faetal on 8/3/2023 at 09:47
You know people are desperate if, on the topic of virus and vaccines, they are taking their cues from Woody Fucking Harrelson.
lowenz on 8/3/2023 at 10:47
WOKE WOKE WOKE! The only thing they want is to say "WOKE" and repeat "WOKE" because it's now the ONLY electoral buzzword they have.
Stupid republicans, bane of USA.
Azaran on 20/4/2023 at 16:05
(
https://timesofindia.indiatimes.com/life-style/health-fitness/health-news/long-covid-signs-are-seen-in-flu-cases-as-well-study/articleshow/99637110.cms?from=mdr) I'm skeptical of this, but could be great news if true
EDIT: You gotta wonder if we're only noticing Long Covid, because of how many people have been infected. This seems to indicate we'd have the same amount of 'long flu' if influenza was as contagious as covid.
Quote:
"Long COVID appears to manifest as a post-viral syndrome
of no greater incidence or severity than seasonal influenza," a release from the European Congress of Clinical Microbiology & Infectious Diseases has said.
Long COVID or post COVID condition is a set of conditions seen in those who are infected with the COVID causing coronavirus. It is also known as PASC or post-acute sequelae of COVID and is characterized by extreme fatigue, and brain fog.
195 adults diagnosed with COVID and 951 adults diagnosed with flu were followed for 12 weeks
For the study, the researchers followed up more than 1000 individuals for 12 weeks and found that a fifth of them, in both the groups of those who were infected with COVID and flu, reported ongoing symptoms and 4% in each of the group "reported having moderate to severe functional limitations in everyday life."
Severe COVID is associated with THIS life threatening disease
"No evidence to prove that Omicron infection leads to severe post-infection than flu"
"After controlling for influential factors including age, sex, First Nations status, vaccination status, and socio-economic profile (based on postcode), the analysis found no evidence to suggest that adults with Omicron were more likely to have ongoing symptoms or moderate to severe functional limitations at 12 weeks after their diagnosis than adults who had influenza," the researchers have said.
Younger population is more likely to report post viral illness after flu
In a sharp contrast to what is being said about post COVID condition and ignore about post-flu condition, the researchers said that the analyses suggested that younger age groups and non-indigenous populations were more likely to report moderate to severe functional limitations after influenza than Omicron.
Vaccination might be the reason
The researchers have said underlying illness and flu vaccination status may have influenced the results.
"The researchers also note the growing evidence that the risk of long COVID has been lower during the Omicron wave compared with earlier SARS-CoV-2 variants, and because the vast majority of people in Queensland were vaccinated when the Omicron variant emerged, the lower severity of long COVID could be due to vaccination and/or the Omicron variant," the release said.
The study was done on the residents of Queensland, Australia where close to 90% were vaccinated during the Omicron led COVID wave.
What are the symptoms of long COVID?
Though the burden of long COVID seems not to be there in the Omicron era, there is a vulnerable section of the population like elderly people and those with a compromised immunity system.
These people should be immediately taken to a hospital when symptoms like fatigue, shortness of breath and cognitive dysfunction are seen. Studies have found more than 200 different symptoms associated with long COVID. Around 10-20% of the people infected with COVID go on to develop long COVID.
How to prevent long COVID?
Long COVID can be prevented by adopting healthy measures like wearing a mask, avoiding going near infected people, keeping the indoor air properly ventilated, taking care of those who are vulnerable but at the same time taking care of your own health as well.
In case of any symptom, do not hesitate to see a doctor.
Cipheron on 20/4/2023 at 17:40
Quote Posted by Azaran
Younger population is more likely to report post viral illness after flu
This one is most likely due to older people having more immunity against flu variants that come around again. It was a factor in the 1918 flu, which disproportionately affected younger people.
Previous Covid exposure may also explain why the more recent variants aren't leading to such severe Long Covid effects either.
SD on 20/4/2023 at 19:30
Let's not neglect confirmation bias either. I had long covid symptoms myself. Only one problem: I've never had covid. But anyone who had had covid might be tempted to attribute those symptoms to covid's after-effects. With so many people apparently having had covid, that is a LOT of people who are going to be blaming covid for any subsequent symptoms they have, regardless of whether covid is actually to blame.
demagogue on 20/4/2023 at 20:36
You can look at that from the other way around though too. In my understanding, or at least according to the story going around in the long covid groups, the most common set of symptoms surrounding long covid are associated with dysautonomia, your autonomic system going screwy, which as I understand it can have many ultimate sources.
But the punchline could be that dysautonomia & the like is a serious health concern that disrupts people's lives no matter its source. It's not like non-covid caused dysautonomic symptoms have to be somehow less serious than the covid-caused ones, or that the latter are somehow more serious. That's kind of a salience bias.
Cipheron on 21/4/2023 at 16:16
It could also be that rather than playing up Long Covid, "Long Flu" has been overlooked or downplayed in the past.
That could have a lot to do with the fact that serious flu is connected with the elderly, so lingering effects are harder to tease out vs old age in general, but it's noted in the article that the bias is towards young people reporting these Long Covid effects, and a sudden drop in a younger person's ability to work is going to be much more noticeable.
Also, only looking at individual to individual cases can actually hide the scale of a problem. For example, if a wave of Covid comes through and infects 10 times as many people as a Flu year does, then that's going to be 10 times as many people affected by the chronic illnesses, even if the 1:1 likelihood is the same.
The problem with statistics is you can "adjust" away levels of risk that are actually important. For example, if you looked at car accidents vs being hit by a falling meteorite, you might say on an adjusted basis, the injuries from car accidents are no greater than the ones from meteorites. But should we draw from that study that the risks of car accidents have been over-played?
So the problem can actually be that zooming in on only people who were already infected, we actually miss part of the big picture: we can no longer make meaningful assessments about what's important. The Covid deaths over 3 years are much higher than three years of severe flu seasons, so even if Covid survivors fare no worse than Flu survivors on average, that's not really proving anything, nor is it saying both diseases bear the same level of risk.
Cipheron on 23/4/2023 at 18:57
Current research on Covid origins:
(
https://journals.asm.org/doi/10.1128/jvi.00365-23)
The first notable research is from attempts to culture SARS-CoV-2 in labs. They note that almost always, certain changes occur as a result of cultivation. But if the stuff was initially cultured in a lab, so it could be studied, then it should have already been subject to those changes:
Quote:
Over the past 3 years, hundreds of research groups around the world have cultured human isolates of SARS-CoV-2 in cell lines. This collective experience has revealed a highly reproducible consequence of viral propagation in culture: the deletion of the portion of the spike gene encoding the furin cleavage site (3). If SARS-CoV-2 had a laboratory origin, it would have been amplified in a laboratory through a process of serial passage typically needed to recover high-titer stocks from environmental samples. In this process, the deletion of the furin cleavage site is expected, offering a signature of laboratory handling. However, early isolates of SARS-CoV-2 show the furin cleavage site to be intact, arguing against introduction into humans after laboratory cell culture.
Also, the virus lacks common adaptations viruses make to laboratory conditions:
Quote:
Traditional laboratory experiments would likely have included the adaptation of a virus in common laboratory animal models such as mice to study it with ease. Thus, a laboratory-derived virus released into the population would reasonably be expected to carry these adaptive markers in their genomes. However, early isolates of SARS-CoV-2 did not carry mutations that confer adaptation to common animal models, such as mutations in the receptor binding domain of spike that improve viral replication in mice
Additionally, the evidence against it being engineered. First, it doesn't have any of the common signatures of engineered work, and second, the means by which it infects spreads was entirely unknown until 2020. So whoever made it must have invented entirely new methods of genetic engineering which leave no trace, while on top of that, coming up with an entirely novel means of viral infection that nobody ever heard of either.
Quote:
Evidence A: lack of any evidence of deliberate genetic engineering.
Genetic engineering involves the use of recombinant DNA techniques to modify the virus. Such techniques often leave telltale evidence in the forms of novel restriction sites, differences in DNA base content, differences in gene organization from natural isolates, selection markers, and foreign nonviral sequences. While various papers have suggested that SARS-CoV-2 carries hallmarks of recombinant DNA technologies, this theory has been thoroughly refuted (7), including by the U.S. intelligence community.
Evidence B: the pathogenesis of SARS-CoV-2 may be dependent on the cleavage site loop length and not only the presence of the furin cleavage site.
The furin cleavage site is an important determinant of virulence (4). A furin cleavage site is absent from the closest known relatives of SARS-CoV-2; however, these closest relatives are, in fact, distantly related. Furin cleavage sites are commonplace in other CoV spike proteins, including those of endemic human betacoronaviruses, and were first identified in the 1980s within a mouse coronavirus (8). Prior to the COVID-19 pandemic, it was commonly thought that the presence of the furin cleavage site was directly linked to the pathogenesis of CoV. However, a recent examination of SARS-CoV-2 has revealed a somewhat complex relationship between the presence of a furin cleavage site and viral pathogenicity. In fact, the context of the cleavage site defines the extent to which this site drives virulence. Specifically, the amino acids N terminal to the cleavage site, which comprise the cleavage loop, are important: both the loop's length and the presence of a glycosylation site within it define the contribution of the furin cleavage site to virulence (9). Since these nuances were not understood prior to 2020, deliberate engineering of the SARS-CoV-2 cleavage site to promote pathogenesis without this critical information is improbable.
faetal on 24/4/2023 at 22:36
Quote Posted by SD
I've never had covid
...that you know of.
