Defective in vitro growth of the hemopoietic progenitor cells in the acquired immunodeficiency syndrome.

Carlo‐Stella, Carmelo; Ganser, Arnold; Hoelzer, Dieter

doi:10.1172/jci113071

Cited by 164 publications

(52 citation statements)

References 39 publications

(30 reference statements)

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“…While the precise mechanisms of such hematopoietic abnormalities remain unclear, several hypotheses have been proposed: (i) decreased levels of appropriate cytokines secondary to altered numbers of T-cell subsets or macrophages, which are commonly seen in HIV type 1 (HIV-1) infection (28); (ii) production of inhibitory factors (14,29); (iii) cytotoxic elimination of the precursor cells by the antibody-dependent cellmediated cytolytic mechanism (7); and (iv) infection of hematopoietic precursor cells with viruses, which leads to death of these cells or their metabolic alteration (7). On the other hand, it has been suggested that primitive bone marrow progenitor cells are most likely not a major reservoir for HIVs (6,13,28).…”

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confidence: 99%

Early Bone Marrow Hematopoietic Defect in Simian/Human Immunodeficiency Virus C2/1-Infected Macaques and Relevance to Advance of Disease

Yamakami

Honda

Takei

et al. 2004

J Virol

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To clarify hematological abnormalities following infection with human immunodeficiency virus (HIV), we examined the hematopoietic capability of bone marrow by using cynomolgus monkeys infected with pathogenic simian/human immunodeficiency virus (SHIV) strain C2/1, an animal model of HIV infection. The relationship between the progress of the infection and the CD4/CD8 ratio of T lymphocytes or the amount of SHIV C2/1 viral load in the peripheral blood was also investigated. A colony assay was performed to assess the hematopoietic capability of bone marrow stem cells during the early and advanced phases of the infection. Colonies of granulocytes-macrophages (GM) were examined by PCR for the presence of the SIVmac239 gag region to reveal direct viral infection. There was a remarkable decrease in the CFU-GM growth on days 1 and 3 postinoculation, followed by recovery on day 56. During the more advanced stage, the CFU-GM growth decreased again. There was minimal evidence of direct viral infection of pooled cultured CFU-GM despite the continuously low CD4/ CD8 ratios. These results indicate that the decrease in colony formation by bone marrow stem cells is reversible and fluctuates with the advance of the disease. This decrease was not due to direct viral infection of CFU-GM. Our data may support the concept that, in the early phase, production of inhibitory factors or deficiency of a stimulatory cytokine is responsible for some of the bone marrow defects described in the SHIV C2/1 model.

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confidence: 99%

Early Bone Marrow Hematopoietic Defect in Simian/Human Immunodeficiency Virus C2/1-Infected Macaques and Relevance to Advance of Disease

Yamakami

Honda

Takei

et al. 2004

J Virol

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“…It has been shown in vitro that a synthetic peptide homologous to a sequence of the envelope protein of HIV suppress the oxidative burst of monocytes (Harrell er fl/,, 1986), Further, the growth of precursor cells in bone marrow may be impaired in patients with HIV infection (Stella, Ganser & Hoelzer, 1987) and this may lead to functionally deficient monocytes and macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…At day 1 and 10, adherent cell nuclei were counted as described by Unkeless & Eisen (1975). The detection limit of this assay was 10'' cells/well (data not shown).…”

Section: Monocyte Culturementioning

confidence: 99%

Reduced oxidative burst responses in monocytes and monocyte-derived macrophages from HIV-infected subjects

Müller¹,

Rollag²,

Frøland

1990

Clinical and Experimental Immunology

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SUMMARYOxidative burst responses of monocytes and monocyte-derived macrophages (MDM) were studied in 40 subjects with HIV infection of different clinical stages, Oxidative burst was assessed as reduction of nitroblue tetrazolium (NBT) with or without stimulants. Results were determined as oxidative burst responses per cell and as a stimulatory ratio between stimulated and unstimulated NBT reduction. Cells from 12 HIV-seronegative homosexual men and 38 blood donors served as control groups. In patients with asymptomatic HIV infection, monocyte oxidative burst responses were reduced compared with the blood donors. In MDM from the same patients, stimulatory ratios were reduced. In AIDS patients, stimulatory ratios of both monocytes and MDM were reduced compared with controls. In contrast to the progressive deterioration of CD4+ lymphocyte counts as well as other immune functions in HIV infection, monocyte oxidative burst responses are impaired already in the asymptomatic phase of the infection, almost to the same extent as in patients with AIDS,

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“…This may lead to anaemia and other haematologic anomalies in HIV infection [14,15]. Also, a model has been developed in which the pathophysiologic processes producing the anaemia in chronic diseases like HIV may be linked to the actions of pro-inflammatory cytokines (IL-1, TNF-α, and IFN-γ) that mediate the immune responses [16].…”

Section: Background Of Studymentioning

confidence: 99%

Anaemia and Pro-inflammatory Cytokines in Human Immunodeficiency Virus Infection

Enumah¹,

Nwauche²,

Okerengwo³

2016

IJI

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Abstract:Anaemia is often seen in HIV infected individuals and cytokines imbalance have been reported to cause haematopoietic stem cells suppression in the bone marrow. This case control study was carried out to determine any possible correlation between haemoglobin and pro-inflammatory cytokines in the development of anaemia in people living with HIV. 54 HIV infected and 34 apparently healthy HIV uninfected individuals were enrolled in this study. Full blood count and levels of three pro-inflammatory cytokines [(IL-α (interleukin-1 alpha), TNF-α (tumour necrosis factor-alpha) and IFN-γ (interferon-gamma)] were determined using MindrayBC-6800 automated Haematology analyser and Enzyme linked Immunosorbent Assay (ELISA) kits (Aviva system Biology, San Diego, CA, USA) respectively. The results obtained showed that prevalence of anaemia was 40.7% in HIV infected subjects, with higher prevalence in females (54.5%) than in males (19.0%). The difference in the mean concentrations of haemoglobin, red blood cell, packed cell volume, IL-α and TNF-α was statistically significant (p<0.05) while white blood cell counts and IFN-γ were not statistically significant (p>0.05) when compared to the control group. Though, there was a higher level of IFN-γ in HIV infected group than in the control group. There were weak correlations between haematological parameters and pro-inflammatory cytokines in the HIV positive group. HIV subjects were later divided into treatment groups: those on highly active antiretroviral therapy (HAART) -ZidovudineLamuvidine-Nevirapine (ZLN) combination, Tenofovir-Lamuvidine-Efavirenz (TLE) combination and those that are not on HAART-treatment naïve patients (TNP). There were statistically significant differences in the mean concentrations of red blood cell and white blood cell across the TLE and TNP groups (p<0.05). There were positive correlations between IFN-γ and HB in TLE group but negative correlations in other two groups. Also, there were positive correlations between IFN-γ and WBC in ZLN group but negative correlations in other two groups. This study suggests that the dysregulated pro-inflammatory cytokine levels caused by HIV itself played a role in causing anaemia in HIV infections.

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Defective in vitro growth of the hemopoietic progenitor cells in the acquired immunodeficiency syndrome.

Abstract: In addition to immunologic derangement, hematological abnormalities have been reported in the majority of patients with ac-

Cited by 164 publications

References 39 publications

Early Bone Marrow Hematopoietic Defect in Simian/Human Immunodeficiency Virus C2/1-Infected Macaques and Relevance to Advance of Disease

Early Bone Marrow Hematopoietic Defect in Simian/Human Immunodeficiency Virus C2/1-Infected Macaques and Relevance to Advance of Disease

Reduced oxidative burst responses in monocytes and monocyte-derived macrophages from HIV-infected subjects

Anaemia and Pro-inflammatory Cytokines in Human Immunodeficiency Virus Infection

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