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Journal of Virology, August 2008, p. 7863-7874, Vol. 82, No. 16
0022-538X/08/$08.00+0 doi:10.1128/JVI.00310-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
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Sheila O. Medeiros,1,
Jose P. Simonetti,3
Hermann G. Schatzmayr,2
Amílcar Tanuri,1 and
Rodrigo M. Brindeiro1*
Laboratory of Molecular Virology, Department of Genetics, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil,1 Laboratory of Flavivirus, Department of Virology, FIOCRUZ, Rio de Janeiro, RJ, Brazil,2 Department of Virology, FIOCRUZ, Rio de Janeiro, RJ, Brazil3
Received 12 February 2008/ Accepted 29 May 2008
Feline immunodeficiency virus (FIV) is the Lentivirus responsible for an immunodeficiency-like disease in domestic cats (Felis catus). FIV is divided into five phylogenetic subtypes (A, B, C, D, and E), based on genetic diversity. Knowledge of the geographical distribution of subtypes is relevant for understanding different disease progressions and for vaccine development. In this study, viral sequences of 26 infected cats from Rio de Janeiro, 8 undergoing treatment with zidovudine (AZT) for at least 5 years, were successfully amplified from blood specimens. gag capsid (CA), pol reverse transcriptase (RT), and env gp120 (V3-V4) regions were analyzed to determine subtypes and to evaluate potential mutations related to antiretroviral drug resistance among treated cats. Subtyping based on phylogenetic analysis was performed by the neighbor-joining and maximum likelihood methods. All of the sequences clustered with subtype B in the three regions, exhibiting low genetic variability. Additionally, we found evidence that the same virus is circulating in animals in close contact. The analysis of FIV RT sequences identified two new putative mutations related to drug resistance located in the RT "finger" domain, which has 60% identity to human immunodeficiency virus (HIV) sequence. Amino acid change K
R at codons 64 and 69 was found in 25% and 37.5% of the treated animals, respectively. These signatures were comparable to K65R and K70R thymidine-associated mutations found in the HIV-1 HXB2 counterpart. This finding strongly suggests a position correlation between the mutations found in FIV and the K65R and K70R substitutions from drug-resistant HIV-1 strains.
Published ahead of print on 11 June 2008.
Supplemental material for this article may be found at http://jvi.asm.org/.
A. N. Martins and S. O. Medeiros contributed equally to this article.
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