Month: April 2022

A group from Department of Laboratory Medicine, University of California, San Francisco, CA, USA. etc. has reported that Gal-9 enhanced SARS-CoV-2 infection.
https://pubmed.ncbi.nlm.nih.gov/35378763/

It was found that Gal-9 enhances SARS-CoV-2 replication in human airway epithelial cells (AECs), mediated by facilitating cellular entry in an ACE2-dependent manner, by enhancing the attachment of SARS-CoV-2 virions to the cell surface by bridging the pathogen surface and receptors on host tissues in a glycosylation-dependent manner.

Clinically speaking, small molecules and anti-Gal-9 monoclonal antibodies (e.g. LYT-200) that antagonize Gal-9 activity may have utility in COVID-19.

A group from Department of Microbiology, Boston University School of Medicine, Boston, MA, USA, etc. has reported CD169/Siglec-1, a myeloid cell specific I-type lectin, facilitated ACE2-independent SARS-CoV-2 fusion and entry in macrophages.
https://pubmed.ncbi.nlm.nih.gov/35378756/

Circulating monocytes, macrophages, and tissue-resident alveolar macrophages are not known to express ACE2, infection receptor of SARS-CoV-2. These cells have been shown to express low levels of TMPRSS2, and moderate levels of endosomal cathepsins which are necessary proteases for SARS-CoV-2 infection. CD169/Siglec-1 (I-type lectin) is highly expressed by splenic red pulp and perifollicular macrophages, subcapsular sinus macrophages and alveolar macrophages. It is also known that CD169/Siglec-1 expression can be upregulated on peripheral blood monocytes under inflammatory conditions, especially in response to type I interferons (IFNs).

In this study, it was examined the mechanisms by which macrophages potentially contribute to inflammation during SARS-CoV-2 infection, using two different human macrophage models, PMA-differentiated THP1 cells (THP1/PMA) and primary monocyte-derived macrophages (MDMs) expressing a myeloid cell-specific receptor, CD169/Siglec-1, in the presence or absence of ACE2.

Pre-treatment with antibodies targeting SARS-CoV-2 S NTD and inhibition of endosomal cathepsins by E64D markedly attenuated S-pseudotyped lentiviral infection in CD169⁺ macrophages, but a TMPRSS2 inhibitor (Camostat) had no effect, suggesting that SARS-CoV-2 S facilitates endosomal viral entry into ACE2-deficient monocyte-derived macrophages (MDMs).
Also, THP1 cells expressing CD169 displayed robust SARS-CoV-2 S binding comparable to levels observed with THP1/ACE2 cells.

Interestingly, CD169-expressing THP1/PMA cells showed low levels of virus dsRNA production that did not significantly increase over the course of infection. However, significant expression of pro-inflammatory cytokines, IL-6, TNFα, IL-1β, and IL-18, was induced in infected CD169⁺ THP1/PMA macrophages compared to the parental THP1/PMA cells, indicating that early viral RNA production is the key trigger of innate immune activation, in other words, SARS-CoV-2 infection of macrophages could induce pro-inflammatory responses finally resulting in cytokine storms.

A group from Department of Chemistry, University of California, Davis, Davis, CA, USA, etc. has reported that the binding of SARS-CoV-2 to the cell membrane is primarily mediated by sialylated glycans with α-(2,6)-sialic acids on the termini positions.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8964299/

It was tested whether the Human milk oligosaccharides (HMOs) could block the RBD of SARS-CoV-2 by preincubating the RBD and the HMOs before introduction to HepG2 cells. Fluorescently labelled RBD was preincubated with 2′-FL, LNnT and 6′-SL separately, then allowed to interact with host cells HepG2. Quantitation of fluorescent signal intensity showed that HMOs blocked binding of RBD to cells presumably reflecting the behavior of the intact virus. The RBD was blocked only slightly by 2′FL (not statistically significant), more by LNnT (significant), and the most by 6′SL . Comparison of LNnT and 6′SL showed that latter one is more effective (significant).

The data suggest that HMOs can potentially function as “decoys” to affect SARS-CoV-2 adherence.

A group from Key Laboratory of Plant Immunity, Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China, etc. has reported that wheat straw return affects rhizo-microbiome.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8951542/

Wheat straw return (WSR), i.e., wheat stalk, was crushed into pieces and added directly to the soil surface in a Wheat–Soybean Rotation System. Little is known about how WSR affects crop-root-associated microbiomes, which are more intimately linked to plant health than field soil.

In this report, there was no significant changes in relative abundance of bacterial genera with WSR, however, it was not true in fungal genera, interestingly.
In detail, the relative abundance of some plant pathogen-associated fungal genera, e.g., Fusarium, and Alternaria, decreased after WSR, while the relative abundance of Acremonium, Mycosphaerella, Pyrenochaetopsis, Pyrenophora, Trichoderma, and Phaeosphaeria increased. These latter fungal genera are known to be associated with cellulose degrading activity.

Where, “U” and “D” mean that the relative abundance significantly increased and decreased, respectively. Rhizosphere (soil close to the root surface (RS)), rhizoplane (root surface (RP)), and endosphere (root interior (ES)).