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Kinetics of US28 Gene Expression during Active Human Cytomegalovirus Infection in Lung‐Transplant Recipients
Author(s) -
Jasper M. Boomker,
Erik A.M. Verschuuren,
Marja G. L. Brinker,
Lou F. M. H. de Leij,
T H Thé,
Martin C. Harmsen
Publication year - 2006
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/503779
Subject(s) - human cytomegalovirus , biology , virology , immunology , viral replication , chemokine , chemokine receptor , exacerbation , lung , transcription (linguistics) , viral load , viral disease , gene , betaherpesvirinae , virus , herpesviridae , inflammation , medicine , genetics , linguistics , philosophy
Targeting viral proteins early during infection may limit exacerbation of human cytomegalovirus infection. The viral chemokine-receptor homologue US28 interferes with leukocyte trafficking and, possibly, viral replication. Because US28 molecules are abundant on the surface of infected cells, this homologue is a potential target for antiviral therapy. To assess the relationship between US28 and disease activity, we measured, by quantitative reverse-transcription polymerase chain reaction, the levels of US28 and immediate-early (IE) 1 gene transcripts in the blood of lung-transplant recipients. We found that, during primary and secondary infection, the IE1 and US28 genes have early transcription kinetics and are expressed at similar levels. This may render US28 an attractive target for antiviral therapy.

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