Thread by @dbdugger

@RealCheckMarker When the kiddos are confined to a wheelchair, mechanically ventilated, and communicate through a computer after developing ALS, it will be after having experienced TDP-43 cleavage in the exact way observed in the HIV+. Boy, they're fucked.

@RealCheckMarker We have known of the productive infection of microglia since 2021.
Microglial Implications in SARS-CoV-2 Infection and COVID-19: Lessons From Viral RNA Neurotropism and Possible Relevance to Parkinson’s Disease frontiersin.org/journals/cellu…

@RealCheckMarker It is well established in HIV medicine that their dysregulation leads to premature brain aging, Alzheimer's, Parkinson's, and Amyotrophic Lateral Sclerosis.
Microglial Cells: The Main HIV-1 Reservoir in the Brain pmc.ncbi.nlm.nih.gov/articles/PMC68…

@RealCheckMarker "Due to their multifunction, any dysfunction in microglia cells will lead to many diverse diseases including brain aging or neurodegenerative diseases such as Alzheimer disease, Parkinson disease and amyotrophic lateral sclerosis."

@RealCheckMarker It has been known for two years that individuals are experiencing the cleavage of TDP-43.
The SARS-CoV-2 main protease induces neurotoxic TDP-43 cleavage and aggregates nature.com/articles/s4139…

@RealCheckMarker The role of TDP-43 propagation in neurodegenerative diseases: integrating insights from clinical and experimental studies
nature.com/articles/s1227…

"The accumulation of TDP-43 aggregates in the central nervous system is a common feature of many neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), Alzheimer’s disease (AD), and limbic predominant age-related TDP-43 encephalopathy (LATE)."

@RealCheckMarker That does say Vpu, correct? Yeah, their asses are headed straight to the MEmory care unit.
HIV-1 Vpu and SARS-CoV-2 ORF3a proteins disrupt STING-mediated activation of antiviral NF-κB signaling
science.org/doi/10.1126/sc…

@RealCheckMarker Same Vpu. Same TDP-43 cleavage.
HIV-1 Vpu induces neurotoxicity by promoting Caspase 3-dependent cleavage of TDP-43 embopress.org/doi/full/10.10…

@RealCheckMarker From the TDP-43 cleavage article. "Accumulating evidence suggests that prion-like spreading of aberrant protein aggregates composed of tau, amyloid-β, and α-synuclein is involved in the progression of neurodegenerative diseases such as AD and PD."

@RealCheckMarker Certainly doesn't help that they have experienced Vpr-like neurological insult like the aggregation of a-synuclein and running around with an AIDS Dementia Complex brain.

@RealCheckMarker SARS-CoV-2 Proteins Interact with Alpha Synuclein and Induce Lewy Body-like Pathology In Vitro pmc.ncbi.nlm.nih.gov/articles/PMC89…

@RealCheckMarker SARS-CoV-2 and the DNA damage response pmc.ncbi.nlm.nih.gov/articles/PMC10…

@RealCheckMarker "HIV-1 causes double-strand breaks as a result of binding of its VPR protein to chromatin [71]. Vpr expression also activates ATM and leads to the formation of repair foci [72]."

@RealCheckMarker Same Vpr. Same a-synuclein aggregation.
HIV-1 Vpr protein impairs lysosome clearance causing SNCA/alpha-synuclein accumulation in neurons pubmed.ncbi.nlm.nih.gov/33890542/

@RealCheckMarker QUINOLINIC ACID IS A BIOMARKER OF COVID-19–ASSOCIATED COGNITIVE IMPAIRMENT croiconference.org/abstract/quino…

@RealCheckMarker As was predicted by Kenneth Podell on September 29th, 2020.
Epub 2020 Sep 29.
Multiple Neuroinvasive Pathways in COVID-19 pubmed.ncbi.nlm.nih.gov/32990925/

@RealCheckMarker "One can draw on the experience with an HIV/AIDS epidemic. The initial understanding of HIV/AIDS was that of the virus affecting the immune system by depleting T cells, which resulted in opportunistic infections of multiple organs, including the brain."

@RealCheckMarker "However, it did not take long to discover that the disease could also attack the brain directly, which resulted in long-term cognitive impairment."

@RealCheckMarker "Subsequently, HIV encephalopathy and AIDS dementia complex leading to long-term cognitive impairment were discovered [87]. Based on the emerging literature, it is reasonable to hypothesize a somewhat similar scenario may unfold in relationship to COVID-19."

@RealCheckMarker Involvement of quinolinic acid in AIDS dementia complex pubmed.ncbi.nlm.nih.gov/15639803/

@RealCheckMarker Same Vpr. Same Quinolinic Acid.
A pilot investigation of the association between HIV-1 Vpr amino acid sequence diversity and the tryptophan-kynurenine pathway as a potential mechanism for neurocognitive impairment pmc.ncbi.nlm.nih.gov/articles/PMC10…

@RealCheckMarker While proteins operate mechanistically as HIV's Vpr and Vpu, others are operating mechanistically as HIV's Tat and Nef contributing to that mentioned above, amyloid deposition and the phosphorylation of tau.

@RealCheckMarker This paper advances three hypotheses as to why amyloid is depositing in the brains of millions.
SARS-CoV-2-Induced Amyloidgenesis: Not One, but Three Hypotheses for Cerebral COVID-19 Outcomes pmc.ncbi.nlm.nih.gov/articles/PMC96…

@RealCheckMarker "Several receptors for SAA have been identified, including scavenger-receptor SR-B1 (involved in cholesterol efflux and removal of SAA), toll-like receptors 2 (TLR2) and 4 (TLR4), and receptor for advanced glycated end-products (RAGE) (all enhancing immune activation)."

@RealCheckMarker SARS-CoV-2 targets ribosomal RNA biogenesis cell.com/cell-reports/p…

@RealCheckMarker "Finally, the Tat protein of human immunodeficiency virus interacts with FBL and U3 snoRNA, impairing prerRNA processing and depleting mature ribosomes."

@RealCheckMarker While it appears all the rage is lying to toddlers and knocking them off with what is an AIDS death, Protein E is contributing to an upregulation of RAGE receptors within the Blood Brain Barrier with resultant amyloid deposition.

@RealCheckMarker Gastro cases hit 20-year high as parasite spreads disease to toddlers smh.com.au/national/gastr…

@RealCheckMarker "There have been 11,747 cryptosporidiosis cases in 2024 compared with 3716 in 2023. A quarter of all cases are in children under four."

@RealCheckMarker Same Tat. Same Cryptosporidium Parvum.
HIV-1 Tat Protein Suppresses Cholangiocyte Toll-Like Receptor 4 Expression and Defense against Cryptosporidium parvum pmc.ncbi.nlm.nih.gov/articles/PMC27…

@RealCheckMarker As has been observed with just about every other well known reservoir in HIV, that astrocytes are being productively infected has been allowed since 2022.
In SARS-CoV-2, astrocytes are in it for the long haul pmc.ncbi.nlm.nih.gov/articles/PMC93…

@RealCheckMarker Among many articles reporting elevation of GFAP.
A Prospective Study on Neural Biomarkers in Patients with Long-COVID Symptoms pmc.ncbi.nlm.nih.gov/articles/PMC10…

@RealCheckMarker Same Tat. Same GFAP.
HIV-1 Tat Induces Unfolded Protein Response and Endoplasmic Reticulum Stress in Astrocytes and Causes Neurotoxicity through Glial Fibrillary Acidic Protein (GFAP) Activation and Aggregation pmc.ncbi.nlm.nih.gov/articles/PMC50…

@RealCheckMarker HIV-1 Tat Upregulates the Receptor for Advanced Glycation End Products and Superoxide Dismutase-2 in the Heart of Transgenic Mice mdpi.com/1999-4915/14/1…

@RealCheckMarker "Recent studies have indicated that HIV-1 Tat-induced RAGE expression within the blood–brain barrier accelerates amyloid beta deposition."

@RealCheckMarker Among the articles discussing the role of Tau in the context of a chronic SARS-Cov-2 infection.
Role of Tau protein in long COVID and potential therapeutic targets pmc.ncbi.nlm.nih.gov/articles/PMC10…

@RealCheckMarker In HIV+, Tat contributes to the phosphorylation of Tau.
HIV and Alzheimer's disease: complex interactions of HIV-Tat with amyloid β peptide and Tau protein pubmed.ncbi.nlm.nih.gov/31016584/

@RealCheckMarker It was in 2021 that evidenced emerged of a protein operating mechanistically as HIV's Nef through evidence of MHC-I down regulation and pulmonary artery hypertension. 2022 brought further evidence through Pepe implicating the Tunneling Nanotube.

@RealCheckMarker It was in 2023 that we learned of foam cell formation as a consequence of cholesterol efflux pathway impairment, for which there is Scavenger Receptor B1 involvement, mentioned above.

@RealCheckMarker SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels nature.com/articles/s4416…

@RealCheckMarker The HIV protein responsible for the development of atherosclerosis and dying from sCJD is listed at citation #33.

@RealCheckMarker "33. Collins, K. L., Chen, B. K., Kalams, S. A., Walker, B. D. & Baltimore, D. HIV-1 Nef protein protects infected primary cells against killing by cytotoxic T lymphocytes. Nature 391, 397–401 (1998)."

@RealCheckMarker In the HIV+, Nef also contributes to the elevation of that mentioned in this article, p-tau 217.
Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection nature.com/articles/s4159…

@RealCheckMarker Abundance of Nef and p-Tau217 in Brains of Individuals Diagnosed with HIV-Associated Neurocognitive Disorders Correlate with Disease Severance pubmed.ncbi.nlm.nih.gov/34843091/

@RealCheckMarker Beyond an abundance of p-tau, there are Trojan Horses.
SARS-CoV-2 spike protein acts as a β-adrenergic receptor agonist: A potential mechanism for cardiac sequelae of long COVID pubmed.ncbi.nlm.nih.gov/39073192/

@RealCheckMarker The intervention above has been proposed as a consequence of Nef being found within astrocytes.
Blockade of beta adrenergic receptors protects the blood brain barrier and reduces systemic pathology caused by HIV-1 Nef protein pubmed.ncbi.nlm.nih.gov/34784367/

@RealCheckMarker "Results suggest that interruption of the beta adrenergic signaling reduces the peripheral organ inflammation caused after Nef expression in astrocytes of the brain."

@RealCheckMarker In the HIV+, Tat and Nef, secreted from astrocytes leads to elevated MCP-I and the trafficking of Trojan Horses into the CNS.
Nef-induced CCL2 Expression Contributes to HIV/SIV Brain Invasion and Neuronal Dysfunction pmc.ncbi.nlm.nih.gov/articles/PMC68…

@RealCheckMarker HIV-1 Tat induces monocyte chemoattractant protein-1-mediated monocyte transmigration across a model of the human blood-brain barrier and up-regulates CCR5 expression on human monocytes pubmed.ncbi.nlm.nih.gov/10453044/

@RealCheckMarker The same monocytes that contributed to profoundness of Asymptomatic Neurocognitive Impairment in Dr. Apple's control arm and of course, was predicted by Kenneth Podell on September 29th, 2020.

@RealCheckMarker Monocytosis in the acute phase of SARS-CoV-2 infection predicts the presence of anosognosia for cognitive deficits in the chronic phase pmc.ncbi.nlm.nih.gov/articles/PMC94…

@RealCheckMarker Cerebrospinal Fluid Offers Clues to Post-COVID ‘Brain Fog’ ucsf.edu/news/2022/01/4…

@RealCheckMarker "All participants underwent an in-person cognitive testing battery with a neuropsychologist, applying equivalent criteria used for HIV-associated neurocognitive disorder (HAND)."

@RealCheckMarker "Surprisingly, the researchers found that 13 of the 22 participants (59 percent) with cognitive symptoms met HAND criteria, compared with seven of the 10 control participants (70 percent)."

@RealCheckMarker Depriving millions of forty years of evidenced based medicine out of concern of the suffering of people forty years ago probably wasn't the best idea.