RNA/DNA Parasites
Alpha-Proteo Microbes
Endosymbiont
Symbiogenesis

Algae
Plastid
Protist
Amoeba
Amoeboid
Amoebozoa
Plasmodium
Myxosporea
Mycoplasma
Slime Mold
Nanobe
Prion

Chromosome Parasite
Parasitic Chromosome
B Chromosome
Hepatitis B
Selfish Genetic Element
Vertically Transmitted Infection

G6PD
Glucose-6-Phosphate Dehydrogenase
Hemolytic Anemia
Human Genetic Resistance to Malaria

Chromosome
Enzyme Catalyst

Cytosolic, Cytosol cytoplasmic matrix or groundplasm.

Genetic variation in human G6PD resulted from generations of adaptation to malarial infection.

Parasitic Chromosomes are often B chromosomes, such that they are not necessarily present in the majority of the species population and are not needed for basic life functions.

Parasitic chromosomes are classified as selfish genetic elements.

Supernumerary
Accessory
Conditionally
Dispensable
Lineage Specific

Human genetic resistance to malaria refers to inherited changes in the DNA of humans which increase resistance to malaria.

Proteomic Analysis of Haptoglobin and Amyloid A Protein Levels in Patients with Vivax Malaria

Cardiovascular complications from malaria include myocarditis.

X-linked genetic deficiency of G6PD makes a human prone to non-immune hemolytic anemia.

Modified F420-dependent G6PD is found in Mycoplasma Tuberculosis.

Common medications that may trigger G6PD-related hemolytic anemia include:

Chloroquine: an immunosuppressant and antimalarial drug

Colchicine: a gout medication

Diaminodiphenyl sulfone (Dapsone): an antibiotic and antimalarial drug

Vitamin K: a dietary supplement

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HIV
Tuberculosis (TB)
Malaria

The global epidemiology of HIV/AIDS and malaria overlap because a significant number of HIV-infected individuals live in regions with different levels of malaria transmission. Although the consequences of co-infection with HIV and malaria parasites are not fully understood, available evidence suggests that the infections act synergistically

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Human Genetic Resistance to Malaria:

G6PD Deficiency
Hemoglobin C/E/S
Haemoglobin Mutation
Beta Thalassemia
Sickle Cell Disease

Innate Resistance to HIV:

CCR5 deletion
TNPO3 mutation

..

The first line of defense against malaria is mainly exerted by abnormal hemoglobins and glucose-6-phosphate dehydrogenase deficiency. The three major types of inherited genetic resistance, sickle cell disease, thalassemias, and G6PD deficiency were present in the Mediterranean world by the time of the Roman Empire.

G6PD gene is located on the X chromosome and exhibits a high amount of variation (polymorphism), resulting in a range of G6PD activity from normal to severely deficient.

..

whats chances both disease pathways data will end up matching back up to the same place?

both CCR5/G6PD mutations appears to begin in Hematopoietic Stem Cells of Bone Marrow, that manufacturers White Blood Cells.

bone marrow is where both Mycoplasma & Candida hide dormant, Protist/Plastid is the suspect.

not the complete Protist/Plastid, but the smallest minimal genome that can misfold chromosomes from RNA to DNA.