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In the new coronavirus (COVID-19), there is a large amount of macrophages in the bronchoalveolar lavage fluid, suggesting that macrophages are greatly involved in the severity. Macrophages are not just phagocytes, they have many subsets, and each has its own functions.

The following group has reported that transcription factors (MAFB and MAF) in macrophages are significantly related to the progression of COVID-19.

https://www.frontiersin.org/articles/10.3389/fimmu.2020.603507/full

MAFB, a transcription factor, promotes a subset of pathogenic pro-fibrotic SPP1+ macrophages, while transcription factor MAF has the function of suppressing inflammatory FCN1+ macrophage subsets. When COVID-19 becomes more severe, the MAFB/MAF ratio increases. In other words, subsets of macrophages are controlled in a direction that accelerates inflammation of lung tissue and simultaneously accelerates fibrosis.
Therefore, they have concluded that it might be effective to silence MAFB and induce overexpression of MAF when treating COVID-19.

The blog management is not a medical doctor, but the following case report may be useful if you infected with the novel coronavirus (COVID-19) and become severe.
https://www.sciencedirect.com/science/article/pii/S2213007120305323?via%3Dihub

In general, steroids are commonly used to reduce inflammation, but long-term use has significant side effects and slows the elimination of the virus in COVID-19.
However, in the late phase of covid-19, there were four cases in which MP (methyl-prednisolone) was highly effective when its pulse therapy was performed at high concentrations for a short period of time (1000 mg, 3 days).
All have recovered and have been discharged from hospital.

It may be good to tell your family.

HIV is a virus with envelope proteins in the same way as SARS-CoV-2, and there have been numerous studies on the structure and glycan modification of that protein. The envelope protein of HIV is called gp160 and is made up of two sub-units, gp41 and gp120. HIV infection is initiated by gp120 binding to CD4 receptors on T cells. Gp120 has 27 N-type glycan modification sites and is known to be strongly glycosylated with high mannose.

A group of Univ. of Alabama at Birmingham has reported about the effects of gp120 glycosylation on infectivity and neutralizing antibodies.
https://pubmed.ncbi.nlm.nih.gov/33205023/

As a result, it was confirmed that the infectivity increased by 7 to 9 times when there was N262 glycan modification.
In addition, it was found that N262 glycan modification reduces the neutralization capacity of HIV neutralizing antibodies.
In particular, PGT151, 35022, 2G12, VRC24, PG16, and PGT145 showed a significant decrease in the capacity.

In this paper, they have discussed possible mechanisms behind these changes using molecular dynamics models.

There is a noteworthy paper on the origin of the novel coronavirus (SARS-CoV-2).
https://zenodo.org/record/4073131?fbclid=IwAR2VprdWCGzl8NlNpzWPz0QudcBRHZ0dnPPCZNz8Yg2oGfleP1_ZxoipzEI

The central points of the discussion are:

RaTG13 (96.2%) hosted by horseshoe bat and MP789 (90.1%) hosted by pangolin are close to SARS-CoV-2.
But,

1. Syn/non-syn ratio of spontaneous gene mutations must not fluctuate significantly across the entire region of the S protein, whereas SARS-CoV-2 vs RaTG13 fluctuates over an order of magnitude.
2. The amino acid sequences in the receptor binding domain (RBD) of S proteins should best bind to the host’s infected receptors, but RaTG13 and pangolin coronavirus do not bind much to ACE2 of their hosts, horseshoe bat or pangolin.
3. The E protein of ZC45, ZXC21, which is coronavirus in bats, is the same as 100% SARS-CoV-2 and could be the backbone of the SARS-CoV-2 gene sequence.
4. How the furin-cleavage site inserted at the junction of the S1/S2 region could not be rationally explained from a view point of viral evolution.

When I start reading this paper, I’m drawn in as if I were reading a detective story.
And finally, you will be convinced that the new coronavirus (SARS-CoV-2) could be an artificial product.

By all means, I recommend you to read it.

It is well known that covid-19 is prone to develop severe diseases in the elderly and underlying diseases (such as diabetes, cerebrovascular diseases and hypertension etc.).
There are various discussions about the difference between the elderly and the young, such as that young people have stronger innate immunity, and in the elderly, the balance between innate and acquired immunity is broken.

The following group believes that why COVID-19 becomes severe in the elderly would be related to the presence or absence of T-cell cross-reactions specific to conventional human coronaviruses (strains such as HCoVs: NL63, OC43).
https://www.nature.com/articles/s41598-020-78506-9

From this study, it was confirmed that T-cell immunity induced by human α-HCoV (NL63) and β-HCoV (OC43) was present in young adults, but virtually not in the elderly, and the frequency of cross-reactive T-cells directed to novel coronavirus (SARS-CoV-2) was minimal in most elderly. Indeed, it is likely to be related to the severity of the elderly.

Difference in IFN-γ response,
<10 (black), 10–30= (dark gray), 30–100 (green), 100–200 (light gray), >200 (Orange) SFU/10^6 PBMC.

It is well known that when the new coronavirus (COVID-19) becomes severe, it causes acute respiratory prompt syndrome and multiple organ failure, resulting in cytokine storms.
To mitigate lung inflammation, the use of inhibitors against certain cytokines, such as IL-6 and GM-CSF, is limited. This is because there are many signaling molecules and pathways are involved in the triggering of cytokine storms.
Therefore, the following group focused on inhibitors of DNA Topoisomerase-1 in order to inhibit the transcription process of genes induced by viral infection “in one go”
https://pubmed.ncbi.nlm.nih.gov/33299999/

Topoisomerase-1 is a necessary enzyme to unwind DNA double helix.
In vivo experiments using hamsters, it was shown that genes expressed high by viral infection were down regulated by the Topoisomerase-1 inhibitor, and thereby SARS-CoV-2-induced lung
inflammation was suppressed.

It is well known that changes in the expression of mucin-type O-glycans can be seen in the initiation, progression, and metastasis of cancers.
A group of AIST has reported a study on the relationship between clinicopathology and O-glycans in pancreatic ductal adenocarcinoma.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0242851

In pancreatic ductal adenocarcinoma, Tn-antigen and sialyl-LewisX antigen are highly expressed.
However, there was no correlation between these expression levels and disease-free survival (DFS).
Interestingly, however, there was a clear correlation between β3Gn-6T glycosyltransferase and DFS, indicating that higher expression of β3Gn-6T resulted in longer DFS.
The β3Gn-6T glycosyltransferase is a necessary enzyme for the synthesis of Core3 O-glycans.

At this stage, the mechanism of why the Core3 structure and its extended structure increase DFS is not known.
Let’s look forward to the progress of research in the future.  That may lead to the outcome of breaking down the general concern that “Glycan is just a physiological expression of disease state”, .