HHV-6 University

 From Perplexity A.I. Explain how backpropagation can be used to create a detailed chronological history of the mistakes made in AIDS research as discussed by Rebecca Culshaw on her Substack Backpropagation, when applied as an analytical framework rather than its strict AI algorithmic sense, can model and reconstruct the chronological history of systemic mistakes made in AIDS research by tracing how specific errors in hypotheses or methodology propagated through successive stages of scientific consensus, policy, and clinical practice. Rebecca Culshaw's approach uses mathematical modeling concepts—including error correction and network feedback—to show how flawed assumptions or data were reinforced, repeated, and amplified in HIV/AIDS research over decades. Conceptual Use of Backpropagation Backpropagation can be used metaphorically to examine how initial misjudgments or biases made in AIDS research created downstream effects that compounded errors across time. By treating each majo...

  Early- and Late-Stage Kaposi's Sarcoma-Derived Cells But Not Activated Endothelial Cells Can Invade De-Epidermized Dermis Early- and Late-Stage Kaposi's Sarcoma-Derived Cells But Not Activated Endothelial Cells Can Invade De-Epidermized Dermis - Journal of Investigative Dermatology Whether Kaposi's sarcoma is a true neoplasm or a reactive endothelial cell outgrowth triggered by inflammatory cytokines remains unclear. In this study, we investigated the differential invasive properties of activated endothelial cells and Kaposi's sarcoma cells in a model of de-epidermized dermis, supplying the cells with matrix barriers similar to those found  in vivo . Cells derived from early “patch-stage” and from late “nodular-stage” Kaposi's sarcoma lesions exhibited similar invasive properties, which indicates that cells with an invasive potential are present in the early stages of tumor development. Slow accumulation of the cells into the extracellular matrix, together with a ...

 

Shaking the Very Foundations of AIDS Orthodoxy : Kaposi's Sarcoma: Two studies of this condition pose a question once considered a heresy: What if HIV is not the cause of the epidemic? - Los Angeles Times

A paradigm shift within the field of HIV/AIDS research could be catalyzed by the critical issues raised in Rebecca Culshaw’s Substack and similar dissenting voices. Culshaw’s challenges to the scientific consensus—the proposition that HIV is not the definitive cause of AIDS—expose systemic vulnerabilities in how scientific dogma is established, maintained, and critiqued. Fundamental Critique of Scientific Consensus Central to Culshaw’s perspective is the assertion that consensus science can become dogmatic, suppressing dissent and marginalizing alternative explanations even when they are scientifically plausible. If HIV’s role as the unique causal agent of AIDS is discredited, the repercussions would extend far beyond infectious disease research. It would necessitate a retraction or reevaluation of countless scientific papers, funding priorities, and public health actions built around this singular hypothesis. Retractions and the Scientific Record A scenario where HIV is not the cause ...

  A scientific paradigm is built on foundational research that frames the field’s questions, interprets data, and sets methods for subsequent generations of practitioners. Unless the pivotal work on which a paradigm rests is formally retracted, it remains a "legitimate problem and solution" source, shaping teaching, research, funding, and institutional memory. Simply producing contradictory data does not erase the impact of the original paradigm; the old framework persists in the literature, is cited, and is used as justification for existing practices—even when anomalies mount. Paradigm Entrenchment and Retraction Paradigms are so entrenched that even dramatic new evidence is often “mopped up” or sidelined through ad hoc auxiliary hypotheses or reforms. When the bedrock work itself is publicly retracted, it signals to the entire research ecosystem that the old paradigm is no longer legitimate, prompting journals, institutions, educators, and policy-makers to revisit the basi...

When a disease is assigned a specific nosology—a formal classification that defines its characteristics, causes, and diagnostic criteria—it becomes difficult to shift the narrative even as new facts begin to undermine that classification. Nosology shapes medical understanding, treatment, and public perception, but it can also rigidify thinking, making the system slow to adapt when anomalies or contradictory evidence arise. AIDS and Nosological Inertia AIDS serves as a clear example. In the early 1980s, the CDC established a case definition for AIDS built around specific clinical presentations and immunologic markers, notably severe immunodeficiency and certain opportunistic infections in previously healthy individuals. The narrative quickly crystallized: AIDS was seen almost exclusively as a disease caused by HIV leading to profound immune suppression. Over time, this nosology—a tight linkage between HIV and the defined clinical syndrome—shaped diagnostic algorithms, drug trials, publi...

From Perplexity A.I. Even if Étienne de Harven was correct and HIV is actually an endogenous retrovirus rather than an exogenous infection, its reactivation in human cells could still have profound effects on the immune system, particularly if it acted as a superantigen. Endogenous Retrovirus Reactivation and Immune Disruption Human endogenous retroviruses (HERVs) are remnants of ancient viral infections integrated into the human genome. Normally, these elements are kept inactive through epigenetic mechanisms, but under conditions such as inflammation, cancer, or immune dysregulation, HERVs can become transcriptionally reactivated. When reactivated, HERVs can trigger immune responses by producing retroviral proteins and viral mimicry signals that activate innate immune pathways such as RIG-I, STING, and cGAS, promoting inflammation and sometimes chronic immune dysregulation. Retroviral Superantigen Function Some endogenous retroviral proteins—including those from certain HERV families—...

From Perplexity A.I. Multifactorial theories of disease, while aiming to describe the complex origins of many conditions, can easily transform scientific inquiry into a "wild goose chase" for endless contributory factors, undermining clear notions of causation and sometimes reducing it to absurdity. The Relentless Search for Factors Multifactorial models often imply that there is an inexhaustible list of minor genetic and environmental influences for any “complex disease,” making it nearly impossible to draw a boundary around what is relevant or mechanistically essential. Researchers are compelled to investigate expansive metabolic maps or networks, sometimes resulting in “spider web–like diagrams” that become so complex they seem arbitrary, and are interpreted with statistical methods that can feel akin to consulting a Ouija board rather than grounding findings in experiment. The more one seeks, the more variables are uncovered—each weakly associated, each potentially “inter...

 From Perplexity A.I.  There is strong evidence that the drugs used in treating AIDS—specifically long-term antiretroviral therapy (ART)—may themselves contribute to the development of comorbidities among people living with HIV. Mechanisms and Patterns Chronic exposure to ART increases risk for several age-related complications: cardiovascular disease, osteoporosis, renal dysfunction, liver disease, neurocognitive disorders, and metabolic syndromes. Known drug-toxicities include bone mineral loss (notably with tenofovir regimens), heightened myocardial infarction risk (with abacavir), and decreased kidney function (with tenofovir disoproxil fumarate). Many HIV drugs cause metabolic derangements (lipodystrophy, insulin resistance, hyperlipidemia) and have direct or indirect impacts on bone density and renal function, especially with decades-long use. Polypharmacy and Drug Interactions Because most HIV patients on ART have at least one comorbidity, they often require several add...

  Will this be the evolving standard of care for AID/CFS/autism? From Perplexity What anti-inflammatory treatments are now recommended in HIV care? The primary anti-inflammatory treatment recommended in HIV care is the early and continuous use of antiretroviral therapy (ART), which substantially reduces systemic inflammation and immune activation—though not to the levels seen in HIV-negative individuals. Among ART regimens, integrase strand transfer inhibitors (INSTIs) like bictegravir and dolutegravir have shown particular benefits in lowering inflammatory markers compared to some older regimens. In addition to ART, specific adjunctive anti-inflammatory therapies may be used in certain scenarios: Statins are under research and sometimes used to address inflammation and reduce cardiovascular risk in HIV-positive patients. Nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and indomethacin can help relieve mild inflammation or symptoms related to HIV, but must be used caut...

 From Perplexity A.I.  How has the consensus on immune activation in HIV changed clinical care? The shift in scientific consensus recognizing chronic immune activation and inflammation as central to HIV disease has substantially changed clinical care. Treatment is no longer focused solely on suppressing viral replication; clinicians now prioritize early antiretroviral therapy (ART), monitoring markers of inflammation, and managing non-AIDS comorbidities linked to immune dysregulation. Earlier Initiation of ART Understanding that chronic immune activation begins early in infection, guidelines now recommend starting ART as soon as possible, rather than waiting for CD4 counts to fall, to reduce inflammation and prevent irreversible immune system damage. Broadened Monitoring and Management Clinicians monitor not just viral load and CD4 counts but also inflammatory biomarkers (e.g., C-reactive protein, sCD14), recognizing their predictive value for cardiovascular, metabolic, and ne...

  Make the argument that HERVs need to be researched jointly with AIDS, CFS and autism. Researching HERVs in conjunction with AIDS, Chronic Fatigue Syndrome (CFS/ME), and autism is essential, as mounting evidence indicates that HERV activation contributes to pathogenesis and disease complexity across all three conditions. Joint investigation will enable deeper understanding of shared mechanisms, clarify diagnostic challenges, and may reveal new therapeutic strategies. Cross-Disease Pathogenic Mechanisms HERVs exert destructive effects in AIDS, CFS, and autism through immune dysregulation, chronic inflammation, neurotoxicity, and epigenetic instability, consistently implicating similar molecular pathways in disease progression. In each condition, abnormal HERV expression triggers maladaptive cytokine profiles and autoimmunity, suggesting a unified avenue for intervention targeting inflammation and immune modulation. Neurodevelopmental disruption and neuronal injury caused by HERVs a...

 Excerpt: Wainberg worked in Gallo's lab in Washington, DC, while on sabbatical from McGill in 1980. Two years later, the term "acquired immunodeficiency syndrome" would be coined to describe a mysterious new killer that seemed to target gay men. Gallo soon became one of the few biomedical researchers to achieve fame outside the scientific community when he was credited, along with Luc Montagnier of the Pasteur Institute in Paris, with the co-discovery of the human immunodeficiency virus. Gallo also led the first team to prove that HIV causes AIDS. It was one of the rare occasions in his professional life when Wainberg chose to back down. There have been other occasions when his tongue has got him into trouble. After the late journalist and author Nicholas Regush published a book called The Virus Within, pouring scorn on the belief that HIV causes AIDS, Wainberg was so furious that he told Maclean's magazine, " Regush is the equivalent of a murderer.  There are p...