Abstract
U937 cell clones in which efficient (plus) vs poor (minus) replication of HIV-1 occurs have been described. We evaluated the role of host factors in their differential ability to support HIV-1 replication. Plus clones constitutively produced TNF-α and viral replication was inhibited by neutralization of endogenous TNF-α. However, HIV-1 replication was strongly upregulated in minus clones by exogenous TNF-α, which also further accelerated the kinetics of infection in plus clones. We observed an increased accumulation of proviral DNA within one round of HIV-1 replication following TNF-a treatment of plus cells. This effect was associated with increased surface density of CXCR4 in both plus and minus clones. Our results identify TNF-α as one correlate that contributes to the higher ability of U937-plus clones to sustain HIV-1 replication. Furthermore, we suggest that TNF-α may affect steps of the viral life cycle that occur earlier than transcription and also enhance HIV-1 replication by increasing the surface density of CXCR4.
| Original language | English |
|---|---|
| Pages (from-to) | 55-59 |
| Number of pages | 5 |
| Journal | Cytokine |
| Volume | 13 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 7 2001 |
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Keywords
- CXCR4
- HIV-1
- TNF-α
- U937
ASJC Scopus subject areas
- Endocrinology
- Molecular Biology
- Immunology
- Immunology and Allergy
Cite this
Tumor necrosis factor-α drives HIV-1 replication in U937 cell clones and upregulates CXCR4. / Biswas, Priscilla; Mantelli, Barbara; Delfanti, Fanny; Cota, Manuela; Vallanti, Giuliana; De Filippi, Camilla; Mengozzi, Manuela; Vicenzi, E.; Lazzarin, A.; Poli, Guido.
In: Cytokine, Vol. 13, No. 1, 07.01.2001, p. 55-59.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Tumor necrosis factor-α drives HIV-1 replication in U937 cell clones and upregulates CXCR4
AU - Biswas, Priscilla
AU - Mantelli, Barbara
AU - Delfanti, Fanny
AU - Cota, Manuela
AU - Vallanti, Giuliana
AU - De Filippi, Camilla
AU - Mengozzi, Manuela
AU - Vicenzi, E.
AU - Lazzarin, A.
AU - Poli, Guido
PY - 2001/1/7
Y1 - 2001/1/7
N2 - U937 cell clones in which efficient (plus) vs poor (minus) replication of HIV-1 occurs have been described. We evaluated the role of host factors in their differential ability to support HIV-1 replication. Plus clones constitutively produced TNF-α and viral replication was inhibited by neutralization of endogenous TNF-α. However, HIV-1 replication was strongly upregulated in minus clones by exogenous TNF-α, which also further accelerated the kinetics of infection in plus clones. We observed an increased accumulation of proviral DNA within one round of HIV-1 replication following TNF-a treatment of plus cells. This effect was associated with increased surface density of CXCR4 in both plus and minus clones. Our results identify TNF-α as one correlate that contributes to the higher ability of U937-plus clones to sustain HIV-1 replication. Furthermore, we suggest that TNF-α may affect steps of the viral life cycle that occur earlier than transcription and also enhance HIV-1 replication by increasing the surface density of CXCR4.
AB - U937 cell clones in which efficient (plus) vs poor (minus) replication of HIV-1 occurs have been described. We evaluated the role of host factors in their differential ability to support HIV-1 replication. Plus clones constitutively produced TNF-α and viral replication was inhibited by neutralization of endogenous TNF-α. However, HIV-1 replication was strongly upregulated in minus clones by exogenous TNF-α, which also further accelerated the kinetics of infection in plus clones. We observed an increased accumulation of proviral DNA within one round of HIV-1 replication following TNF-a treatment of plus cells. This effect was associated with increased surface density of CXCR4 in both plus and minus clones. Our results identify TNF-α as one correlate that contributes to the higher ability of U937-plus clones to sustain HIV-1 replication. Furthermore, we suggest that TNF-α may affect steps of the viral life cycle that occur earlier than transcription and also enhance HIV-1 replication by increasing the surface density of CXCR4.
KW - CXCR4
KW - HIV-1
KW - TNF-α
KW - U937
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UR - http://www.scopus.com/inward/citedby.url?scp=0035819237&partnerID=8YFLogxK
U2 - 10.1006/cyto.2000.0798
DO - 10.1006/cyto.2000.0798
M3 - Article
VL - 13
SP - 55
EP - 59
JO - Cytokine
JF - Cytokine
SN - 1043-4666
IS - 1
ER -