH, 2000, GENETICS, V155, P431
  40. Zhang M, 2004, GLYCOBIOLOGY, V14, P1229, DOI 10.1093/glycob/cwh106