Covid19, bats, birds and mitochondria

As an avowed mitochondriac I see the little organelle’s hand in a lot of pies and so may it be for Coronavirus in particular and viruses in general.

A relationship between mitochondrial performance and Corvid susceptibility is a real possibility. Below are the facts that present themselves for the ‘joining of the dots’ as one might say.

Birds, swallows and crows are reservoirs for influenza viruses as bats are for coronaviruses. None are hosts to these viruses specifically as they live happily enough with a wide range of viruses and normally show no symptoms of illness from any of them.

In recent years the mystery of just why these creatures can tolerate high viral loads and only occasionally shed them is being unravelled. They appear under normal conditions only to mount a mild immune response to these infections but under stress (food shortage, reproduction, habitat loss) they can become unwell and shed the viruses. All of the above is well known as is the ability for these viruses to jump across species into humans when they are being shed.

The ‘dots’ I would like to join would be to link known human susceptibilities to Coronavirus in particular and to the bat or bird host’s biochemistry.

Human susceptibility to Coronavirus increases with age. This is the number one vulnerability followed by diabetes and obesity. All three conditions are characterised by chronic inflammation. Indeed ageing can be described as an inflammatory disease. Hence there has been for years intense interest in both anti-inflammatory drugs and in anti-oxidant foodstuffs since these purport to mitigate the effects of pro-inflammatory ‘free-radicals’ within the cell.

Within a cell the chief source of free-radicals is the mitochondria and the cell takes great steps to mitigate their damage by capturing the radicals and rendering them harmless using extremely abundant and fast acting enzymes as well as simple chemicals. Even so, the damage is substantial and repair of proteins and DNA is ongoing throughout life. With age, poorly functioning mitochondria, degenerating back up systems and repair failures tip the balance towards inflammation.

The mitochondria in birds and bats are radically different to those in man and mice. Size for size, and despite having ultra-energetic lifestyles ( flying ) birds and bats have very long lives. Pigeons live for 20+ years, Parrots 100+.  A tiny bat can live for 40 years; the Pipistrel bat more than 15 years. Compare this with 2 years for a mouse and 40 for a human ( in the wild condition not modern medicalised society).

Why? Simply they have much better mitochondria. Bat and avian mitochondria produce far fewer free radicals, they are simply better built and place lower oxidative stress on their cell host. Early in life, when the bats start flying,  weaker mitochondria are apparently weeded out and only the smaller better ones reproduce within the cell. Eventually their mitochondria populations are much ‘fitter’ than for animals that don’t fly.

Conversely, for mammals that don’t do very much at all, (maybe think modern sedentary worker) there is no pressure to select for the best, after all, demands such as flying will not be made.

The key here is to see mitochondria within an organism as a reproducing population subject to evolutionary selective pressures within a cell, in the same way as this would apply to free living organisms in the outside environment. They can all be nearly as good as their best or exist in populations able to tolerate less than perfect versions.

Another fact to add to the mix is that mitochondria are not sugar-eaters (saccharophiles) so much so that cancer cells which survive almost exclusively on sugar effectively inhibit mitochondrial replication. Diabetic and pre-diabetic conditions are associated with mitochondria-unfriendly high sugar levels.

Another clue that mitochondria are figuring in the Covid context is reported extreme sarcopena ( muscle wastage)  for those on ventilators with Covid19. This is a sure sign of mitochondrial-mediated apoptosis ( cell death) of muscle cells. Sarcopena from middle age is ‘waiting to happen’ depending on how much activity is being demanded of the muscles.

It follows that amongst the old, the diabetic and the obese it is highly likely that their mitochondria are as un-bat-like as they can be.

So regarding Coronavirus human vulnerability, it tracks mitochondrial capacity in a way that feels more than coincidental. Conversely, human ‘invulnerability’ is associated with the youngest most active population which will naturally have the ‘best’ mitochondria.

In conclusion joining the dots is not the same as providing an explanation but there feels like there is a link between mitochondrial well being and viral tolerance. Just what it is is unknown but I’m off to the gym to practise flying and am keeping off the sugar.