Thread by @dbdugger

As a member of the HIV positive community and advocate for those living with a chronic SARS-Cov-2 infection, I can say that while the origins remain up for debate, there is much that isn't up for debate.

https://twitter.com/CarlosdelRio7/status/1805194495182401879

Not the first time we have observed a virus that depletes CD4 cells, it is persistent, there is an aversion to non-pharmaceutical interventions, vaccines aren't protective, and there is forward transmission.

That it would be prudent to borrow from forty years of evidenced based medicine to preserve the autonomy, immune competence, and cognition of millions, including the family members, friends, colleagues, and the clinicians of the HIV positive was advanced early on.

It was on September 28th, 2020, that you and others in HIV medicine were put on alert that SARS-Cov-2 possessed the ability to deplete the CD4 compartment, as does HIV.
SARS-CoV-2 Uses CD4 to Infect T Helper Lymphocytes
medrxiv.org/content/10.110…

Certainly not the only time. You and others were one again notice in March of 2022.
ACE2-independent infection of T lymphocytes by SARS-CoV-2
nature.com/articles/s4139…

Since September of 2022, you have been able to view Covid-19 appear directly under HIV on Merck Medical's website.
merckmanuals.com/professional/h…

Acquired lymphocytopenia
The most common causes include:
Protein-energy undernutrition
HIV infection
COVID-19
Certain other viral infections

"Patients with COVID-19 also frequently have lymphocytopenia (35 to 83% of patients) (2). Lower lymphocyte counts portend a poor prognosis and an increased likelihood of requiring ICU admission and of dying from the disease."

"The cause of the lymphocytopenia is not completely understood, but COVID-19 can directly infect lymphocytes, and a cytokine-related apoptosis of the cells is likely."

On September 29, 2020, Kenneth Podell advanced the idea that individuals would live with the functional equivalent of HIV Associated Neurocognitive Decline. Subsequent journal articles would prove his prescience.
Multiple Neuroinvasive Pathways in COVID-19 pubmed.ncbi.nlm.nih.gov/32990925/

"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."

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

"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."

Not only does SARS-Cov-2 deplete the CD4 compartment, ignored journal articles have demonstrated its proteins operating mechanistically in the same way as HIV's Nef, Tat, and Vpr.

In December of 2021, the same month China repurposed Azvudine, and seventh months after TDF was suggested to be efficacious, Chertow published the findings of multiple autopsies.
SARS-CoV-2 infection and persistence throughout the human body and brain
assets.researchsquare.com/files/rs-11390…

He implicated the two most well known reservoirs in HIV, that of the Central Nervous System, and Gut Associated Lymphoid Tissues.

The Central Nervous System reservoir of those living with a chronic HIV and SARS-Cov-2 infection expand through the same mechanism of transcytosis, the Tunneling Nanotube, implicated by Ana Pepe in 2022, and suggestive of a protein operating mechanistically as HIV's Nef.

A number of journal articles have specifically mentioned HIV's Nef, including this one related to the formation of foam cells, observed in the HIV positive as a consequence of cholesterol efflux pathway impairment, which can also lead to sCJD.

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

"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)."

science.org/doi/full/10.11…

"Several viruses, such as the influenza virus, HIV, and herpes simplex virus (31), can use TNTs to transfer their genomes to naïve cells, a mechanism of direct cell-to-cell communication that allows evasion of host immunity and to avoid pharmaceutical targeting."

"This evidence supports our hypothesis that SARS-CoV-2, similar to other viruses such as HIV (30, 72), is an inducer of TNT formation, to facilitate its spreading between TNT-connected cells."

"On the basis of our observations, the transfer of SARS-CoV-2 occurs via TNTs through both extracellular adhesion (i.e., surfing) and intracellular transport in agreement with what has been already shown for HIV."

"For example, HIV is able to not only “hijack” TNTs but also gap junctional communication to spread toxic signals to uninfected astrocytes."

An untold number of HIV positive individuals will present to a clinician today who finds themselves with every cell type that constitutes the CNS reservoir in those living with HIV being productively infected by SARS-Cov-2.

Both SARS-Cov-2 and HIV productively astrocytes. Known to contribute to glymphatic system disturbances and along with microglia impair oligodendrocytes through a "bystander effect."
In SARS-CoV-2, astrocytes are in it for the long haul ncbi.nlm.nih.gov/pmc/articles/P…

Like with HIV, the Trojan Horse Hypothesis is recognized and has been since 2021, with monocyte derived macrophages differentiating into perivascular macrophages and stomping on the brain until folks end up with dementia.

The primary target of HIV, perivascular macrophages are believed to be responsible for the appearance and disappearance of virus within the CNS, due to their relatively quick turnover.
Macrophages and Monocytes: “Trojan Horses” in COVID-19 ncbi.nlm.nih.gov/pmc/articles/P…

As is observed with HIV, SARS-Cov-2 productively infects brain pericytes. Known to harbor latent virus, they also contribute to Cerebral Blood Flow Disturbances and Blood Brain Barrier degradation.

Infection of Brain Pericytes Underlying Neuropathology of COVID-19 Patients pubmed.ncbi.nlm.nih.gov/34769052/

Known since 2021, like with HIV, SARS-Cov-2 productively infects microglia, the consequences being well established.
SARS-CoV-2 Infection of Microglia Elicits Proinflammatory Activation and Apoptotic Cell Death pubmed.ncbi.nlm.nih.gov/35510852/

An untold now find themselves predisposed to Parkinson's as a consequence of their dysregulation and basal ganglia persistence, observed by Chertow almost three years ago, and to which the substantia nigra belongs.

An untold find themselves predisposed to Alzheimer's as a consequence of their dysregulation and amyloid deposition, known since 2022.
Amyloidogenesis of SARS-CoV-2 Spike Protein
pubs.acs.org/doi/10.1021/ja…

Additionally, with their dysregulation comes a predisposition to Amyotrophic Lateral Sclerosis.

As you are well aware, HIV's Tat really does a number on folks, in a number of ways. From a neurological standpoint, it contributes to reactive gliosis, microglial ferroptosis, excess CA2+ release, and cerebrovascular toxicity in the presence of amyloid deposits.

I don't have to tell you that it also contributes to ribosomal RNA biogenesis disturbances, like this.
SARS-CoV-2 targets ribosomal RNA biogenesis cell.com/cell-reports/f…

"Finally, the Tat protein of human immunodeficiency virus interacts with FBL and U3 snoRNA, impairing pre-rRNA processing and depleting mature ribosomes."

Reactive gliosis and neuroinflammation: prime suspects in the pathophysiology of post-acute neuroCOVID-19 syndrome ncbi.nlm.nih.gov/pmc/articles/P…

Synaptic Transport of Human Immunodeficiency Virus-Tat Protein Causes Neurotoxicity and Gliosis in Rat Brain ncbi.nlm.nih.gov/pmc/articles/P…

COVID-19 related neurological manifestations in Parkinson’s disease: has ferroptosis been a suspect? nature.com/articles/s4142…

HIV-1 Tat-mediated microglial ferroptosis involves the miR-204-ACSL4 signaling axis pubmed.ncbi.nlm.nih.gov/37023693/

SARS-CoV-2 Viroporin E Induces Ca2+ Release and Neuron Cell Death in Primary Cultures of Rat Hippocampal Cells Aged In Vitro mdpi.com/1422-0067/25/1…

"Highly infectious viruses such as the human immunodeficiency virus (HIV), Ebola virus, or hepatitis C virus encode proteins that function as ion channels."

HIV-1 Tat-Mediated Calcium Dysregulation and Neuronal Dysfunction in Vulnerable Brain Regions pubmed.ncbi.nlm.nih.gov/26028040/

How in the world did Kenneth Podell know a protein was operating mechanistically in the same way as HIV's Vpr, leading to an AIDS Dementia Complex diagnosis in the form of Lewy Body Dementia? Remarkable, to say the least.

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

"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."

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

HIV-1 Vpr protein impairs lysosome clearance causing SNCA/alpha-synuclein accumulation in neurons ncbi.nlm.nih.gov/pmc/articles/P…

Dementia with Lewy bodies after COVID-19 infection with catatonia: A case report onlinelibrary.wiley.com/doi/full/10.10…

HIV-1 Encephalopathy and Aids Dementia Complex ncbi.nlm.nih.gov/books/NBK50770…

Rough times ahead for those who drew parallels to ME/CFS, ignoring Asymptomatic Neurocognitive Impairment and allowing for what are AIDS Defining Illness, like TB, to present in children, of all people.

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

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

"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)."

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