Published in
American Society for Microbiology, Journal of Virology, 18(78), p. 10023-10033, 2004
DOI: 10.1128/jvi.78.18.10023-10033.2004
American Society for Microbiology, Journal of Virology, 12(83), p. 6323-6323, 2009
DOI: 10.1128/jvi.00695-09
Links
- ORCID
- American Society for Microbiology | PDF
- American Society for Microbiology | PDF
- ORCID
- [www.ncbi.nlm.nih.gov] | PDF
- [www.ncbi.nlm.nih.gov] | PDF
- [europepmc.org] | PDF
- [europepmc.org] | PDF
- [www.researchgate.net] | PDF
- [www.ncbi.nlm.nih.gov] | PDF
- [www.ncbi.nlm.nih.gov] | PDF
- [www.ncbi.nlm.nih.gov] | PDF
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Human Cytomegalovirus UL131-128 Genes Are Indispensable for Virus Growth in Endothelial Cells and Virus Transfer to Leukocytes
,
Giulia Campanini,
Antonella Sarasini,
Markus Wagner,
Andrea Gallina,
Gabriele Milanesi,
Ulrich Koszinowski,
Fausto Baldanti,
Giuseppe Gerna
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Abstract
ABSTRACT Human cytomegalovirus (HCMV), a ubiquitous human pathogen, is the leading cause of birth defects and morbidity in immunocompromised patients and a potential trigger for vascular disease. HCMV replicates in vascular endothelial cells and drives leukocyte-mediated viral dissemination through close endothelium- leukocyte interaction. However, the genetic basis of HCMV growth in endothelial cells and transfer to leukocytes is unknown. We show here that the UL131-128 gene locus of HCMV is indispensable for both productive infection of endothelial cells and transmission to leukocytes. The experimental evidence for this is based on both the loss-of-function phenotype in knockout mutants and natural variants and the gain-of-function phenotype by trans -complementation with individual UL131, UL130, and UL128 genes. Our findings suggest that a common mechanism of virus transfer may be involved in both endothelial cell tropism and leukocyte transfer and shed light on a crucial step in the pathogenesis of HCMV infection.