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A group from University of California, San Francisco has reported effects of B.1.427/B.1.429 SARS-CoV-2 variants onto infectivity and neutralization.
https://pubmed.ncbi.nlm.nih.gov/33991487/

Famous SARS-CoV-2 variants are B.1.1.7(originally detected in UK), B.1.351(South Africa), and P.1(Brazil) variants. The B.1.1.7 variant is characterized by N501Y mutation, and the B.1.351 and P.1 carry E484K, K417N/K417T in addition to N501Y mutations.
B.1.427/B.1.429 variants appeared in California from September, 2020 are characterized by S13I, W152C, L452R mutations in the spike protein coding domain, and L452R is in RBD.

These variants showed 18.6%–24% increased transmissibility relative to wild-type circulating strains, and antibody neutralization assays revealed 4.0- to 6.7-fold decrease in neutralizing titer from convalescent patients and 2.0-fold decreases in neutralizing titers from vaccine recipients, respectively

The reason of this change could be due to structural changes in the RBD which are caused by formation of a hydrophobic patch on the surface of spike RBD by L452 together with F490 and L492.

A group from Juntendo University School of Medicine, etc. has found a unique glycosylation pattern in relapse-prone breast cancer comparing with non-relapsed cancer with using lectin microarrays.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0250747

Breast cancer is one of the most common malignant tumors among women. Triple-negative breast cancer (TNBC) is a relapse-prone breast cancer subset that accounts for about 15–20% of all breast cancers and is defined by tumors lacking estrogen receptor expression, progesterone receptor expression, and increased expression of human epidermal growth factor receptor-2 (HER2). An adjuvant therapy, cytotoxic chemotherapy is the only available treatment option for TNBC patients, because they do not respond to hormone or anti-HER2 treatment.

Authors found that TJA-II, which has binding specificity to Fucα1-2Gal and/or β-GalNAc glycans, shows higher intensity in cell extracts from surgical specimens of relapsed TNBC patients than in non-relapsed patients, and histochemical TJA-II staining of adjacent sections confirmed this difference. Since two more lectins, WFA and BLP, showed similar tendency to TJA-II, some glycoproteins having β-linked terminal GalNAc are to be in the background of this finding. The next stage is definitely to find out new target molecules for the effective therapy of the relapse-prone TNBC subset.

A group from Vrije Universiteit Amsterdam, Netherlands has studied alterations in the dendritic cells (DCs) signal paths after α2-3Sia binding.
https://www.frontiersin.org/articles/10.3389/fimmu.2021.673454/full

DCs possess the extraordinary capacity to recognize various pathogens with its pattern recognition receptors (PPRs) and present those antigens with MHC to tell the information to T-cells.
Sialic acids are increasingly attracting attention with their role in the immune regulation of cancer. During cancer progression, tumor cells often highly increase their sialic acid expression to create an immunosuppressive tumor microenvironment. Sialic acids are also advantageous for pathogens to evade from immune attacks. Bacteria obtain sialic acids by de novo synthesis or from an environmental source, and thereby can hide and escape from immune surveillance.

Authors analyzed alterations in the DC phosphoproteins, Kinase signatures, and JAK-STAT signaling pathway due to α2-3Sia stimulation in the presence of Lipopolysaccharide (LPS). LPS is often used as a model antigen (as an endotoxin) to activate immunity.

Overview of the result was summarized as follows.
Phosphorylation was enhanced upon α2-3Sia stimulation, while simultaneous α2-3sia and LPS stimulation resulted in less phosphorylation, indicating that recognition of a2-3Sia by DC alters TLR 4 triggering and DC signaling. α2-3Sia stimulated DCs compared to control with simultaneous α2-3sia and LPS stimulation showed decreased scoring of kinases ERK, AKT1, PKCB, GSK3, PKCD, PAK1, PKA, GSK3, GRK, IκB, and RAF1, and those affected kinase signatures were involved in the chemokine signal pathway. α2-3sia stimulation affected the JAK-STAT signaling by lowering the phosphorylation status of STAT3 and STAT5A.

Although the things are so complicated, these changes result in downregulation of IL-12 (inflammatory cytokine) pathway and inversely upregulation of IL-10 (anti-inflammatory cytokine) pathway, leading allover features to the direction of suppressing inflammation.
 

A group from IRCCS Azienda Ospedaliero-Universitaria di Bologna, Italy has reported on differences in lung microbiome between COVID-19 patients and COVID-19 negative persons.
https://www.nature.com/articles/s41598-021-89516-6

Several indexes have been developed to discuss about similarity among groups and characteristics of each group.
Similarity Percentage analysis highlighted that the lung microbiome of COVID-19 patients was characterized by a higher relative abundance of Pseudomonas spp. compared to COVID-19-negative persons. On the other hand, the lung microbiome of COVID-19-negative persons was mainly characterized by the enrichment of lung commensal bacteria (such as Haemophilus influenzae, Veillonella dispar, Granulicatella spp., Porphyromonas spp., and Streptococcus spp).

The linear discriminant analysis (LDA) highlighted that the lung microbiome of COVID-19 patients was characterized by the presence of Pseudomonas alcaligenes, Sphingobacterium spp., Clostridium hiranonis, Acinetobacter schindleri, Enterobacteriaceae of unknown genus and Acinetobacter spp.

A common feature between these two analysis indexes was Pseudimonas spp. This means that enrichment of opportunistic gram-negative pathogens frequently associated with multidrug resistance increase in COVID-19 patients and the lung commensal bacteria decrease inversely.

A group from Hokkaido University, etc. has reported on changes in the expression levels of ACE2 and TMPRSS2 with agonists for Toll-like receptors (TLRs) and with Fluticasone Propionate (FP)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8107375/

It is said that SARS-CoV-2 cell entry depends on two proteins present on the surface of host cells, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). Authors has investigated effects of activation of innate immune signal path onto the expression levels of ACE2 and TMPRSS2, and also if there is any effect of FP administration on that.

As sample cells, primary human nasal epithelial cells (HNECs) were collected from the nasal mucosa. HNECs were stimulated by Poly(I:C), which is a double-stranded RNA (dsRNA) often used as a agonist for TLRs in a model of viral infection.

ACE2 and TMPRSS2 protein expression levels were evaluated by using immunofluorescent analysis. The ACE2 intensity in HNECs was significantly promoted by Poly(I:C) (a 2.884±0.505-fold change vs. untreated cells, p=0.003), but there were no significate changes in the TMPRSS2 expression levels. And, this Poly(I:C)-induced change in ACE2 was significantly suppressed by FP (a 0.405±0.312-fold change vs. Poly(I:C)-treated cells, p=0.044).

Further studies are required to evaluate whether FP suppresses SARS-CoV-2 viral cell entry in vivo.

A group from Stanford University School of Medicine, etc. has reported about passive immunity of infants born to mothers infected with SARS-CoV-2.
https://pubmed.ncbi.nlm.nih.gov/33972953/

An important aspect of immunity against infectious pathogens in young infants relies on effective maternal antibody production, transfer of maternal antibodies across the placenta to the fetus, and persistence of passive immunity in the infant. Authors have investigated SARS-CoV-2 antibody transplacental transfer ratios with respect to the timing of maternal infection during gestation, antibody response to SARS-CoV-2 infection in the newborns, and persistence of passively- and actively-acquired SARS-CoV-2 antibodies in infants.

The study enrolled 145 mothers with SARS-CoV-2 infection and 147 of their infants. There was a significant positive correlation between IgG levels in the 125 paired maternal and cord blood samples (Rs=0.93, p<0·0001). Transplacental IgG transfer ratios were calculated in 77 IgG positive mother-infant dyads, and the median transfer ratio was 1.0 (95% CI 0.86-1.09). The transfer ratio was significantly higher in the mothers who were severe-critically symptomatic (n=4) compared to mothers who were asymptomatic (n=23) (1.6 vs. 1.0, p=0.003) or mild-moderately symptomatic (n=50) (1.6 vs. 0.9, p=0.002). The transfer ratios based on time elapsed from the first maternal positive PCR to delivery were 0.6 (<60 days, n=22), 1.2 (60-180 days, n=27), and 0.9 (>180 days, n=5). These studies demonstrate that cross-placental SARS-CoV-2 IgG transfer occurs throughout gestation, and a higher transfer efficiency is achieved when infection onset is more than two months prior to delivery. These findings have important implications in determining optimal timing of vaccination in pregnant mothers and infants.