Parasite Prevention-Cure with natural low cost high efficiency IUI Individual Universal Immunotherapy C-Life-IUI-CBM-SAV-SAS-SAT.
In-vivo/ex-vivo immune-regeneration system can eliminate/reverse harmful agents, including living organisms, pathogens like parasites, virus, fungus, bacteria, non-living threats as toxins and the effects of trauma or aging. Specialized antibodies and immune cells can eliminate and weaken parasites.
Parasites like Protozoa/Malaria generate Life abandonments of more than 600k/year, Schistozomose 200k and Ascaris Lumbricoides/ascariasis/round worms over 60k. Helminthiasis is an infestation of parasitic worms in human body, nematodes/roundworms, cestodes/tapeworms or trematodes/flukes.
Parasites, viruses, bacteria, fungi and other pathogens can attack the human body. These parasites include Protozoa and Helminths. Protozoa, single-celled organisms, cause diseases such as malaria, caused by Plasmodium and amoebiasis, caused by Entamoeba Histolytica.
Helminths are parasitic worms, including roundworms, tapeworms, flukes, that can cause diseases like schistosomiasis, caused by Schistosoma and ascariasis caused by Ascaris Lumbricoides. They can be eliminated in-vivo by antibodies/immune cells, such as IgE/Eosinophils, also supplemented ex-vivo.
MALARIA, Plasmodium Falciparum, protozoan parasite responsible for the most severe form, has a life cycle with different sizes. Sporozoites, the infectious form is injected by mosquitoes, 10-15/1 micro-meters length/diameter. Inside human body, grow/multiply in liver and produce merozoites 1.5/1mi-m.
Immune cells as macrophages/neutrophils engulf/destroy Plasmodium with phagocytosis. Antibodies as IgE can bind to the parasite, marking it for destruction by immune cells. Cytokine signaling molecules help also activate immune cells that kill the parasite.
CHAGAS Trypanosoma cruzi, parasite responsible for Chagas disease, employs several strategies to evade and inhibit the immune system. T. cruzi invades host cells and resides within a membrane-bound compartment called parasitophorous vacuole, helping it avoid detection by host immune system.
- cruzi uses antioxidant enzymes to protect itself from reactive oxygen and nitrogen within host cell, allowing it to survive phagolysosome environment. It expresses surface molecules like calreticulin, GP160 proteins, which disrupt/delays immune response Antibodies/Pathogen-Associated Molecular Patterns activated.
- cruzi stimulates immunoregulatory receptors, which further delays progression of protective immune response. It induces polyclonal B cell activation and hypergammaglobulinemia, leading to production of non-specific antibodies that are inefficient in controlling the infection.
- cruzi expresses multiple related epitopes, which complicates generation of specific neutralizing antibodies, it modulates macrophage activation, impairing their ability to control infection, allowing it to establish chronic infection, that can lead to severe cardiac/gastrointestinal/neurological complications.
+12000/year die from Chagas disease, around 30% with chronic Chagas disease develop cardiac complications, such as heart failure/arrhythmia/sudden cardiac death. If treated early is curable, but cases go undiagnosed until chronic phase. +28k/year new cases, +7M infected/year and +80M at risk of infection.
Initial/acute/lytic phase Lytic Antibodies as IgM are reactive to galactose epitopes on the parasite, can mediate the lysis of trypomastigote forms and are found at higher levels in patients with the indeterminate form of Chagas disease, suggesting a probable effective protective role.
But T.cruzi Antibodies that can stimulate the proliferation of T and B lymphocytes, which is crucial for mounting an effective immune response, may have a less effective role, as IgG via Helper-T cells and B-Cells suggesting a vulnerability/inefficiency that is exploited by the parasite to propagate.
CD4+ T Cells also known as Helper T cells play a role in immune response, including activation of B cells, macrophages and CD8+ T Cells, which is essential for controlling the infection by directly killing infected cells. T.cruzi parasite tends to evade Helper T/B cells, Macrophages and T-cells tend to remain inactivated.
Macrophages are involved in phagocytosing the parasite, presenting antigens to T cells and initiating adaptive immune response, but T. cruzi can modulate macrophage activation, impairing ability to control infection. Polyclonal B cell can be activated but lead to production of non-specific inefficient antibodies.
- cruzi could enter body and be taken up by macrophages, immune cells responsible for engulfing/destroying pathogens, but it can alter activation state of macrophages. M1 macrophages produce inflammatory cytokines and reactive oxygen to kill pathogens, M2 is involved in tissue repair and is anti-inflammatory.
- cruzi can induce a shift in macrophages towards the M2 phenotype, resulting in reduced production of pro-inflammatory cytokines and increased production of anti-inflammatory cytokines. As a result, macrophages become less effective at killing the parasite and more permissive to its survival.
CHAGAS CURE STRATEGY since in-vivo macrophages/Helper-T-cell/B-cells, IgG antibodies can be inefficient immune responses, but antigen-specific IgM antibodies and antigen loaded T-cells can be efficient, antigen loaded T-cells, D-cells and antigen specific IgM antibodies can be supplemented ex-vivo.
Macrophages are crucial for initial immune response, but T. cruzi can manipulate them to favor a less effective M2 anti-inflammatory state, reducing their ability to kill the parasite. T.cruzi induction of polyclonal B-cells activation can result in production of non-specific inefficient antibodies as IgG.
Ex-vivo activation and expansion of T-cells with specific antigens can enhance their ability to target and kill infected cells, potentially overcoming immune evasion strategies. Ex-vivo antigen-loaded T-cells can be a more precise and targeted immune response to treat Chagas disease and other infections.
- cruzi does not produce Prostaglandins but it can induce overproduction of PG2 series prostaglandins that are immunosuppressive to aid immune evasion. Blocking over production can improve immune response from Macrophages, Helper-T, B-Cells and IgG antibodies. Neutrophils/IgE could also be effective as in Malaria.
C-Life Cubic Cell Culture Life
C-Life can combine CBM, Cell Bank Medculture and IUI, Individual Universal Immunotherapy to create ex-vivo supplementation to the similar in-vivo process, but in a reduced space/time to increase efficiency and to eliminate harmful agent including parasites, adding efficient quantities/types.
IUI Individual Universal Immunotherapy
Immune cells are extracted from the patient and exposed to antigens or a small load of pathogens in a controlled environment outside the body. This process helps train immune cells to recognize and attack the pathogen, determining quantity/type that is most effective.
These trained immune cells are then activated and expanded in number to ensure a robust response when reintroduced into the body. The activated and expanded immune cells are infused back into the patient. These cells/antibodies are now better quantified/equipped to recognize/combat the pathogen.
In-vivo immune and regeneration system can eliminate parasites efficiently, given average space/time quantity/quality of antibodies/immune cells/stromal-stem cells versus pathogens/parasites, circumstantial to +95% efficiency. Under 5% may need complement of ex-vivo similar system.
The immune system produces several substances/proteins/cells to combat macro parasites, such as helminths parasitic worms, as Immunoglobulin E. IgE antibodies bind to the surface of the parasite and mark it for destruction by immune cells such as Eosinophils, Mast Cells and Basophils.
Granulocyte Eosinophils, white blood cells, are activated by IgE and release toxic granules that can damage or kill parasites. Mast Cells/Basophils also bind to IgE, release histamine/other chemicals that contribute to inflammation and help expel the parasite from the body.
Cytokines, signaling molecules, such as interleukins, IL-4, IL-5, IL-13, play a crucial role in coordinating the immune response against parasites. These substances and immune cells work together to identify, attack and eliminate macro parasites from the body.
Protective capsules/pills of IgE antibodies and Eosinophils could reach the intestines
via mouth, rectum suppository/catheter, vascular system via nano-intra-skin patch, sub-lingual pill, nasal spray for IgE antibodies or micro-intra venal for granulocyte Eosinophils, to attack parasites.
Malaria Plasmodium Falciparum developed strategies to evade the human immune system in-vivo, that can be countered ex-vivo to accelerate in-vivo response, as antigenic variation where the parasite changes proteins on its surface. Ex-vivo antigens/antibodies/cells can help recognize/target them.
After infecting red blood cells, Malaria Plasmodium parasite can hide inside them, shielding itself from direct attack by immune cells. But ex-vivo immune system can supplement red cells, cytokines, antibodies and immune cells, trained to identify intra/extra cell parasite phases.
Infected red blood cells can stick to uninfected ones and to walls of blood vessels, preventing their clearance by the Spleen, a key organ in filtering out infected cells. Ex-vivo immune system can supplement red cells, cytokines, antibodies, immune cells, trained to identify intra/extra cell parasites.
Inhibition of apoptosis by Malaria Plasmodium can prevent the programmed cell death of infected liver cells, allowing it to survive and multiply within the host. But ex-vivo immune system can supplement red cells, cytokines, antibodies and immune cells, trained to identify intra/extra cell parasite phases.
Natural individual antigens, antibodies, antigen loaded adaptive immune cells, innate immune cells can be prepared ex vivo, exposing them to an inferior load of pathogens, to then be re-introduced in-vivo to overwhelm the pathogens with a pre-tested efficient strategy in terms of quantity and quality/type.
CBM Cell Bank Medculture
Cultivating cells/proteins ex-vivo, replicating the in-vivo defense process, can increase efficiency against parasites, being more efficient than traditional artificial allopathic treatments that also have collateral effects. Biologic Medicine of Permanent Life is based on natural technology paradigm.
SAV Super Auto Vaccine
Malaria current vaccines target specific proteins on the parasite surface. Empirical efficacy and real world effectiveness/efficiency is proportional to the dosage/load of antigen/adjuvant leading to a proportional/higher immune response. Quantity, quality/type and coverage determine +80% efficiency.
Current malaria vaccines target the CircumSporozoite Protein (CSP) on the surface of the Plasmodium falciparum sporozoites, stimulating the immune system to produce antibodies that block the sporozoites from infecting liver cells. Immune cells help destroy infected liver cells.
SAS Super Auto Supplement
In addition to supplementing antibodies and antigen loaded immune cells, nano mRNAs intra-skin and micro/macro molecules/proteins/cells intra-venal can replicate proven in-vivo processes ex-vivo, to raise efficiency in eliminating parasites, avoiding low efficiency, collateral effect artificial treatments.
SAT Super Auto Test
Mescope, microfluid saliva, blood, urine, mucus, sweat, tear and fecal matter can identify parasites, proteins/antigens via photonic imaging of cell phone, accessory lenses and network HAI, Human Artificial Intelligent enlargement/analysis, complemented by mini testing in mini-laboratory.
