title: Short communication: Different mutation patterns in subtype CRF06_cpx after mother-to-child transmission.
abstract: Abstract Development of drug resistance mutation patterns (DRMP) in HIV after treatment failure depends on the drugs used in the failing regimen. However, selected patterns may not be unique; there is evidence that selection of DRMP for nelfinavir is dependent on subtype and/or background polymorphisms. Here we describe the selection of DRMP in a mother and son infected with subtype CRF06_cpx by mother-to-child transmission. Four years after delivery the mother received stavudine/lamivudine/nelfinavir as first-line therapy. Genotypic resistance tests (GRT) during follow-up showed selection of M184V/L283I in reverse transcriptase (RT) and H63Q/A71V/L90M in protease (PR). The child started treatment 8 months after birth with stavudine/didanosine/nelfinavir followed by an intensification period with efavirenz. Due to toxicity, efavirenz was removed from the regimen again. GRT during follow-up showed selection of L74V/K103N/M184V/M230L in RT and M46I/H63Q/N88S in PR. The viral load (VL) of the mother was initially undetectable followed by intermediate replication (1000-21,000 copies/ml), whereas the child had both periods of undetectable VL and low-level replication. Although both patients were infected with the same virus and treated with the same protease inhibitor, different DRMPs were selected. Whether the nucleoside backbone, course of antiretroviral therapy, or different host environment is responsible for this variability must be determined in larger studies.
authors.affiliation: J.W. Goethe University Hospital, Institute for Medical Virology, 60596 Frankfurt, Germany. M.Stuermer@em.uni-frankfurt.de
authors.forename: Martin
authors.initials: M
authors.lastname: Stürmer
authors.forename: Amina
authors.initials: A
authors.lastname: Carlebach
authors.forename: Schlomo
authors.initials: S
authors.lastname: Staszewski
authors.forename: Richard
authors.initials: R
authors.lastname: Linde
authors.forename: Christoph
authors.initials: C
authors.lastname: Königs
authors.forename: Hans W
authors.initials: HW
authors.lastname: Doerr
authors.forename: Martin
authors.initials: M
authors.lastname: Däumer
authors.forename: Annemarie
authors.initials: A
authors.lastname: Berger
mesh_terms: D019943:Amino Acid Substitution / Q000235:genetics; D023241:Antiretroviral Therapy, Highly Active; D000998:Antiviral Agents / Q000627:therapeutic use*; D024882:Drug Resistance, Viral; D005260:Female; D006678:HIV / Q000235:genetics* / Q000302:isolation & purification; D015658:HIV Infections / Q000188:drug therapy* / Q000635:transmission / Q000821:virology*; D016333:HIV Protease / Q000235:genetics; D006801:Humans; D007223:Infant; D018445:Infectious Disease Transmission, Vertical; D008297:Male; D009035:Mothers; D020125:Mutation, Missense; D009679:Nuclear Family; D010802:Phylogeny; D012641:Selection, Genetic; D017385:Sequence Homology; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D016333:HIV Protease