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As with many aspects of the new coronavirus, researchers are trying to pull together data to understand the medium-term health effects more fully.
[...] Its impact on the heart still isn't clear, Dr Gallo says, but studies published in recent weeks describe abnormalities in the hearts of patients who have completely cleared the virus.
"[The researchers] asked them about their just general wellbeing and a lot of the patients are commenting on just being generally exhausted and having shortness of breath, some of them having palpitations, atypical chest pain," she says.
What's more, many of these patients weren't that sick with COVID-19 — most of them had managed their illness at home, rather than needing hospital treatment.
[...] Other persistent symptoms people report have to do with the brain: "brain fog", sleeplessness and headaches.'
[...]Fatigue, which is more than just a feeling of tiredness, and can be associated with things like a "foggy" brain, slowed reflexes and headaches, is usually a useful response to infections.
"There's a good reason for that — mounting an immune response to fight an infection takes a huge amount of energy," Dr Landowski says.
"The body wants you to do as little as possible, so you can conserve energy and divert it to the immune system.
Then, once the infection is eliminated, the fatigue dissipates.
"However, in some people, the switch that returns the body back to normal seems to fail, resulting in chronic fatigue."
[...] "Regardless of which cells it's infecting, if it's infecting cells in the brain, it could be causing damage, which could have long-term consequences," Dr Lawson said.
Even if the virus doesn't infect brain cells directly, inflammation caused by the virus could also cause damage to the brain.
Some experts are concerned the medium-term effects on the brain might have consequences that reach further.
In an article in the Journal of Alzheimers Disease Reports, experts raise the question of whether people who've had COVID-19, particularly those whose symptoms included loss of taste or smell, will be at greater risk of conditions including Alzheimer's disease after they recover.
The last-linked article from above (which is open-access), is excerpted here with links sprinkled on some of the unusual terms:
Some of the earliest neurologic findings were in those experiencing COVID-19-related anosmia and dysgeusia [2]. Important to this equation is that COVID-19 may prove to be a risk factor for future neurodegenerative disorders, beyond that which would be expected in the context of other comorbidities and genetic predispositions. Anosmia and the biological processes resulting in this symptom contribute to grey matter loss in cortical regions [3], which is similar to where pathognomonic amyloid plaques are often discovered [4]. Olfactory dysfunction has also been found to be associated with the graduation from mild cognitive impairment (MCI) to AD, serving as a potential identifier for preclinical stages [5].
[...] It has become clear that many age-related conditions are found among those testing positive for COVID-19, though some of these are also related to lifestyle and family history. ... Systolic hypertension in midlife, rather than only late life, is associated with 18% and 25% increased risk of AD, respectively ... These cardiovascular risk factors are directly related to cerebrovascular consequences, such as hypoperfusion, a symptom strongly associated with MCI and AD [14]. Plasma exchange and albumin for AD patients with hypoperfusion, for example, has been shown to improve cognitive deficits and initiate cerebrospinal fluid (CSF) amyloid-β (Aβ)...
Journal Reference:
Jack C. Lennon. Neurologic and Immunologic Complications of COVID-19: Potential Long-Term Risk Factors for AlzheimerΓÇÖs Disease [open], Journal of Alzheimer's Disease Reports (DOI: 10.3233/ADR-200190)
Got it! The millennials surviving COVID-19 today may have higher chances of an early onset of dementia than the baby boomers of today.
(Score: -1, Redundant) by Anonymous Coward on Monday August 03 2020, @06:52PM (7 children)
So now t-cell immunity doesnt confer protection either? Just like the WHO tweeted about antibodies... What is the point of it if not to confer protection like for every other virus?
Also, no idea what the second quote is supposed to prove. Can you clarify what you think it says?
(Score: 0) by Anonymous Coward on Monday August 03 2020, @07:12PM (6 children)
Your semi-literacy is not my problem. It's yours.
(Score: 0) by Anonymous Coward on Monday August 03 2020, @07:24PM (5 children)
Well you quoted something that says the cross reactive t-cells originally raised towards cold viruses are important for proper immune response. So, I guess you agree with me then...
(Score: 0) by Anonymous Coward on Monday August 03 2020, @07:52PM (4 children)
English, motherfucker. Can you read it? Apparently not.
Your ignorance is stunning. Get a clue. If you can. I won't hold my breath.
(Score: -1, Troll) by Anonymous Coward on Monday August 03 2020, @08:14PM (3 children)
"Rather, diversity of T-cell responses in terms of recognition rate of SARS-CoV-2 T-cell epitopes was decreased in patients with more severe COVID-19 symptoms (Fig. 4h, Extended Data Fig. 4b), providing evidence that development of protective immunity requires recognition of multiple SARS- CoV-2 epitopes."
Whatever, you apparently have no idea what those words you quoted mean. I hope for your sake you are trolling instead of being profoundly stupid.
(Score: 0) by Anonymous Coward on Monday August 03 2020, @11:57PM (2 children)
This means that while SARS COV2 *may* share epitopes [britannica.com] with other Coronaviruses, antibodies must be able to identify/connect to multiple epitopes, some that are unique to SARS COV2 in order to convey significant levels of immunity. Which fully supports what I said. Which is why I quoted it in the first place.
You're a troll and/or a moron. Don't care which. No more feeding for you, asshole. Get back under your bridge!
(Score: -1, Troll) by Anonymous Coward on Tuesday August 04 2020, @12:30AM
It means if you had prior immunity to other coronaviruses that cross react with sars2, then you have "diversity of T-cell responses", which is evidence for "protective immunity".
So no, that is not what you said.
(Score: -1, Troll) by Anonymous Coward on Tuesday August 04 2020, @12:33AM
Also it was about t-cells, not even about antibodies. It is so obvious you have no idea what you read.