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The X4 phenotype of HIV type 1 evolves from R5 in two children of mothers, carrying X4, and is not linked to transmission

Clevestig, P; Maljkovic, I; Casper, C; Carlenor, E; Lindgren, S; Naver, L; Bohlin, A B; Fenyö, Eva Maria LU ; Leitner, T and Ehrnst, A (2005) In AIDS Research and Human Retroviruses 21(5). p.371-378
Abstract
Previously, we found that emergence of the X4 viral phenotype in HIV-1-infected children was related to the presence of X4 in their mothers (C. H. Casper et al., J Infect Dis 2002; 186: 914-921). Here, we investigated the origin of the X4 phenotype in the child, analyzing two mother-child pairs (Ma-Ca, Mb-Cb) where the mothers carried X4 and their children developed X4 after an initial presence of R5. We used nested polymerase chain reaction of the env V3 region to generate 203 HIV-1 clones for sequencing (Ma, n = 44; Ca, n = 73; Mb, n = 61; Cb, n = 25) from DNA of peripheral blood mononuclear cell (PBMC) lysates, altogether 167 clones, or from cDNA of plasma RNA, 36 clones. PBMC and plasma isolate sequences from each time point enabled us... (More)
Previously, we found that emergence of the X4 viral phenotype in HIV-1-infected children was related to the presence of X4 in their mothers (C. H. Casper et al., J Infect Dis 2002; 186: 914-921). Here, we investigated the origin of the X4 phenotype in the child, analyzing two mother-child pairs (Ma-Ca, Mb-Cb) where the mothers carried X4 and their children developed X4 after an initial presence of R5. We used nested polymerase chain reaction of the env V3 region to generate 203 HIV-1 clones for sequencing (Ma, n = 44; Ca, n = 73; Mb, n = 61; Cb, n = 25) from DNA of peripheral blood mononuclear cell (PBMC) lysates, altogether 167 clones, or from cDNA of plasma RNA, 36 clones. PBMC and plasma isolate sequences from each time point enabled us to assign the probable phenotype to clone sequences in a phylogenetic tree. The transmission and evolution were reconstructed using the maximum likelihood method. In mother-child pair Ma-Ca, one maternal R5 isolate clustered with the child's R5 sequences, at the earliest time when R5 was isolated in the child, confirming this as a likely source of the transmitted R5 phenotype. At age 3, an X4 population was present in the child that had evolved from the child's own R5-associated population, clearly distinct from the maternal X4 sequences. The second mother-child pair (Mb-Cb) displayed a similar pattern. Amino acid substitution patterns corroborated the conclusions from the phylogenetic tree. Thus, in both children, the X4 virus developed from their own R5 population, and was not caused by transmission of X4. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
AIDS Research and Human Retroviruses
volume
21
issue
5
pages
371 - 378
publisher
Mary Ann Liebert, Inc.
external identifiers
  • pmid:15929699
  • wos:000229825700005
  • scopus:20444393084
ISSN
1931-8405
DOI
10.1089/aid.2005.21.371
language
English
LU publication?
yes
id
7d191257-2fa9-46d4-bb91-009968ec94e4 (old id 234039)
date added to LUP
2007-09-21 10:42:34
date last changed
2017-01-01 04:59:15
@article{7d191257-2fa9-46d4-bb91-009968ec94e4,
  abstract     = {Previously, we found that emergence of the X4 viral phenotype in HIV-1-infected children was related to the presence of X4 in their mothers (C. H. Casper et al., J Infect Dis 2002; 186: 914-921). Here, we investigated the origin of the X4 phenotype in the child, analyzing two mother-child pairs (Ma-Ca, Mb-Cb) where the mothers carried X4 and their children developed X4 after an initial presence of R5. We used nested polymerase chain reaction of the env V3 region to generate 203 HIV-1 clones for sequencing (Ma, n = 44; Ca, n = 73; Mb, n = 61; Cb, n = 25) from DNA of peripheral blood mononuclear cell (PBMC) lysates, altogether 167 clones, or from cDNA of plasma RNA, 36 clones. PBMC and plasma isolate sequences from each time point enabled us to assign the probable phenotype to clone sequences in a phylogenetic tree. The transmission and evolution were reconstructed using the maximum likelihood method. In mother-child pair Ma-Ca, one maternal R5 isolate clustered with the child's R5 sequences, at the earliest time when R5 was isolated in the child, confirming this as a likely source of the transmitted R5 phenotype. At age 3, an X4 population was present in the child that had evolved from the child's own R5-associated population, clearly distinct from the maternal X4 sequences. The second mother-child pair (Mb-Cb) displayed a similar pattern. Amino acid substitution patterns corroborated the conclusions from the phylogenetic tree. Thus, in both children, the X4 virus developed from their own R5 population, and was not caused by transmission of X4.},
  author       = {Clevestig, P and Maljkovic, I and Casper, C and Carlenor, E and Lindgren, S and Naver, L and Bohlin, A B and Fenyö, Eva Maria and Leitner, T and Ehrnst, A},
  issn         = {1931-8405},
  language     = {eng},
  number       = {5},
  pages        = {371--378},
  publisher    = {Mary Ann Liebert, Inc.},
  series       = {AIDS Research and Human Retroviruses},
  title        = {The X4 phenotype of HIV type 1 evolves from R5 in two children of mothers, carrying X4, and is not linked to transmission},
  url          = {http://dx.doi.org/10.1089/aid.2005.21.371},
  volume       = {21},
  year         = {2005},
}