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. 2021 Apr 16:12:614522.
doi: 10.3389/fmicb.2021.614522. eCollection 2021.

Interrogating the Impact of Intestinal Parasite-Microbiome on Pathogenesis of COVID-19 in Sub-Saharan Africa

Affiliations

Interrogating the Impact of Intestinal Parasite-Microbiome on Pathogenesis of COVID-19 in Sub-Saharan Africa

Dawit Wolday et al. Front Microbiol. .
No abstract available

Keywords: COVID-19; SARS-CoV-2; helminths; hyperinflammation; microbiome; parasites; pathogenesis; protozoa.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer SB declared a past co-authorship with the author DW to the handling editor.

Figures

Figure 1
Figure 1
Impact of parasite-driven microbiome diversity and composition on COVID-19 severity. Certain protozoa, such as commensal Entamoeba spp. and cryptosporidium spp. and helminths that enrich the gut with the so called beneficial microbiome profile and with dominant TH2 and Treg pre-existing condition, might mute hyperactive immune response upon infection with SARS-CoV-2. In this milieu, SARS-CoV-2 replication is controlled. Another possibility is that TH2 and Treg responses might suppress anti-SARS-CoV-2 immunity and thereby hasten COVID-19 severity. On the contrary, gut dysbiosis as a result of some pathogenic protozoa, such as Entamoeba histolytica or helminths, or patients without parasite coinfection with underlying preexisting THl immune response might facilitate cytokine storm and aggravate COVID-19 severity. In patients with gut dysbiosis, SARS-CoV-2 replication is significantly increased. AAM/M2 Mø, alternatively-activated macrophages; Breg, regulatory B cell; ES, Excretory/Secretory parasite product; IFN, interferon; IL, interleukin; IP, interferon-γ-inducible protein; MCP, monocyte chemoattractant protein; MIP, macrophage inhibitory protein; Mø, macrophage; RBC, red blood cells; TH, T helper lymphocytes; TGF, transformation growth factor; TNF, tumor necrosis factor; Treg, regulatory T cell.

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