Indirectly. Pro inflammatory cytokines favour bone absorbing osteoclasts over osteoblasts, so the balance shifts over towards osteoporosis. This is another reason why long term low level inflammation (hold my beer) is not good for you.
Thanks Carp. I have a question, because I have a problem with this "asymptomatic infection" term. When the study states "These changes were observed even in mice with mild and asymptomatic infections.", does this mean that the mouse caught Covid through mucosal infection and went on to develop this bone issue while not showing any covid symptoms. OR, was the mouse injected with Covid? If the mouse was injected with Covid, then it stands to reason that the mouse would not be showing symptoms, but woudl still be suffering from the effects of the covid virus throught the parts of the body that received the injected virus. Also, when they inject the mouse is the dsed according to size in comparison to the dose that a human would generally pick up through normal infection?
Not being picky, just generally inquizative to the specifics.
Hi Rob. The non-control, ACE expressing TG mice were exposed to virus preparations intranasally at doses increasing in a logarthymic fashion from 10^3 for them to 10^4 to 10^5 PFU. They remained as active as the controls and putting weight normally on their limbs (ie no pain) yet their femur bones still sustained a bone loss of 25%! Their osteoclasts were still reabsorbing bone. The controls expressed no bone loss and the researchers ruled out inactivity as a cause.
Extrapolated to humans you would experience bone density loss without knowing it until you have a fall etc and fracture something. Or in kids they may have skeletal deformations, growth retardation or will be prone to fracture. Ugh.
So - did they determine the causative factor? Is this spike?
If spike, then can we expect to see this problem in the injected?
Inquiring bears would like to know. (it may be rhetorical)
Indirectly. Pro inflammatory cytokines favour bone absorbing osteoclasts over osteoblasts, so the balance shifts over towards osteoporosis. This is another reason why long term low level inflammation (hold my beer) is not good for you.
https://joe.bioscientifica.com/configurable/content/journals$002fjoe$002f201$002f3$002f309.xml?t:ac=journals%24002fjoe%24002f201%24002f3%24002f309.xml
Thanks Carp. I have a question, because I have a problem with this "asymptomatic infection" term. When the study states "These changes were observed even in mice with mild and asymptomatic infections.", does this mean that the mouse caught Covid through mucosal infection and went on to develop this bone issue while not showing any covid symptoms. OR, was the mouse injected with Covid? If the mouse was injected with Covid, then it stands to reason that the mouse would not be showing symptoms, but woudl still be suffering from the effects of the covid virus throught the parts of the body that received the injected virus. Also, when they inject the mouse is the dsed according to size in comparison to the dose that a human would generally pick up through normal infection?
Not being picky, just generally inquizative to the specifics.
Cheers
Hi Rob. The non-control, ACE expressing TG mice were exposed to virus preparations intranasally at doses increasing in a logarthymic fashion from 10^3 for them to 10^4 to 10^5 PFU. They remained as active as the controls and putting weight normally on their limbs (ie no pain) yet their femur bones still sustained a bone loss of 25%! Their osteoclasts were still reabsorbing bone. The controls expressed no bone loss and the researchers ruled out inactivity as a cause.
Extrapolated to humans you would experience bone density loss without knowing it until you have a fall etc and fracture something. Or in kids they may have skeletal deformations, growth retardation or will be prone to fracture. Ugh.