Why are children infected, but not affected, by Covid19 – the fetal hemoglobin hypothesis (and melatonin?)

(Aug 2020: I dont think this fetal hemoglobin hypothesis is correct anymore – a better explanation is the thymus.)

One of surprising (and blessed features) of Covid19 is that children are infected, but not affected. I cite three papers…

1. “The numbers of children with COVID‐19 pneumonia infection are small…Symptoms are mainly mild or even asymptomatic, which allow children to be a risk factor for transmission”
2. “patients younger than 18 years old; 1,118 cases, 2.2% were severe and 1.2% were critical, 1 death”
3. 10 children – “empirical” lesser symptoms in 5 children who were given antibiotics compared to those who were not.
4. “In children “2+ weeks in respiratory swabs & up to 1 month in stool!”
5. “No infections were detected in either survey in 234 tested children ranging from 0 to 10 years“

The hypothesis is this:“Fetal hemoglobin that binds oxygen more strongly than adult hemoglobin”…

Alpha-feto protein is another angle.

…saves children (and sickle-cell patients where it persists longer) from heme-binding (O2 sequestering) proteins of anaerobic bacteria (Prevotella, et al), which can also break down hemoglobin.

This derives from the hypothesis of battle of oxygen between anaerobic, O2 hating bacteria – and us.

The type of hemoglobin changes through our life cycle. HbF (fetal hemoglobin) is predominant in a new-born, and comes down within a year to our adult life percentage (less than 1%)

But, not always…

“The degree of HbF persistence varies greatly between adult individuals and this variability is largely genetically controlled”

Substantiated by data from metagenomes.

Interestingly, no heme binding protein was found in 5 patients in their early stage – indicating the bacteria turns on expression sensing something as the disease progresses – maybe oxygen?

Also, why is #Covid19 low in malaria endemic regions?

There are many possibilities (one of that is the newly proposed CD147 entry protein – which is the same in malaria). But also that fetal hemoglobin is high in people with sickle-cell sickness

If fetal hemoglobin falls to 1% by 1 year, why are elder children also safe?

The change from fetal to adult hemoglobin is epigenetic, guided by the BCL11a gene. Its reversible. I believe thats what might be happening, with age it gets more and more fixed.

Added the melatonin to this – based on suggestion on twitter.