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A group from University of Liverpool has reported results of random forests model (one of machine learning methods) to predict the animal host of SARS-CoV-2.
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009149

A figure below shows stacked bar plots of predicted probabilities of each host category for coronavirus RNA sequences, assuming bird, camelid, carnivore, human, rodent, swine, yangochiroptera, and yinpterochiroptera as potential hosts. It is clearly shown that MARS-CoV has camelid host, SARS-CoV has carnivore host, and SARS-CoV2 seems to have a bat host (suborder Yinpterochiroptera). While the random forests model supports bats as the ultimate origin of SARS-CoV-2, the involvement of intermediate hosts remains unclear.

A group from Rowan University, Stratford, USA, etc. has suggested that Maackia amurensis lectin (MAL, MAA, MASL as abbreviated names) could be effctive in inhibiting SARS-CoV-2 infection.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019238/

Oral squamous cells were used as a model cell in this study. Transcriptome analysis was done to investigate effects of MAL onto ACE2, ADAM17, Furin, and Glycosyltransferases (GalNAc-T, ST6GalNAc-1, and ST6GalNAc-2）.
Interestingly, it was shown that those decreased in a MAL dose dependent manner. For instance, at a dose of 1925nM of MAL, ACE2 mRNA level decreased by 60％, ADAM17 by 40％, and ST6GalNAc-1 by 60%. As a result of these events, MAL decreases inflammatory signaling events that would otherwise lead to activation of the IL6 amplifier implicated in COVID-19 induced ARDS

MAL is known to have binding specificity to α2-3Sia.

A group from San Martino Policlinico Hospital, Genoa, Italy, etc. has reported on characteristics of bronchoalveolar lavage fluid (BALF) collected from COVID-19 patients.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8049078/

BALF cellularity was mainly composed of neutrophils and macrophages (neutrophils were more abundant than macrophages). The median value of macrophage percentages was higher in non-survivors compared to survivors (35% vs 20%). However, we must be cautious that all the differences shown in a table below are not statistically significant.

A group from Northwest University, Xi’an, China, etc. has reported a potential glycan biomarker for Esophageal squamous cell carcinoma (ESCC)
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https://www.frontiersin.org/articles/10.3389/fchem.2021.637730/full

Saliva was used as a sample in this study, and saliva was centrifuged to remove insoluble components and a protease inhibitor was added. Lectin microarrays using 37 lectins were used for investigating differences in glycosylation patterns between healthy volunteers (HV) and ESCC patients. As a result, it was found that DSA and ECA lectins are specific to ESCC, and Galβ1-4GlcNAc-containing N-glycans could be potential biomarkers for ESCC.

A group from University Göttingen, etc. has alarmed a possibility in reinfection of mutated SARS-CoV-2 in farmed mink to human.
https://pubmed.ncbi.nlm.nih.gov/33857422/

Transmission of SARS-CoV-2 from humans to farmed mink has been observed in Europe and USA. Substitution D614G, which is dominant in SARS-CoV-2 from humans, was also found in viruses from mink, and a mink-specific mutation Y453F (mutant D614G+Y453F) or Y453F in conjunction with H69Δ, H70Δ (mutant D614G+H69Δ/H70Δ/Y453F) were also found in mink. The Y453F mutation locates in RBD, and reduced inhibition by human serum samples tested. The neutralizing titer IC₅₀ increased by 1.62 times with this mutation, and the neutralizing titer of REGN10933, which is one component of a cocktail therapy (REGN-COV2), also increased with this mutation.

New emerging variants generated through transmission from humans to wild animals could represent a future threat to human health.

A group from Vector State Research Center of Virology and Biotechnology, etc. has investigated binding specificity of SARS-CoV-2 Spike protein to a various glycans with using ELISA assays.
SARS-CoV-2 Spike protein does not bind to sialic acid, unlike the case of influenza virus, but has affinity to a lactosamine family (Galβ1-3GlcNAc, Galβ1-4GlcNAc, etc.).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905424/ 

A group from Peking Union Medical College, etc. has reported on differences in SARS-CoV-2 infectivity between M1 macrophages and M2 macrophages including alveolar epithelial type II (AT2) cells.
https://www.nature.com/articles/s41421-021-00258-1

Generally speaking, M1 macrophages are inflammatory and M2 macrophages are anti-inflammatory. Comparing AT2, M1 macrophages, and M2 macrophages, SARS-CoV-2 infection and its replication was higher in macrophages than AT2, M1 macrophages took up SARS-CoV-w2 with higher efficiency than M2 macrophages, and the viral loads increased in an exponential fashion in M1 macrophages but in a flat fashion in M2 macrophages. It is considered that ACE2 could be the receptor that mediates the infection with SARS-CoV-2, and ACE2 has been reported to be expressed also by macrophages. However, there were no difference in the infectivity between ACE2-overexpressing macrophages and ACE2-knockeddown macrophages. So, virus takeup through phagocytosis could initiate SARS-CoBV-2 infection.
Authors related the difference in the infectivity between M1 and M2 to difference in cell softness, endosomal, and lysosomal pH.

A group from Niigata University, etc. has reported that Dectin-2 is related to Infection of Influenza virus and the induction of inflammatory responses.
https://www.jstage.jst.go.jp/article/biomedres/42/2/42_53/_pdf/-char/en

Although the importance of relationship between hemagglutinin (HA) and sialic acids has been emphasized, agents targeting HA and sialic acids are not effective in suppressing severe influenza unless they are administered within 48 h after symptoms begin. Antigen-presenting cells (APCs), such as dendritic cells (DCs) and macrophages, recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) of dead cells or damaged tissues, and activate inflammatory immune responses. Toll-like receptors (TLRs), Nod-like receptors (NLRs), and C-type lectin receptors (CLRs) are known as such pattern recognition receptors.

Since HA is strongly high mannosylated, there must be a signal path activating inflammatory immune responses through the interaction between C-type Lectins and glycosylated. C-type Lectin family includes DC-SIGN, Dectin-1, Dectin-2, Mincle, etc. Authors have found that Dectin-2 expressed on BM-DCs recognizes glycosylated HA from the type A and type B strains, and induce production of inflammatory cytokines. Dectin-2 recognized high mannose polysaccharides.
A figure below shows that production of inflammatory cytokines is greatly reduce by knocking out Dectin-2.