Tumor necrosis factor-α drives HIV-1 replication in U937 cell clones and upregulates CXCR4

Priscilla Biswas; Barbara Mantelli; Fanny Delfanti; Manuela Cota; Giuliana Vallanti; Camilla De Filippi; Manuela Mengozzi; E. Vicenzi; A. Lazzarin; Guido Poli

doi:10.1006/cyto.2000.0798

Tumor necrosis factor-α drives HIV-1 replication in U937 cell clones and upregulates CXCR4

Priscilla Biswas, Barbara Mantelli, Fanny Delfanti, Manuela Cota, Giuliana Vallanti, Camilla De Filippi, Manuela Mengozzi, E. Vicenzi, A. Lazzarin, Guido Poli

IRCCS Ospedale San Raffaele

Research output: Contribution to journal › Article › peer-review

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	https://doi.org/10.1006/cyto.2000.0798
Publication status	Published - Jan 7 2001

Keywords

CXCR4
HIV-1
TNF-α
U937

ASJC Scopus subject areas

Endocrinology
Molecular Biology
Immunology
Immunology and Allergy

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10.1006/cyto.2000.0798

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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 › peer-review

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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.",

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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

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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.

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Tumor necrosis factor-α drives HIV-1 replication in U937 cell clones and upregulates CXCR4

Abstract

Keywords

ASJC Scopus subject areas

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