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Titolo:
JC virus multiplication in human hematopoietic progenitor cells requires the NF-1 class D transcription factor
Autore:
Monaco, MCG; Sabath, BF; Durham, LC; Major, EO;
Indirizzi:
NINCDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA NINCDS Bethesda MD USA 20892 Med & Neurosci, NIH, Bethesda, MD 20892 USA
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 20, volume: 75, anno: 2001,
pagine: 9687 - 9695
SICI:
0022-538X(200110)75:20<9687:JVMIHH>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEAR FACTOR-I; ADENOVIRUS DNA-REPLICATION; TONSILLAR STROMAL CELLS; HUMAN CYTOMEGALO-VIRUS; AFFINITY BINDING-SITE; HUMAN POLYOMAVIRUS; B-LYMPHOCYTES; GENE FAMILY; GLIAL-CELLS; PROTEIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Major, EO NINCDS, Lab Mol Med & Neurosci, NIH, Bldg 36,Room 5W21, Bethesda, MD 20892USA NINCDS Bldg 36,Room 5W21 Bethesda MD USA 20892 esda, MD 20892USA
Citazione:
M.C.G. Monaco et al., "JC virus multiplication in human hematopoietic progenitor cells requires the NF-1 class D transcription factor", J VIROLOGY, 75(20), 2001, pp. 9687-9695

Abstract

JCV, a small DNA virus of the polyomavirus family, has been shown to infect glial cells of the central nervous system, hematopoietic progenitor cells, and immune system lymphocytes. A family of DNA binding proteins called nuclear factor-1 (NF-1) has been linked with site-coding specific transcription of cellular and viral genes and replication of some viruses, including JC virus (JCV). It is unclear which NF-1 gene product must be expressed by cells to promote JCV multiplication. Previously, it was shown that elevated levels of NF-1 class D mRNA were expressed by human brain cells that are highly susceptible to JCV infection but not by JCV nonpermissive HeLa cells. Recently, we reported that CD34(+) precursor cells of the KG-1 line, when treated with the phorbol ester phorbol 12-myristate 13-acetate (PMA), differentiated to cells with macrophage-like characteristics and lost susceptibility to JCV infection. These studies have now been extended by asking whether loss of JCV susceptibility by PMA-treated KG-1 cells is linked with alterations in levels of NF-1 class D expression. Using reverse transcription-PCR, we have found that PMA-treated KG-1 cells express mRNA that codes for all four classes of NF-I proteins, although different levels of RNA expression were observed in the hematopoietic cells differentiated into macrophages. Northern hybridization confirms that the expression of NF-1 class D gene is lower in JCV nonpermissive PMA-treated KG-1 cells compared with non-PMA-treated cells. Further, using gel mobility shift assays, we were able to show the induction of specific NF-I-DNA complexes in KG-1 cells undergoing PMAtreatment. The binding increases in direct relation to the duration of PMAtreatment. These results suggest that the binding pattern of NF-1 class members may change in hematopoietic precursor cells, such as KG-1, as they undergo differentiation to macrophage-like cells. Transfection of PMA-treatedKG-1 cells with an NF-1 class D expression vector restored the susceptibility of these cells to JCV infection, while the transfection of PMA-treated KG-1 cells with NF-1 class A, B, and C vectors was not able to restore JCV susceptibility. These data collectively suggest that selective expression of NF-1 class D has a regulatory role in JCV multiplication.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 09:00:13