| pubmed-article:16815724 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16815724 | lifeskim:mentions | umls-concept:C0011139 | lld:lifeskim |
| pubmed-article:16815724 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:16815724 | lifeskim:mentions | umls-concept:C0009013 | lld:lifeskim |
| pubmed-article:16815724 | lifeskim:mentions | umls-concept:C0038826 | lld:lifeskim |
| pubmed-article:16815724 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:16815724 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:16815724 | lifeskim:mentions | umls-concept:C0205250 | lld:lifeskim |
| pubmed-article:16815724 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:16815724 | pubmed:dateCreated | 2006-8-4 | lld:pubmed |
| pubmed-article:16815724 | pubmed:abstractText | Superinfection with human immunodeficiency virus type 1 (HIV-1) in human subjects, defined as reinfection with a heterologous strain of HIV-1, has become a topic of great interest. To illustrate the significance of this occurrence, we performed HIV-1 superinfection of L-2 cells, which were isolated from MT-4 cells persistently infected with subtype B HIV-1 as a cell clone continuously producing defective HIV-1 particles. L-2 cells carrying provirus with a one-base insertion in the pol protease were superinfected with HIV-1 derived from primary isolates of subtype B or CRF01_AE. The kinetics of the superinfection in L-2 were very slow compared with those of primary infections in MT-4. Interestingly, L-2 shifted after superinfection to become a producer of highly cytopathogenic HIV-1. Molecular characterization revealed that superinfection occurred in only about 10% of the CRF01_AE-superinfected L-2, which carried provirus of both subtypes and produced viral particles containing genomic RNA of both subtypes. Surprisingly, such cytopathogenic HIV-1 showed predominantly the original subtype B phenotype. Thus, the mechanism of the production of cytopathic HIV-1 seemed to be mediated by trans complementation with pol products of superinfected CRF01_AE. These findings suggest the significance of long-lived infected cells as recipients for superinfection that could result in the generation of new HIV-1 variants with high virulence in patients who are off therapy or do not adhere to treatment, and may indicate the need for precautions against such superinfection. | lld:pubmed |
| pubmed-article:16815724 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16815724 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16815724 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16815724 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16815724 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16815724 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:16815724 | pubmed:issn | 1286-4579 | lld:pubmed |
| pubmed-article:16815724 | pubmed:author | pubmed-author:IkutaKazuyosh... | lld:pubmed |
| pubmed-article:16815724 | pubmed:author | pubmed-author:KameokaMasano... | lld:pubmed |
| pubmed-article:16815724 | pubmed:author | pubmed-author:GotoToshiyuki... | lld:pubmed |
| pubmed-article:16815724 | pubmed:author | pubmed-author:WarachitJiran... | lld:pubmed |
| pubmed-article:16815724 | pubmed:author | pubmed-author:IwabuYukieY | lld:pubmed |
| pubmed-article:16815724 | pubmed:author | pubmed-author:LiGui-MeiGM | lld:pubmed |
| pubmed-article:16815724 | pubmed:author | pubmed-author:TsujiShotaroS | lld:pubmed |
| pubmed-article:16815724 | pubmed:author | pubmed-author:ShojiSanaeS | lld:pubmed |
| pubmed-article:16815724 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16815724 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:16815724 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16815724 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16815724 | pubmed:pagination | 1773-82 | lld:pubmed |
| pubmed-article:16815724 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:16815724 | pubmed:meshHeading | pubmed-meshheading:16815724... | lld:pubmed |
| pubmed-article:16815724 | pubmed:meshHeading | pubmed-meshheading:16815724... | lld:pubmed |
| pubmed-article:16815724 | pubmed:meshHeading | pubmed-meshheading:16815724... | lld:pubmed |
| pubmed-article:16815724 | pubmed:meshHeading | pubmed-meshheading:16815724... | lld:pubmed |
| pubmed-article:16815724 | pubmed:meshHeading | pubmed-meshheading:16815724... | lld:pubmed |
| pubmed-article:16815724 | pubmed:meshHeading | pubmed-meshheading:16815724... | lld:pubmed |
| pubmed-article:16815724 | pubmed:meshHeading | pubmed-meshheading:16815724... | lld:pubmed |
| pubmed-article:16815724 | pubmed:meshHeading | pubmed-meshheading:16815724... | lld:pubmed |
| pubmed-article:16815724 | pubmed:meshHeading | pubmed-meshheading:16815724... | lld:pubmed |
| pubmed-article:16815724 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16815724 | pubmed:articleTitle | Superinfection of human immunodeficiency virus type 1 (HIV-1) to cell clone persistently infected with defective virus induces production of highly cytopathogenic HIV-1. | lld:pubmed |
| pubmed-article:16815724 | pubmed:affiliation | Department of Virology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka, Japan. | lld:pubmed |
| pubmed-article:16815724 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16815724 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16815724 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16815724 | lld:pubmed |
