Chronic ethanol intoxication enhances the production of cytokine-induced neutrophil chemoattractant and macrophage inflammatory protein-2 by hepatocytes after human immunodeficiency virus-1 glycoprotein 120 vaccination

Alcohol ◽  
2001 ◽  
Vol 24 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Abraham P Bautista ◽  
Enze Wang
Keyword(s):  
Human Immunodeficiency Virus ◽  
Chronic Ethanol ◽  
Ethanol Intoxication ◽  
Inflammatory Protein ◽  
Immunodeficiency Virus ◽  
Chronic Ethanol Intoxication ◽  
Macrophage Inflammatory Protein ◽  
Human Immunodeficiency Virus 1

scholarly journals Levels of Macrophage Inflammatory Protein 1α (MIP-1α) and MIP-1β in Intervillous Blood Plasma Samples from Women with Placental Malaria and Human Immunodeficiency Virus Infection

2003 ◽  
Vol 10 (4) ◽  
pp. 631-636 ◽  
Author(s):  
Sujittra Chaisavaneeyakorn ◽  
Julie M. Moore ◽  
Lisa Mirel ◽  
Caroline Othoro ◽  
Juliana Otieno ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Blood Plasma ◽  
Plasma Levels ◽  
Placental Malaria ◽  
Hiv Positive ◽  
Inflammatory Protein ◽  
Immunodeficiency Virus ◽  
Macrophage Inflammatory Protein ◽  
Hiv Negative

ABSTRACT Macrophage inflammatory protein-1α (MIP-1α) and MIP-1β play an important role in modulating immune responses. To understand their importance in immunity to placental malaria (PM) and in human immunodeficiency virus (HIV)-PM coinfection, we investigated levels of these chemokines in the placental intervillous blood plasma (IVB plasma) and cord blood plasma of HIV-negative PM-negative, HIV-negative PM-positive, HIV-positive PM-negative, and HIV-positive PM-positive women. Compared to HIV-negative PM-negative women, the MIP-1β concentration in IVB plasma was significantly elevated in HIV-negative PM-positive women and HIV-positive PM-positive women, but it was unaltered in HIV-positive PM-negative women. Also, PM-infected women, irrespective of their HIV status, had significantly higher levels of MIP-1β than HIV-positive PM-negative women. The MIP-1α level was not altered in association with either infection. The IVB plasma levels of MIP-1α and MIP-1β positively correlated with the cord blood plasma levels of these chemokines. As with IVB plasma, only cord plasma from PM-infected mothers had significantly elevated levels of MIP-1β compared to PM-negative mothers, irrespective of their HIV infection status. MIP-1β and MIP-1α levels in PM-positive women were positively associated with parasite density and malaria pigment levels. Regardless of HIV serostatus, the IVB MIP-1β level was significantly lower in women with PM-associated anemia. In summary, an elevated level of MIP-1β was associated with PM. HIV infection did not significantly alter these two chemokine levels in IVB plasma.

Dynamics Study on the Anti-Human Immunodeficiency Virus Chemokine Viral Macrophage-Inflammatory Protein-II (VMIP-II) Reveals a Fully Monomeric Protein†

Biochemistry ◽  
1999 ◽  
Vol 38 (1) ◽  
pp. 442-453 ◽  
Author(s):  
Andy C. LiWang ◽  
Jian Jing Cao ◽  
Hong Zheng ◽  
Zhaohai Lu ◽  
Stephen C. Peiper ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Inflammatory Protein ◽  
Immunodeficiency Virus ◽  
Macrophage Inflammatory Protein

scholarly journals Macrophage Inflammatory Protein 1α Inhibits Postentry Steps of Human Immunodeficiency Virus Type 1 Infection via Suppression of Intracellular Cyclic AMP

2005 ◽  
Vol 79 (9) ◽  
pp. 5625-5631 ◽  
Author(s):  
Carol-Ann Amella ◽  
Barbara Sherry ◽  
David H. Shepp ◽  
Helena Schmidtmayerova
Keyword(s):  
Human Immunodeficiency Virus ◽  
Life Cycle ◽  
Cyclic Amp ◽  
Human Immunodeficiency Virus Type ◽  
Intracellular Camp ◽  
Inflammatory Protein ◽  
Immunodeficiency Virus ◽  
Macrophage Inflammatory Protein ◽  
Hiv 1

ABSTRACT Primary isolates of human immunodeficiency virus type 1 (HIV-1) predominantly use chemokine receptor CCR5 to enter target cells. The natural ligands of CCR5, the β-chemokines macrophage inflammatory protein 1α (MIP-1α), MIP-1β, and RANTES, interfere with HIV-1 binding to CCR5 receptors and decrease the amount of virions entering cells. Although the inhibition of HIV-1 entry by β-chemokines is well documented, their effects on postentry steps of the viral life cycle and on host cell components that control the outcome of infection after viral entry are not well defined. Here, we show that all three β-chemokines, and MIP-1α in particular, inhibit postentry steps of the HIV-1 life cycle in primary lymphocytes, presumably via suppression of intracellular levels of cyclic AMP (cAMP). Productive HIV-1 infection of primary lymphocytes requires cellular activation. Cell activation increases intracellular cAMP, which is required for efficient synthesis of proviral DNA during early steps of viral infection. Binding of MIP-1α to cognate receptors decreases activation-induced intracellular cAMP levels through the activation of inhibitory G proteins. Furthermore, inhibition of one of the downstream targets of cAMP, cAMP-dependent PKA, significantly inhibits synthesis of HIV-1-specific DNA without affecting virus entry. These data reveal that β-chemokine-mediated inhibition of virus replication in primary lymphocytes combines inhibitory effects at the entry and postentry levels and imply the involvement of β-chemokine-induced signaling in postentry inhibition of HIV-1 infection.

scholarly journals Macrophage inflammatory protein-1alpha is induced by human immunodeficiency virus infection of monocyte-derived macrophages

Blood ◽  
1996 ◽  
Vol 87 (5) ◽  
pp. 2011-2019 ◽  
Author(s):  
B Canque ◽  
M Rosenzwajg ◽  
A Gey ◽  
E Tartour ◽  
WH Fridman ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Virus Replication ◽  
Transforming Growth Factor ◽  
Virus Production ◽  
Tnf Alpha ◽  
Hiv Replication ◽  
Gm Csf ◽  
Inflammatory Protein ◽  
Immunodeficiency Virus ◽  
Macrophage Inflammatory Protein

Disparate findings have been reported as to whether human immunodeficiency virus (HIV) affects cytokine production by macrophages (MA). We investigated production of different cytokines and of macrophage inflammatory protein (MIP)-1alpha by HIV-1Ba-L-or HIV-1Ada-infected blood-derived MA. Relative to controls, only MIP-1alpha levels increased twofold to > 10-fold in supernatants 2 to 3 weeks postinfection (PI), at the time of maximum virus production; levels of the other chemokines (RANTES, interleukin (IL)-8) and cytokines (IL-1alpha, IL-3, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), G-CSF, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1) investigated were not affected. MIP-1alpha mRNA signal assessed by reverse transcriptase-polymerase chain reaction (RT-PCR) was, however, only occasionally greater in cells from infected cultures relative to controls. MIP-1alpha levels in supernatants remained in the same range as in control cultures when more than 10 mmol/L Zidovudine was added 24 hours PI, which indicates involvement of virus replication in the effect. Anti-MIP-1alpha antibody labeling identified a 10% to 25% subset of MA, strongly expressing HLA-DR and CD4, and also stained by anti-IL-6 and anti-TNF-alpha antibodies. Two weeks PI, dual staining showed that the majority of the 5% to 20% cells that were p24+ belonged to the MIP-1alpha+ population, which may define a MA subset capable to better sustain HIV replication. MIP-1alpha induced by HIV replication in MA might play a role in the pathophysiology of HIV infection; in impaired hematopoiesis; or as a CD4+ and CD8+ lymphocyte chemoattractant, by recruiting either or both HIV-susceptible and cytotoxic T lymphocytes to virus replication sites.

scholarly journals Involvement of both the V2 and V3 Regions of the CCR5-Tropic Human Immunodeficiency Virus Type 1 Envelope in Reduced Sensitivity to Macrophage Inflammatory Protein 1α

2000 ◽  
Vol 74 (4) ◽  
pp. 1787-1793 ◽  
Author(s):  
Yosuke Maeda ◽  
Mohamed Foda ◽  
Shuzo Matsushita ◽  
Shinji Harada
Keyword(s):  
Human Immunodeficiency Virus ◽  
Chemokine Receptors ◽  
Luciferase Reporter ◽  
Replication Assay ◽  
Inflammatory Protein ◽  
Immunodeficiency Virus ◽  
Macrophage Inflammatory Protein ◽  
Hiv 1

ABSTRACT To determine whether C-C chemokines play an important role in the phenotype switch of human immunodeficiency virus (HIV) from CCR5 to CXCR4 usage during the course of an infection in vivo, macrophage inflammatory protein (MIP)-1α-resistant variants were isolated from CCR5-tropic (R5) HIV-1 in vitro. The selected variants displayed reduced sensitivities to MIP-1α (fourfold) through CCR5-expressing CD4-HeLa/long terminal repeat–β-galactosidase (MAGI/CCR5) cells. The variants were also resistant to other natural ligands for CCR5, namely, MIP-1β (>4-fold) and RANTES (regulated upon activation, normal T-cell expressed and secreted) (6-fold). The env sequence analyses revealed that the variants had amino acid substitutions in V2 (valine 166 to methionine) and V3 (serine 303 to glycine), although the same V3 substitution appeared in virus passaged without MIP-1α. A single-round replication assay using a luciferase reporter HIV-1 strain pseudotyped with mutant envelopes confirmed that mutations in both V2 and V3 were necessary to confer the reduced sensitivity to MIP-1α, MIP-1β, and RANTES. However, the double mutant did not switch its chemokine receptor usage from CCR5 to CXCR4, indicating the altered recognition of CCR5 by this mutant. These results indicated that V2 combined with the V3 region of the CCR5-tropic HIV-1 envelope modulates the sensitivity of HIV-1 to C-C chemokines without altering the ability to use chemokine receptors.

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