Open (More or Less) Post on Covid 153
Jul. 9th, 2024 10:10 am![[personal profile]](https://www.dreamwidth.org/img/silk/identity/user.png){kind=small}
ecosophia
We are now winding up the third year of these open posts. As the phrase "died suddenly" repeats in the mass media like a mantra, statistics for work days lost to illness and all-cause mortality mount up in heavily vaccinated nations, and more and more ugly facts about the official response to Covid spill out into public, we are entering what may well turn out to be the most difficult period of the Covid disaster -- the phase in which denial rises in lockstep with the death rate, and a great many people try not to admit what has been done to them by the people and institutions they trusted. It could get ugly, folks. So it's time for another open post. The rules are the same as before:
1. If you plan on parroting the party line of the medical industry and its paid shills, please go away. This is a place for people to talk openly, honestly, and freely about their concerns that the party line in question is dangerously flawed and that actions being pushed by the medical industry et al. are causing injury and death. It is not a place for you to dismiss those concerns. Anyone who wants to hear the official story and the arguments in favor of it can find those on hundreds of thousands of websites.
2. If you plan on insisting that the current situation is the result of a deliberate plot by some villainous group of people or other, please go away. There are tens of thousands of websites currently rehashing various conspiracy theories about the Covid-19 outbreak and the vaccines. This is not one of them. What we're exploring is the likelihood that what's going on is the product of the same arrogance, incompetence, and corruption that the medical industry and its tame politicians have displayed so abundantly in recent decades. That possibility deserves a space of its own for discussion, and that's what we're doing here.
3. If you plan on using rent-a-troll derailing or disruption tactics, please go away. I'm quite familiar with the standard tactics used by troll farms to disrupt online forums, and am ready, willing, and able -- and in fact quite eager -- to ban people permanently for engaging in them here. Oh, and I also lurk on other Covid-19 vaccine skeptic blogs, so I'm likely to notice when the same posts are showing up on more than one venue.
4. If you don't believe in treating people with common courtesy, please go away. I have, and enforce, a strict courtesy policy on my blogs and online forums, and this is no exception. The sort of schoolyard bullying that takes place on so many other internet forums will get you deleted and banned here. Also, please don't drag in current quarrels about sex, race, religions, etc. No, I don't care if you disagree with that: my journal, my rules.
With that said, the floor is open for discussion.
(no subject)
Date: 2024-07-12 12:49 pm (UTC)-A Spaniard.
Re: Population Immunity
Date: 2024-07-12 01:28 pm (UTC)Re: Population Immunity
Date: 2024-07-12 01:31 pm (UTC)I also find it disturbing that such a basic search as "Y. pestis immune suppression" (without the quotes) turns up nothing. It should at least turn up a few dozen irrelevant results!
Re: Viral Evolution in a Crowded World
Date: 2024-07-12 01:33 pm (UTC)"...This all means that past pandemics are, at best, a very weak guide for what will happen with this one."
Boldly going where no man has gone before we are.
This is starting to remind me of a certain happening (involving genetic tinkering) in a book, Retro something, written by some bearded dude, that began a cascade of events that changed, well, everything.
jeffinWA
Re: Viral Evolution in a Crowded World
Date: 2024-07-12 01:53 pm (UTC)But to each their own.
Something weird happened with Omicron for sure though. It was a very sudden change.
(no subject)
Date: 2024-07-12 02:28 pm (UTC)"Here, we showed that SARS-CoV-2 infected T lymphocytes, mainly CD4 + T cells, in an ACE2-independent manner. SARS-CoV-2 infection triggered pronounced T-cell death, which potentially contributed to lymphopenia in patients with COVID-19. T-cell infection may also pose profound influences on patients. Infected T lymphocytes not only lost the ability to control viral infection but may also carry viruses to other parts of the body through blood circulation. In addition, this ACE2-independent infection mode may compromise the therapeutic effect of neutralizing antibodies targeting at spike-ACE2 binding. These may synergistically result in more severe infection outcomes in patients with COVID-19.
It has been debated whether SARS-CoV-2 impaired the functionality of immune cell populations through direct infection. Our results provided evidence to show that SARS-CoV-2-infected T cells, as viral RNA, viral sgRNA, viral protein, and the infectious virus could be detected from T cell upon infection or from patient PBCs, although the production of infectious virus particles may stay at a low level. Several recent studies also revealed that multiple immune cells carry viral antigen or viral RNA, including neutrophils, macrophages, inflammatory monocytes, plasma B cells, T cells, and NK cells through postmortem histology analysis and single-cell/single-nuclear RNA-seq to lung or BALF.13,14,15 This suggests that SARS-CoV-2 should have a broad tropism of target cells, including major immune cells populations.
Human ACE2 and TMPRSS2 proteins were recognized as the main proteins that mediated SARS-CoV-2 cell entry.14 The newly discovered binding molecules AXL and NRP1 are still dependent on ACE2 as the main receptor.18,19 Our discovery of ACE2-independent infection of T cells is surprising, but is also supported by previous discoveries that there are SARS-CoV-2 RNA+ cells which did not co-express ACE2 and TMPRSS2.15 In our data, SARS-CoV-2 showed significant infection of activated T cells, suggesting there should be a new entry mechanism in T cells. The identification of LFA-1, as an entry molecule that contributed to a SARS-CoV-2 infection of T cells would be important for developing clinical therapeutics, although future questions remain. For example, what is the LFA-1 binding protein in SARS-CoV-2 virion if it is not the spike protein. Since LFA-1 is expressed in a number of other leukocytes, it can be expected that other immune cells (including macrophages or monocytes) could also be infected by SARS-CoV-2 potentially through binding with LFA-1. These questions should be addressed in future studies.
The infection of CD4 + T lymphocytes by SARS-CoV-2 virus may be a major contributor of virus induced pathogenesis. Armed T cells play a pivotal role against pathogen infection.10 As shown in our data, these T cells are likely to be targets of SARS-CoV-2 infection and undergo apoptosis in the HIF-1a-dependent pathway. These events may lead to T-cell dysfunction, depletion, and eventually lymphopenia in patients. In addition, the dying CD4 + T lymphocytes could trigger excessive inflammation that leads to severe immunopathogenesis in patients. Notably, the population of CD8 + T lymphocytes is also significantly decreased in COVID-19 patients. Unlike CD4 + T lymphocytes, these cells were not determined to contain SARS-CoV-2 viral antigen in flow cytometry. The mechanism underlying SARS-CoV-2 infection-induced CD8 + T lymphocytes depletion is currently unknown. Besides viral infection, several mechanisms, including the presence of endogenous or exogenous glucocorticoids, over-activated neutrophil releasing inhibitors of T cell activation (Arginase 1 and CD274) and cytokine-regulated selective differentiation of bone marrow cells, might also contribute to lymphocytes depletion.11,23 Further in-depth investigation is needed to address the potentially multi-mode mechanisms that lead to lymphopenia in the COVID-19 patients. Considering the apparent correlation between lymphopenia and disease progression in COVID-19 patients, it is important to develop strategies to prevent virus-induced lymphopenia."
https://www.nature.com/articles/s41392-022-00919-x
I'm not the only person thinking this is the airborn-AIDS idea, judging from the posts this paper generated on twitter:
https://nature.altmetric.com/details/124489153/twitter
(no subject)
Date: 2024-07-12 02:36 pm (UTC)https://www.lifesitenews.com/news/canadian-ag-asks-court-to-dismiss-lawsuit-against-govt-for-imposing-covid-jab-travel-mandate/
~F
RE: site blocking
Date: 2024-07-12 03:34 pm (UTC)Does ecosophia.dreamwidth.org have a static IP address?
This would be a series of numbers with periods, that looks like "123.456.78.0.1"
I've read that one way to block a website is to make it unsearchable by name, but if that's done, it is still possible to type in the IP address and get there. I don't have the skills to ferret it out myself, but perhaps someone with computer skills could post it?
Re: Novak Djokovic
Date: 2024-07-12 03:51 pm (UTC)Re: Population Immunity
Date: 2024-07-12 05:12 pm (UTC)(no subject)
Date: 2024-07-12 05:14 pm (UTC)https://journals.asm.org/doi/full/10.1128/iai.01517-07
Interaction between Yersinia pestis and the Host Immune System
"By the bite of an infected rodent flea, Y. pestis may invade directly into the host through the barrier structure of the host skin and encounter phagocytes such as polymorphonuclear leukocytes (PMNs) (predominantly neutrophils) and macrophages at the site of invasion. Most of them might be killed by neutrophils. However, the facultative intracellular Y. pestis preferentially infects host macrophages, possibly via recognition of specific surface-associated CCR5 molecules (33), and survives inside of macrophages at the early stage of infection. After proliferation and expression of various virulence determinants in macrophages, Y. pestis can be released into the extracellular compartment and spread systemically with acquisition of phagocytosis resistance. During this process, Y. pestis may circumvent destruction by the components of the host innate immune system"
Is this what you were looking for?
Re: Population Immunity
Date: 2024-07-12 05:29 pm (UTC)(no subject)
Date: 2024-07-12 06:48 pm (UTC)Re: Population Immunity
Date: 2024-07-12 07:40 pm (UTC)Re: site blocking
Date: 2024-07-12 07:45 pm (UTC)(no subject)
Date: 2024-07-12 07:45 pm (UTC)Re: Population Immunity
Date: 2024-07-12 07:54 pm (UTC)Somehow the overview above between brackets makes sense to me. It is not just the vaxxed but also the unvaxxed that need to be careful athough the unvexxed are better of
(no subject)
Date: 2024-07-12 07:58 pm (UTC)Re: site blocking
Date: 2024-07-12 08:03 pm (UTC)Non-authoritative answer:
Name: dreamwidth.org
Addresses: 3.221.63.47
3.231.247.77
34.206.235.108
34.231.5.204
Aliases: ecosophia.dreamwidth.org
(no subject)
Date: 2024-07-12 08:20 pm (UTC)"The Rolling Stones were the mummy's boys – they were all college students from the outskirts of London."
Re: site blocking
Date: 2024-07-12 09:04 pm (UTC)1) None of those IP addresses work; all return an error in my browser, and I checked them in a regular and a private TOR window.
2) If there was a fixed IP it should have one and only one numeric address, not four.
2) I am pretty sure the answer will be No, because ecosophia is a subdomain of dreamwidth.org, and I don't think subdomains can have fixed IPs.
ecosophia.dreamwidth.org has to bring you to dreamwidth.org, and that host completes the connection.
---
HOWEVER...
If you can get to dreamwidth.org, you can search for the site ecosophia from there, and I am pretty sure it is then ecosophia that resolves the search. That MAY get past any blocking at the DNS level.
I can't test that for sure since I have no problem accessing the site.
Re: Population Immunity
Date: 2024-07-12 09:43 pm (UTC)Re: site blocking
Date: 2024-07-12 09:45 pm (UTC)Re: site blocking
Date: 2024-07-12 11:57 pm (UTC)It won't work because they are not part of the same network either
(no subject)
Date: 2024-07-12 11:59 pm (UTC)That would be very welcome, thank you, archivist!