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Table 1 Impact of viral infection in HSCs

From: Spotlight on the impact of viral infections on Hematopoietic Stem Cells (HSCs) with a focus on COVID-19 effects

Viral infection

viral infection effect on HSCs

Ref

VSV

Long-term HSCs show increased expression of the IL-10 receptor after infection with VSV. The anti-inflammatory cytokine human cytokine synthesis inhibitory factor (CSIF; also known as IL-10) may reduce immunopathology while simultaneously boosting HSC self-renewal

[46]

MCMV

It was shown that the BM expressed MCMV-specific IL-12(p40), IL-10, CCL-2, -3, and -4. Consequently, even in the absence of an effective IFNAR route, these mediators may confer long-term-HSCs function by direct activation or indirectly through immune cell attraction and immigration

[46]

HIV

When the TCR gene is delivered into HSCs via a Lentiviral vector, the HSCs differentiate into a large number of CD8 + T cells with the ability to recognize and kill HIV antigen cells

[81]

CRISPR/ Cas9 gene editing methods are used in human CD34 HSPCs and attained effective CCR5 ablation for the treatment of HIV infection

[83]

T cells derived from transduced HPSC may be inhibited in their ability to proliferate HIV by using RevM10

EVE

EVD

The NSG-A2 mice, which were genetically modified to include human HSCs, generated the essential cell components for a fully functional adaptive human immune response. These mice exhibited pathogenesis typical of Ebola virus infection, including viremia, cell and organ destruction, and a high degree of time sensitivity

[47]

LCM

The loss of HPSCs and HSCs, as measured by phenotypic, is one of the most significant negative changes in the BM stroma. Additionally, LCMV infection has a long-lasting effect on the surviving HSCs, impairing their capacity to displace other cells

[48]

SARS-CoV-2

Evidence suggested that Ang II was responsible for controlling CD115 in HSCs. Reducing the deleterious impact induced by Ang II has on SARS-CoV-2 infection

[75]

Pathological stimuli of the Nlrp3 inflammasome could produce cytokine storm and pyroptosis in HSCs, and the SARS-CoV-2 may infect a pool of HSPCs independently and directly

[63, 64]

Infected cells generated by planting SARS-CoV-2 in rat kidney cells and Vero cells showed a decline in infection after 24 to 72 h, regardless of the initial infection dose

[65]

HSCs and myeloid progenitors may be stimulated by β-glucan

[66]