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Ultra‐deep sequencing reveals hidden HIV‐1 minority lineages and shifts of viral population between the main cellular reservoirs of the infection after therapy interruption
Author(s) -
Rozera Gabriella,
Abbate Isabella,
Ciccozzi Massimo,
Presti Alessandra Lo,
Bruselles Alessandro,
Vlassi Chrysoula,
D'Offizi Gianpiero,
Narciso Pasquale,
Giombini Emanuela,
Bartolini Barbara,
Ippolito Giuseppe,
Capobianchi Maria R.
Publication year - 2012
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.23292
Subject(s) - viral quasispecies , biology , phylogenetic tree , virology , population , deep sequencing , pyrosequencing , virus , genetic heterogeneity , genome , genetic variation , gene flow , genetics , antiretroviral therapy , genetic variability , gene , viral load , genotype , medicine , environmental health , phenotype
Viral quasispecies population dynamics between monocytes and T‐lymphocytes were analyzed in patients after highly active antiretroviral therapy (HAART) interruption, during a follow‐up of 3–6 months. V3 env region underwent ultra‐deep pyrosequencing. Co‐receptor usage prediction was performed by Position Specific Score Matrix Analysis. Phylogenetic trees were constructed to evaluate the relationships between the variants. Gene flow was also investigated. Even though at the moment of therapy interruption monocyte‐derived HIV‐1 genomes presented higher genetic heterogeneity than that of T‐lymphocytes, at subsequent times, this difference in genetic heterogeneity disappeared, due to different waves of expansion and reduction of quasispecies variability associated with monocytes and T‐lymphocytes. Phylogenetic analysis and gene flow evaluation supported the hypothesis of extensive interchange of variants between cellular compartments of the infection. A spread of proviral X4 lineages hidden in monocytes to T cells was observed, but this was not associated with an overall shift towards CXCR4 using variants during the observation period. J. Med. Virol. 84:839–844, 2012. © 2012 Wiley Periodicals, Inc.