Saturday, July 22, 2023

Covid's Effects on Lymphocytes

A bit more on Cov-AIDS from Daniel Brittain Dugger because people need to be aware of the similarities between these diseases to, just maybe, provoke them to do everything they can to reduce transmission: mask, vax, and ventilate and clean the air. 

Long story short, Covid affects your immune system, making anyone who gets it open to getting all sorts of other things that their body would normally protect them from. The fewer times you get an infection, and the lower the dose of infection, the better off you'll be. DBD is arguing against the use of Paxlovid. Elsewhere he notes that those on HIV PrEP have the lowest rate of SARS-CoV-2 acquisition. It's just an argument being presented here, and I'm not an expert on it, so talk to your doctor if Paxlovid is right for you! This is a very complex one, so I explained some of the terms along the way. 

From October 2020

"As a member of the HIV community, who has endeavored to not only educate themselves about their own condition but that of a chronic SARS-CoV-2 infection, it troubles me that there is a population in decline that does not receive the attention it deserves: that of the CD4 lymphocyte."

CD4 lymphocytes are part of the T-lymphocyte cells that are produced in the bone marrow and fight off bacteria and viruses. And their decline could point to the problems seen in Long Covid.

"The consequences of such spells a recipe for disaster. The fact that a SARS-CoV-2 infection shared the same pathophysiological process of productively infecting the CD4 T Lymphocyte, leading to its apoptosis was observed in September 2020. While the discussion of viral persistence continues to be debated, it was actually known as soon as there was enough resistance to wipe out the first monoclonals. SARS-CoV-2 lacks the ability to read. We created the resistance through abrupt therapeutic discontinuation.

Depletion of the CD4 population and viral persistence allows me to borrow from 40 years of evidenced based medicine to demonstrate how we could have literally not botched this any more.

In those individuals for whom there is depletion of the CD4 compartment, there is a critical date that must be paid attention to in the event that individual is going to experience CD4 normalization, maintain a high CD4 nadir [low point], and maintain their cognition. That date is referred to as the Estimated Date of Seroconversion [development of antibodies]. Deferral of antivirals outside of the one year anniversary slams the door on normalization and prevents optimal vaccine-induced seroconversion. . . . 

In Philadelphia, Tom Hanks developed Kaopsi's Sarcoma as a consequence of Human Herpes Virus-8 and elevated Vascular Endothelial Growth Factor. A CD4 nadir of 500 cells or less will predispose you to this cancer. While we have yet to observe folks with KS lesions, we have seen an uptick of cancers caused by opportunistic infections. When the CD4 nadir is between 300 and 500, there is the possibility of tuberculosis reactivation. We have seen an explosion of TB. One in five is a carrier of TB. When the CD4 nadir is between 100 and 250, things start to get interesting: Coccidioidomycosis [Valley fever], Cryptococcal meningitis, Esophageal candidiasis, Mycobacterium avium complex [MAC lung disease], Progressive Multifocal Leukoencephalopathy, thanks to some dude named John Cunningham [a brain infection caused by the JC virus]. 

When the CD4 nadir gets to 50, you find yourself vulnerable enough to experience histoplasmosis, blastomycosis, Cytomegalovirus retinitis. As vulnerable as these folks in Michigan

As someone who has educated themselves about 'brain fog,' I find it unconscionable that individuals continue to couch the neurological insult as ME/CFS. Why? Because they do not care about the control arm in Dr. Appel's study. Because of the novelty of the virus, Dr. Apple relied upon the test for HIV Associated Neurocognitive Decline, which relies upon the tunneling nanotube and depletes CD4 cells, just as SARS-CoV-2. 70% of the control arm met the diagnostic criteria for Asymptomatic Neurocognitive Impairment. For those who experience further disease progression, it will be Mild Neurocognitive Decline and last, the functional equivalent of AIDS Dementia Complex. In fact, some have already made it there, as they have heme oxygenase and quinolinic acid in their Cerebrospinal Fluid. 


from here

Why else might I look at this from the perspective of HIV? I want to get back to normal, and folks are preventing that.

Each cell type that constitutes the central nervous system reservoir in HIV does so for SARS-CoV-2. The one that has not received enough attention is that of the microglia [patrol the brain for pathogens]. Not only is it resistant to apoptosis [programmed cell death], which means a Latency Reversal Agent is now needed, it leads to drug resistance. As soon as therapy is discontinued, the peripheral blood is reseeded and folks can spew virus from their lungs. 

While monocyte derived macrophages were discussed, there was not a mention of their ability to act as a trojan horse not cause osteoporosis. We have seen the consequences of this play out as people have struggled with issues with their teeth. You will be hard pressed to find a greater concentration of osteoclasts than in the mandible [jaw]. More than likely, the kids in LV had leaky guts, disintegrating jaws, underwent dental procedures and ended up with streptococcus intermedius brain abscesses. Paying more attention to the loss of Bone Mineral Density would have been prudent since measurements at the hip and spine are done in clinical trials for HIV antivirals. What better way to end up with a hip fracture?

Speaking of decline, there is another thing that we are not discussing, that of decline in the eGFR [kidney efficiency]. Antivirals are initiated as early as possible to preserve kidney function, as they are productively infected by both viruses. Antivirals impact the kidneys. Additionally, Soluble Urokinase Plasminogen Activator Receptor does not do wonders for your cognition.  

I really wish folks would read more, as the literature and prescribing guidelines are there for consumption. Protease inhibitors ARE disfavored for a number of reasons. First, we haven't a clue who lives with a resistant strain. Second, due to microglia involvement, therapy will be required for life. Those who support protease inhibitors do not care about the individual taking the pill. You complain about endothelial damage, but allow the CD4 nadir to drop and put them on a Ritonavir based regimen that will cause endothelial damage within 30 days. Personally, I would prefer to live in a society not plagued with lipodystrophic diabetics. Cannot say the same for those pushing Paxlovid. 

Finally, you will not arrest cortical thinning nor allow for hypometabolic frontal lobe resolution with a monotherapy. The literature is quite clear. Unfortunately, nobody reads. 

Yes, it is unfathomable that we find ourselves in this position and incompetence is the only thing that can be blamed. God Bless the United States of Anosmics [smell blindness] and What Would be AIDS-Defining Illnesses were the virus HIV." 

Check out the book, And the Band Played On, for more on the how activists change the framing of how AIDS was discussed in the 80s. We seem to be following the same path, so it reads as a guidebook for what to do next. 

From August 2020:

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