Donor-type aplasia after stem cell transplantation in aplastic anaemia

Ghosh, Kanjaksha

doi:10.4103/jpgm.jpgm_64_21

Journal of Postgraduate Medicine

2021

DOI: 10.4103/jpgm.jpgm_64_21

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Donor-type aplasia after stem cell transplantation in aplastic anaemia

Kanjaksha Ghosh

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2022

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Human Cytomegalovirus Infection of Epithelial Cells Increases SARS-CoV-2 Superinfection by Upregulating the ACE2 Receptor

Greenwood

Crozier

Elder

et al. 2022

The Journal of Infectious Diseases

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SARS-CoV-2, the causative agent of COVID-19, has caused widespread morbidity and mortality since its onset in late 2019. Here, we demonstrate that prior infection with human cytomegalovirus (HCMV) substantially increases infection with SARS-CoV-2 in vitro. HCMV is a common herpesvirus carried by 40-100% of the population which can reactivate in the lung under inflammatory conditions, such as those resulting from SARS-CoV-2 infection. We show in both endothelial and epithelial cell types that HCMV infection upregulates ACE2, the SARS-CoV-2 cell entry receptor. These observations suggest that HCMV reactivation events in the lung of healthy HCMV carriers could exacerbate SARS-CoV-2 infection and subsequent COVID-19 symptoms. This effect could contribute to the disparity of disease severity seen in ethnic minorities and those with lower socio-economic status, due to their higher CMV seroprevalence. Our results warrant further clinical investigation as to whether HCMV infection influences the pathogenesis of SARS-CoV-2.

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Human Cytomegalovirus Infection of Epithelial Cells Increases SARS-CoV-2 Superinfection by Upregulating the ACE2 Receptor

Greenwood

Crozier

Elder

et al. 2022

The Journal of Infectious Diseases

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show abstract

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Donor-type aplasia after stem cell transplantation in aplastic anaemia

Cited by 1 publication

References 7 publications

Human Cytomegalovirus Infection of Epithelial Cells Increases SARS-CoV-2 Superinfection by Upregulating the ACE2 Receptor

Human Cytomegalovirus Infection of Epithelial Cells Increases SARS-CoV-2 Superinfection by Upregulating the ACE2 Receptor

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