|Posted on June 15, 2021 at 10:35 AM|
Neurology & Stroke
Stealth Adapted Viruses – Possible Drivers of Major Neuropsychiatric Illnesses Including Alzheimer’s Disease
W John Martin
Institute of Progressive Medicine, South Pasadena, USA
Correspondence: W John Martin, Institute of Progressive Medicine, 1634 Spruce Street, South Pasadena, CA 913, USA, Tel 626-616-2868
Received: May 22, 2015 | Published: June 22, 2015
Citation: Martin WJ (2015) Stealth Adapted Viruses – Possible Drivers of Major Neuropsychiatric Illnesses Including Alzheimer’s Disease. J Neurol Stroke 2(3): 00057. DOI: 10.15406/jnsk.2015.02.00057
Mainstream neurologists and psychiatrists have largely refrained from serious consideration of a virus cause of common brain diseases. This is mainly because of the general lack of any accompanying immune system stimulated inflammatory reaction within the brain. This article exposes a weakness in this argument by describing the process of “stealth adaptation” of viruses. Deletion or mutation of relatively few virus components can result in derivative viruses, which are no longer effectively recognized by the cellular immune system. Consequently, there is no triggering of the inflammatory response. Furthermore, the brain is uniquely susceptible to symptomatic illness caused by stealth adapted viruses. An understanding of stealth adaptation greatly expands the potential scope of viral illnesses. It also underscores the value of using virus cultures as a diagnostic tool and of taking appropriate measures to avoid transmission of infection. More importantly, therapeutic measures are available for suppressing both stealth adapted and conventional virus infections through enhancement of the alternative cellular energy (ACE) pathway. Such measures are available for clinical evaluation in treating many of the major illnesses affecting the brain, including Alzheimer’s disease.
Keywords: Alzheimer’s disease; Neurology; Psychiatry; Cellular immunity; Immune evasion; Inflammation; Alternative cellular energy; ACE; Stealth adapted viruses; Herpes simplex virus; HSV; EnerceuticalsTM; KELEA; CFS; Chronic fatigue syndrome; Dementia; Encephalopathy
KELEA: Kinetic Energy Limiting Electrostatic Attraction; ACE: Alternative Cellular Energy; CFS: Chronic Fatigue Syndrome; CPE: Cytopathic Effect; HSV: Herpes Simplex Virus; SCMV: African Green Monkey Simian Cytomegalovirus; HCMV: Human Cytomegalovirus; CTL: Cytotoxic T Lymphocytes; CSF: Cerebrospinal Fluid; CPE: Cytopathic Effect; ALS: Amyotrophic Lateral Sclerosis; ACE: Alternative Cellular Energy; UV: Ultraviolet; ICE: Insufficiency of Cellular Energy
With the possible exception of cancer, diseases of the brain comprise most of the worst feared human aliments. Whether it is the increasing likelihood of autism occurring in children ; or Alzheimer’s disease occurring in the elderly , the current medical paradigms are failing to provide effective answers. Nor has significant progress been made in addressing many other tragic illnesses, such as schizophrenia, bipolar psychosis, Parkinson’s disease and amyotrophic lateral sclerosis (ALS). Society is further challenged by a range of somewhat less severe but still disabling illnesses, including chronic fatigue syndrome (CFS), fibromyalgia, depression, drug addiction, criminal behaviors and intellectual impairments affecting both learning and work performances.
Various investigators have suggested a possible infectious origin of several of the aforementioned neuropsychiatric illnesses [3-11]. Because of the absence of noticeable inflammation, however, it is usually argued that if infectious agents are indeed involved, their effects must be indirect and quite possibly delayed. For example, common infections occurring during pregnancy can clearly lead to elevated levels of various cytokines as part of the immune response. There are supporting data that maternal cytokines may significantly inhibit normal fetal brain development, with potential later life consequences [12-14]. Other researchers have suggested that certain infectious agents might potentially trigger the production of antibodies, which cross-react with neuronal components, thereby interfering with normal brain function. Such self-reacting antibodies may continue to form as part of an ongoing autoimmune process [15-17]. None of these scenarios envisions viruses as the direct cause of ongoing cellular injury...........
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