New Updates: why-covid-19-is-hitting-men-harder

Coronavirus: Why Men are More Vulnerable to Covid-19

male vs female:

sex difference in covid-19

For the past year, it has been proven that females are a lot stronger in combating SARS-CoV2, causing fewer deaths than males. The severity is also seen higher in men for the hepatitis C virus.

Scientists opinion that there are cellular and genetic distinctions between males and females.

  • Cells specialized in the innate immune system respond faster in females upon stimulations by viruses. These cells bind to affected cells and stimulate more significant production of antiviral signals.
  • Neutrophils from women are more responsive to interferon signals. The concentration of sex hormones attributed some difference. For example, the hormone estrogen (more in female) reduces the susceptibility to viral infections. In addition, the neutrophils exposed to estradiol has matured phenotypes and responded better to interferon stimulation.
  • Females showed upregulation of genes involved in immune response. Females with two X chromosomes produce more TLR7 than men with single X chromosome. This is because the TLR7 gene escapes the silencing of X-linked genes.
  • Plasmacytoid dendritic cells expressing TLR7 are more in women than men. Toll-like receptor 7 (TLR7) detects single-strand RNA in cytoplasm, which raises the siren announcing that the virus entered the cells.

The heightened immune response is a double-edged sword; 80% of all autoimmune disease patients are women. The diseases which involve immune system interaction progress faster in females – as we see in AIDS. Increased T-cell activation and TLR7 signaling accounted for the critical difference.

Reference:

https://www.the-scientist.com/features/sex-differences-in-immune-responses-to-viral-infection-68466

COVID strain Greek

World health organization's New Naming for COVID19

Mind the name of the Strain

The  SARS-CoV-2 variants are evolving with mutations that escape immune cells easily. The scientific (variant names) terminologies being used are difficult to remember – the strains are being called based on their geographical origin.

I hope most of you are wondering how these difficult names are being popped up in the first place. It is through software. The process is to upload the fasta file (genomic sequence), and the software using an algorithm assign the name based on phylogeny – know more about the dynamic nomenclature details reading this article

https://www.biorxiv.org/content/10.1101/2020.04.17.046086v1

To avoid confusion of using complex variants names and quell the geographical stigmas, the WHO adviced to use the Greek alphabets for policymakers, the general public, and non-experts who had difficulty identifying variant names. Some of the variants which are of concern are below:

Label

Lineage

Documented samples

Alpha

B.1.1.7

UK

Beta

B.1.351

South Africa

Gamma

P.1

Brazil

Delta

B.1.617.2

India

Reference: https://www.nature.com/articles/d41586-021-01483-0

https://pangolin.cog-uk.io/

https://www.gisaid.org/hcov19-variants/

Hallmarks of Sever COVID-19:

The inflammatory state of COVID patients are measured through C-reactive proteins (Inflammatory marker) and  D-Dimer, which measures the protein fragments that arise from blood clots. However, these markers can only give us the disease severity.

Researchers are on the verge of a breakthrough in identifying early biomarkers that can distinguish patients destined to develop the critical disease.

Below are few markers which are validated in clinical subjects:

  • IL-6, IL-8, and TNF-α cytokines: Validated in clinical samples
  • IL-10 and IP-10: Requires validation in larger groups

Reference: https://www.the-scientist.com/news-opinion/the-immune-hallmarks-of-severe-covid-19-67937

Hallmarks of COVID

Is gut leakage a reason for Multisystem-inflammatory syndrome in Children?

The reasons for multisystem inflammatory syndrome in children are still uncertain. Children’s stool samples showed the presence of viral RNA after weeks of SARS-CoV2 infection. Researchers are trying to find how the viral particles in the gut make their way into the blood.

A load of viral RNA, antigens, and markers of leaky gut increased in children, suggesting that trafficking of spike proteins through the leaky gut into the bloodstream could cause the multisystem inflammatory syndrome.

The researchers identified higher levels of Zonulin in MIS-C kids than in normal kids. Zonulin is a protein implicated in celiac disease, associated with increased permeability of the gut. Encouraged with the above finding, the blockers of Zonulin (larazotide) in 17 months old MIS-C patient with complex medical history. The patient responded positively, with decreased symptoms of MIS-C and plasma spike antigen levels. Larazotide is phase 3 clinical trial and found to be safe to treat celiac disease.

The clinicians are testing the similar treatment in four other patients after approval of FDA for compassionate use. The findings look promising, but without placebo control, it isn’t easy to interpret the efficacy.

Reference: https://www.the-scientist.com/news-opinion/sars-cov-2-antigens-leaking-from-gut-to-blood-might-trigger-mis-c-68845

Multisystem-inflammatory syndrome in Children
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