On Hepatitis C Virus Evolution: The Interaction between Virus and Host towards Treatment Outcome
Carregando...
Citações na Scopus
10
Tipo de produção
article
Data de publicação
2013
Título da Revista
ISSN da Revista
Título do Volume
Editora
PUBLIC LIBRARY SCIENCE
Autores
BITTAR, Cintia
JARDIM, Ana Carolina Gomes
YAMASAKI, Lilian Hiromi Tomonari
CARARETO, Claudia Marcia Aparecida
LEMEY, Philippe
CARVALHO-MELLO, Isabel Maria Vicente Guedes de
RAHAL, Paula
Citação
PLOS ONE, v.8, n.4, article ID e62393, 13p, 2013
Resumo
Background: Hepatitis C is a disease spread throughout the world. Hepatitis C virus (HCV), the etiological agent of this disease, is a single-stranded positive RNA virus. Its genome encodes a single precursor protein that yields ten proteins after processing. NS5A, one of the non-structural viral proteins, is most associated with interferon-based therapy response, the approved treatment for hepatitis C in Brazil. HCV has a high mutation rate and therefore high variability, which may be important for evading the immune system and response to therapy. The aim of this study was to analyze the evolution of NS5A quasispecies before, during, and after treatment in patients infected with HCV genotype 3a who presented different therapy responses. Methods: Viral RNA was extracted, cDNA was synthesized, the NS5A region was amplified and cloned, and 15 clones from each time-point were sequenced. The sequences were analyzed for evolutionary history, genetic diversity and selection. Results: This analysis shows that the viral population that persists after treatment for most non-responder patients is present in before-treatment samples, suggesting it is adapted to evade treatment. In contrast, the population found in before treatment samples from most end-of-treatment responder patients either are selected out or appears in low frequency after relapse, therefore changing the population structure. The exceptions illustrate the uniqueness of the evolutionary process, and therefore the treatment resistance process, in each patient. Conclusion: Although evolutionary behavior throughout treatment showed that each patient presented different population dynamics unrelated to therapy outcome, it seems that the viral population from non-responders that resists the treatment already had strains that could evade therapy before it started.
Palavras-chave
Referências
- Aaskov J, 2006, SCIENCE, V311, P236, DOI 10.1126/science.1115030
- Appel N, 2005, J VIROL, V79, P896, DOI 10.1128/JVI.79.2.896-909.2005
- Bittar C, 2010, BMC INFECT DIS, V10, DOI 10.1186/1471-2334-10-36
- Bowen DG, 2005, J HEPATOL, V42, P408, DOI 10.1016/j.jhep.2004.12.013
- COFFIN JM, 1995, SCIENCE, V267, P483, DOI 10.1126/science.7824947
- Craig S, 2003, J VIROL, V77, P4463, DOI 10.1128/JVI.77.7.4463-4467.2003
- Domingo E, 1997, ANNU REV MICROBIOL, V51, P151, DOI 10.1146/annurev.micro.51.1.151
- Drummond AJ, 2007, BMC EVOL BIOL, V7, DOI 10.1186/1471-2148-7-214
- Duverlie G, 1998, J GEN VIROL, V79, P1373
- Eigen M, 1988, SEQUENCE SPACE QUASI
- EIGEN M, 1993, SCI AM, V269, P42
- Enomoto N, 1996, NEW ENGL J MED, V334, P77, DOI 10.1056/NEJM199601113340203
- ENOMOTO N, 1995, J CLIN INVEST, V96, P224, DOI 10.1172/JCI118025
- Ewing B, 1998, GENOME RES, V8, P175
- Ewing B, 1998, GENOME RES, V8, P186
- Gale MJ, 1997, VIROLOGY, V230, P217, DOI 10.1006/viro.1997.8493
- Guindon S, 2003, SYST BIOL, V52, P696, DOI 10.1080/10635150390235520
- Hall T. A., 1999, NUCL ACIDS S SER, V41, P95, DOI 10.1111/J.1469-8137.2009.02874.X
- Ide Y, 1996, GENE, V182, P203, DOI 10.1016/S0378-1119(96)00555-0
- INCHAUSPE G, 1991, P NATL ACAD SCI USA, V88, P10292, DOI 10.1073/pnas.88.22.10292
- Jardim ACG, 2009, INFECT GENET EVOL, V9, P689, DOI 10.1016/j.meegid.2008.11.001
- Kato N, 2001, ACTA MED OKAYAMA, V55, P133
- Le Guillou-Guillemette H, 2007, WORLD J GASTROENTERO, V13, P2416
- MARTELL M, 1992, J VIROL, V66, P3225
- Marucci EA, 2008, GENET MOL RES, V7, P970
- Neumann AU, 1998, SCIENCE, V282, P103, DOI 10.1126/science.282.5386.103
- Polyak Stephen J, 2003, Clin Liver Dis, V7, P67, DOI 10.1016/S1089-3261(02)00075-2
- Pond SLK, 2005, BIOINFORMATICS, V21, P676, DOI 10.1093/bioinformatics/bti079
- Satoh S, 2000, VIROLOGY, V270, P476, DOI 10.1006/viro.2000.0287
- Shirota Y, 2002, J BIOL CHEM, V277, P11149, DOI 10.1074/jbc.M111392200
- SIMMONDS P, 1993, J GEN VIROL, V74, P2391, DOI 10.1099/0022-1317-74-11-2391
- Smith DB, 1997, J GEN VIROL, V78, P321
- Tamura K, 2011, MOL BIOL EVOL, V28, P2731, DOI 10.1093/molbev/msr121
- Thompson JD, 1997, NUCLEIC ACIDS RES, V25, P4876, DOI 10.1093/nar/25.24.4876
- Togawa R, 2007, BIOMOL ELECTROPHEROG
- Tong X, 2006, VIRUS RES, V115, P122, DOI 10.1016/j.virusres.2005.07.012
- Worobey M, 2008, NATURE, V455, P661, DOI 10.1038/nature07390