Detection of human T-cell lymphotropic virus type 1 in plasma samples

Carregando...
Imagem de Miniatura
Citações na Scopus
19
Tipo de produção
article
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER SCIENCE BV
Citação
VIRUS RESEARCH, v.163, n.1, p.87-90, 2012
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Human T-cell lymphotropic virus type 1 (HTLV-1) is-an RNA virus responsible for diseases such as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and adult T-cell leukemia/lymphoma (ATL). Cell-to-cell contact and Tax-induced clonal expansion of infected cells are the main modes of virus replication, making virus detection during the viremic stage difficult. Consequently, the proviral load is the current virologic marker for disease monitoring, but the mechanisms of progression have not been established yet. Thus, this study investigated the presence of virus in plasma from asymptomatic HTLV-1 carriers and from HAM/TSP patients. Real-time PCR was performed on DNA from 150 plasma samples; 12(8%) had detectable DNA amplification, including 6(4%) asymptomatic HTLV-1 carriers and 14(26%) HAM/TSP patients (p < 0.005). Of the 33 samples submitted for nested PCR, six (18%, p = 0.02) were positive for HTLV-1 RNA in the plasma. Additionally, 26 plasma samples were treated with DNAse enzyme to eliminate any DNA contamination before RNA extraction. Two of them (8%) showed amplification for HTLV-1 (p = 0.5). Therefore, this study described for the first time the detection of free HTLV-1 RNA in plasma from HTLV-1-infected subjects, regardless of their clinical status. Thus, HTLV-1 viral replication does occur in plasma, and other transmission pathways for HTLV-1 should be investigated further.
Palavras-chave
HTLV-1, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), Real-time PCR, Nested PCR, HTLV-1 plasma viral load
Referências
  1. Bangham CRM, 2003, J GEN VIROL, V84, P3177, DOI 10.1099/vir.0.19334-0
  2. Best I, 2006, CLIN EXP IMMUNOL, V146, P226, DOI 10.1111/j.1365-2249.2006.03208.x
  3. Dehee A, 2002, J VIROL METHODS, V102, P37, DOI 10.1016/S0166-0934(01)00445-1
  4. GESSAIN A, 1985, LANCET, V2, P407
  5. Ghez D, 2010, RETROVIROLOGY, V7, DOI 10.1186/1742-4690-7-99
  6. Hall WW, 1996, J ACQ IMMUN DEF SYND, V13, pS204
  7. IWASAKI Y, 1993, BRAIN PATHOL, V3, P1, DOI 10.1111/j.1750-3639.1993.tb00719.x
  8. KAPLAN JE, 1990, J ACQ IMMUN DEF SYND, V3, P1096
  9. KIRA J, 1991, ANN NEUROL, V29, P194, DOI 10.1002/ana.410290214
  10. Lezin A, 2005, J INFECT DIS, V191, P1830, DOI 10.1086/429962
  11. Manel N, 2004, M S-MED SCI, V20, P277, DOI 10.1051/medsci/2004203277
  12. Matsuzaki T, 2001, J NEUROVIROL, V7, P228
  13. Mellors JW, 1997, ANN INTERN MED, V126, P946
  14. Montanheito PA, 2005, BRAZ J MED BIOL RES, V38, P1643
  15. Nagai M, 1998, J NEUROVIROL, V4, P586, DOI 10.3109/13550289809114225
  16. Novoa P, 2007, J MED VIROL, V79, P182, DOI 10.1002/jmv.20775
  17. Olindo S, 2005, J NEUROL SCI, V237, P53, DOI 10.1016/j.jns.2005.05.010
  18. OSAME M, 1986, LANCET, V1, P1031
  19. Pais-Correia AM, 2010, NAT MED, V16, P83, DOI 10.1038/nm.2065
  20. Takenouchi N, 2003, J NEUROVIROL, V9, P29, DOI 10.1080/13550280390173418
  21. Tosswill JHC, 1998, J VIROL METHODS, V75, P21, DOI 10.1016/S0166-0934(98)00093-7
  22. TUKE PW, 1992, J VIROL METHODS, V40, P163, DOI 10.1016/0166-0934(92)90065-L