Higher macrophage inflammatory protein (MIP)-1α and MIP-1β levels from CD8<sup>+</sup>T cells are associated with asymptomatic HIV-1 infection

Cocchi, Fiorenza; DeVico, Anthony L.; Yarchoan, Robert; Redfield, Robert; Cleghorn, Farley; Blattner, William A.; Garzino-Demo, Alfredo; Colombini-Hatch, Sandra; Margolis, David M.; Gallo, Robert C.

doi:10.1073/pnas.240469997

Cited by 129 publications

(106 citation statements)

References 60 publications

(56 reference statements)

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“…HIV-1 infection and the resultant IFN-␣ responses are known to induce the production of cytokines. Proinflammatory factors, such as IL-1␤, tumor necrosis factor alpha (TNF-␣), and CXCL10 (IP-10), appear to be detrimental to the host (55,56), while MIP-1␣ is likely beneficial (57). To assess these responses in our model, we analyzed plasma samples at 11 dpi for the presence of 11 different human cytokines.…”

Section: Fig 4 Ifn-␣14 Suppression Of Established Hiv-1 Infection (Amentioning

confidence: 99%

Interferon Alpha Subtype-Specific Suppression of HIV-1 InfectionIn Vivo

Lavender¹,

Gibbert

Peterson³

et al. 2016

J Virol

112

188

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Section: Fig 4 Ifn-␣14 Suppression Of Established Hiv-1 Infection (Amentioning

confidence: 99%

Interferon Alpha Subtype-Specific Suppression of HIV-1 InfectionIn Vivo

Lavender¹,

Gibbert

Peterson³

et al. 2016

J Virol

112

188

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“…Several studies have demonstrated that increased production of RANTES, MIP-1␣, and MIP-1␤ correlates with resistance to infection or a more favorable clinical prognosis, likely because of competition of the chemokines with HIV-1 for binding to CCR5 (2)(3)(4)(5)(6).…”

mentioning

confidence: 99%

Induction of G ₁ cycle arrest in T lymphocytes results in increased extracellular levels of β-chemokines: A strategy to inhibit R5 HIV-1

Heredia

Davis

Amoroso

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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The ␤-chemokines RANTES (regulated on activation, normal T cell expressed and secreted), macrophage inflammatory protein-1␣ (MIP-1␣), and MIP-1␤ are the natural ligands of the HIV-1 coreceptor CCR5 and compete with the virus for receptor binding. We show that secretion of the ␤-chemokines by activated lymphocytes starts before cellular DNA synthesis is detected and demonstrate that transient prolongation of the G1 phase of the cell cycle by treatment with cytostatic drugs results in increased levels of the three chemokines in culture supernatants. Supernatants collected from peripheral blood mononuclear cells exposed to hydroxyurea, which arrests the cell cycle in late G 1, contained high levels of ␤-chemokines. These supernatants were able to inhibit HIV-1 replication when added to cultures of infected lymphocytes. The observed antiviral effect likely was due to the increased levels of ␤-chemokines RANTES, MIP-1␣, and MIP-1␤ because (i) supernatants greatly inhibited the replication of HIV-1 BaL, whereas they affected HIV-1 IIIb replication only slightly; (ii) neutralizing antibodies against the chemokines abrogated the antiviral effect of the supernatants; and (iii) the hydroxyurea concentrations shown to up-regulate chemokine levels were not sufficient to inhibit virus replication by depletion of intracellular nucleotide pools. Although antiviral properties have been reported previously for the cytostatic agents shown here to up-regulate ␤-chemokine levels, our results provide an additional mechanism by which these drugs may exert antiviral activity. In summary, increased extracellular levels of anti-HIV-1 ␤-chemokines resulting from transient prolongation of the G1 phase of the lymphocyte cell cycle by treatment with cytostatic drugs may help to control the replication of CCR5-using strains of HIV-1.

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“…Because the ß-chemokines are major components of the HIV-1 suppressive soluble factor extensively studied nowadays (6)(7)(8)(9)(10)(11)(12), the present study was undertaken to determine the relationship between plasma concentrations of MIP1a and RANTES and viral load in Brazilian HIV-1-infected subjects.…”

mentioning

confidence: 99%

CCR5 genotype and plasma ß-chemokine concentration of Brazilian HIV-infected individuals

Mikawa

Tagliavini

Costa

2002

Braz J Med Biol Res

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The 32-bp deletion in the HIV-1 co-receptor CCR5 confers a high degree of resistance to HIV-1 infection in homozygous individuals for the deleted allele and partial protection against HIV-1 during disease progression in heterozygotes. Natural ligands for CCR5, MIP-1a, MIP-1ß and RANTES, have been shown to inhibit HIV replication in CD4+ T cells. In the present study, we examined the CCR5 genotype by PCR and the plasma levels of RANTES and MIP-1a by ELISA among blood donors (N = 26) and among HIV-1-infected individuals (N = 129). The control group consisted of healthy adult volunteers and HIV-1-infected subjects were an asymptomatic and heterogeneous group of individuals with regard to immunologic and virologic markers of HIV-1 disease. The frequency of the CCR5 mutant allele (D32ccr5) in this population was 0.032; however, no D32ccr5 homozygote was detected. These results could be related to the intense ethnic admixture of the Brazilian population. There was no correlation between circulating ß-chemokines (MIP-1a, RANTES) and viral load in HIV-infected individuals. RANTES concentrations in plasma samples from HIV+ patients carrying the homozygous CCR5 allele (CCR5/CCR5) (28.23 ng/ml) were higher than in the control samples (16.07 ng/ml; P<0.05); however, this HIV+ patient group (mean 26.23 pg/ml) had significantly lower concentrations of MIP-1a than those observed in control samples (mean 31.20 pg/ml; P<0.05). Both HIV-1-infected and uninfected individuals heterozygous for the D32ccr5 allele had significantly lower concentrations of circulating RANTES (mean 16.07 and 6.11 ng/ml, respectively) than CCR5/CCR5 individuals (mean 28.23 and 16.07 ng/ml, respectively; P<0.05). These findings suggest that the CCR5 allele and ß-chemokine production may affect the immunopathogenesis of HIV-1.

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Higher macrophage inflammatory protein (MIP)-1α and MIP-1β levels from CD8⁺T cells are associated with asymptomatic HIV-1 infection

Cited by 129 publications

References 60 publications

Interferon Alpha Subtype-Specific Suppression of HIV-1 InfectionIn Vivo

Interferon Alpha Subtype-Specific Suppression of HIV-1 InfectionIn Vivo

Induction of G ₁ cycle arrest in T lymphocytes results in increased extracellular levels of β-chemokines: A strategy to inhibit R5 HIV-1

CCR5 genotype and plasma ß-chemokine concentration of Brazilian HIV-infected individuals

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Higher macrophage inflammatory protein (MIP)-1α and MIP-1β levels from CD8+T cells are associated with asymptomatic HIV-1 infection

Cited by 129 publications

References 60 publications

Interferon Alpha Subtype-Specific Suppression of HIV-1 InfectionIn Vivo

Interferon Alpha Subtype-Specific Suppression of HIV-1 InfectionIn Vivo

Induction of G 1 cycle arrest in T lymphocytes results in increased extracellular levels of β-chemokines: A strategy to inhibit R5 HIV-1

CCR5 genotype and plasma ß-chemokine concentration of Brazilian HIV-infected individuals

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Higher macrophage inflammatory protein (MIP)-1α and MIP-1β levels from CD8⁺T cells are associated with asymptomatic HIV-1 infection

Induction of G ₁ cycle arrest in T lymphocytes results in increased extracellular levels of β-chemokines: A strategy to inhibit R5 HIV-1