Haematological manifestations of human immune deficiency virus infection

Vishnu, Prakash; Aboulafia, David M.

doi:10.1111/bjh.13783

Cited by 59 publications

(67 citation statements)

References 139 publications

(146 reference statements)

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“…Due to the infection of the BM accessory cells, impaired stromal function and alteration of the hematopoietic growth factor network was frequently observed in the BM of patients with HIV-1 infection[41–43]. These events directly lead to disruption of normal hematopoiesis in the BM[44, 45].…”

Section: Resultsmentioning

confidence: 99%

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Paradoxical myeloid-derived suppressor cell reduction in the bone marrow of SIV chronically infected macaques

et al. 2017

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Myeloid derived suppressor cells (MDSCs), which suppress anti-tumor or anti-viral immune responses, are expanded in the peripheral blood and tissues of patients/animals with cancer or viral infectious diseases. We here show that in chronic SIV infection of Indian rhesus macaques, the frequency of MDSCs in the bone marrow (BM) was paradoxically and unexpectedly decreased, but increased in peripheral blood. Reduction of BM MDSCs was found in both CD14+MDSC and Lin-CD15+MDSC subsets. The reduction of MDSCs correlated with high plasma viral loads and low CD4+ T cell counts, suggesting that depletion of BM MDSCs was associated with SIV/AIDS disease progression. Of note, in SHIVSF162P4-infected macaques, which naturally control viral replication within a few months of infection, the frequency of MDSCs in the bone marrow was unchanged. To investigate the mechanisms by which BM MDSCs were reduced during chronic SIV infection, we tested several hypotheses: depletion due to viral infection, alterations in MDSC trafficking, and/or poor MDSC replenishment. We found that the possible mobilization of MDSCs from BM to peripheral tissues and the slow self-replenishment of MDSCs in the BM, along with the viral infection-induced depletion, all contribute to the observed BM MDSC reduction. We first demonstrate MDSC SIV infection in vivo. Correlation between BM CD14+MDSC reduction and CD8+ T cell activation in tissues is consistent with decreased immune suppression by MDSCs. Thus, depletion of BM MDSCs may contribute to the pathologic immune activation during chronic SIV infection and by extension HIV infection.

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Section: Resultsmentioning

confidence: 99%

“…HIV-1 infected patients usually develop hematopoietic dysfunction, which is mainly mediated by the altered production of stromal cell-derived hematopoietic growth factors, infection of the BM accessory cells, and impaired stromal functionality[41–43, 56]. This abnormality could lead to defects of MDSC replenishment.…”

Section: Discussionmentioning

confidence: 99%

Paradoxical myeloid-derived suppressor cell reduction in the bone marrow of SIV chronically infected macaques

et al. 2017

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“…The pathophysiology of the haematological abnormalities have not been fully elucidated, but has been suggested to be complex and multifactorial. [4] The pathophysiology of cytopenias can broadly be divided into two groups: factors (i) directly associated with the impact of HIV on HSPC function, and (ii) not directly associated with HSPC function. The suggested mechanisms directly resulting from HIV are briefly discussed in this review, while factors not directly associated with HSPC function are summarised in Fig.…”

Section: S42mentioning

confidence: 99%

“…Cytopenias are the most common haematological abnormality associated with HIV infection and may affect any of the major blood lineages leading to anaemia, thrombocytopenia and/or neutropenia. [4,5] The prevalence of cytopenias in treatmentnaïve HIV-infected adult cohorts, reported between 2010 and 2018, in English-speaking eastern and southern sub-Saharan African countries, is summarised in Fig. 3.…”

Section: Haematological Abnormalitiesmentioning

confidence: 99%

HIV and haematopoiesis

et al. 2019

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Human immunodeficiency virus (HIV) infection not only leads to a compromised immune system, but also disrupts normal haematopoiesis, resulting in the frequent manifestation of cytopenias (anaemia, thrombocytopenia and neutropenia). Although there is a definite association between the severity of cytopenia and HIV disease stage, this relationship is not always linear. For example, cytopenias such as thrombocytopenia may occur during early stages of infection. The aetiology of these haematological abnormalities is complex and multifactorial, including druginduced impaired haematopoiesis, bone marrow suppression due to infiltration of infectious agents or malignant cells, HIV-induced impaired haematopoiesis, and several other factors. In this review, we describe the frequencies of anaemia, thrombocytopenia and neutropenia reported for HIV-infected, treatment-naïve cohorts studied in eastern and southern sub-Saharan African countries. We present a rational approach for the use of diagnostic tests during the workup of HIV-infected patients presenting with cytopenia, and discuss how HIV impacts on haematopoietic stem/progenitor cells (HSPCs) resulting in impaired haematopoiesis. Finally, we describe the direct and indirect effects of HIV on HSPCs which result in defective haematopoiesis leading to cytopenias. S Afr Med J 2019;109(8 Suppl 1):S41-S46. https://doi.org/10.7196/SAMJ.2019.v109i8b.13829 Fig. 1. Schematic illustration of the differentiation of haematopoietic stem/progenitor cells (HSPCs) into mature blood cell types. (MPP = multipotent progenitor; CMP = common myeloid progenitor; CLP = common lymphoid progenitor; MEP = megakaryocyte-erythroid progenitor; GMP = granulocytemacrophage progenitor; NK = natural killer cell.)

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“…The treatment leads to viral suppression but does not completely restore the immune damage, so ineffective immune response could be the reason why HIV patients have an increased risk of developing different types of tumours [30, 31]. The role of HIV in the development of neoplastic pathologies can be linked to severe immunodeficiency with consequent impairment of immunological surveillance against infectious agents (with predisposition to the appearance of virus-associated tumours) and the cells with malignant transformation [32-34], although its role in the process of carcinogenesis has not yet been completely clarified.…”

Section: Discussionmentioning

confidence: 99%