PatientsLikeMe ™

MY STORY
Year 1996 viral load 6,200------- T-cells 375 had been infected for 6 months with fevers constantly I asked my doctor and other with HIV why are my T-cell so low with a very small viral load and why do I have a constant fever? This question I needed answered, and no doctor or anyone could tell me why.
Year 2003 viral load undetectable T-cells 605 had been on Protease inhibitors for 7 years now went from Crixavan to Nelfinavir cholesterol at 320 triglycerides at 600 I tried niacin at 500mg. 3 to 5 times a day to try and get my cholesterol and triglycerides down. I started a workout program on my new bowflex I got some amino acids at Orchard nutrition center; these were branched chain Liucine, Isoleucin, Valine and some L-Glutamine with some L-tryptophan. I took these amiono acids prior to my workouts that consisted of 50 minutes 3 days a week. August17th 2003 I was stung 6 times by what seemed to be bald faced hornets this seemed to improve my immune system greatly no more colds lasting 5 months just 3 days of low grade fever now. I had read many articles on the venom and how in many studies it had raised IL-2 in non allergic people. This may have accounted for the raise in T-cells.

HIV related loss of T cells and lymphocytes

People/With HIV, The normal path of Trytophan De novo synthesis is altered by indoleamine 2,3-dyoxygenase, Tryptophan is then changed in the kyunrenine pathway to Tryptophan 2,3-dioxygenase "aka TDO." Indoleamine 2,3-dioxygenase is the first and rate-limiting enzyme of tryptophan catabolism through kynurenine pathway, thus causing depletion of tryptophan which can cause halted growth of microbes as well as T cells. This not only will cause a tryptophan depletion, but niacin depletion as well. It is then this niacin depletion that interferes with NAD+ synthesis.

The normal path of Trytophan is changed to 5-Hydroxytryptophan (5-HTP), through hydroxylase, then 5-Hydroxytryptophan is decarboxylated to Serotonin by the enzyme aromatic amino acid (vitamin B-6) then is changed to Melatonin This reaction occurs both in nervous tissue and in the liver. Trytophan can also take the kynurenine pathway and convert to Niacin even when small amounts of Indoleamine 2,3-dioxygenase is present. This does not interfere with NAD+ synthesis.

With HIV integrase, PARP (Poly (ADP-ribose) polymerase) is needed for HIV integrase when elevated, The overactivation of PARP can deplete the stores of cellular NAD+ in T-cells and lymphocyets thus induce a progressive ATP depletion.ROS (reactive oxygen species) free radicals TNF-a, IFN-γ are also elevated with HIV causing cell damage.

As part of its DNA repair function, PARP consumes nicotinamide adenine dinucleotide (NAD) to make ADP-ribose polymers that covalently attach to nuclear proteins and add negative charge to areas of DNA damage. This drains the NAD+ pool, which may compromise the further repair of DNA. A major decrease in NAD+ levels also has serious consequences for mitochondrial function. Since NAD+ is an electron carrier in mitochondrial respiration and a source of reducing equivalents, it contributes to the maintenance of the redox state of mitochondria, the formation of the mitochondrial membrane potential and the generation of ATP. ATP is also consumed in the synthesis of NAD+ from NAM in an endogenous biochemical pathway to replenish the NAD+ consumed by PARP activity. A major drain on NAD+ pools would, therefore, eventually compromise energy production, resulting in the death of these cells.

Gaining immunity

I feel these findings of the essential amino acid Trytophan depletion if avoided, before, or during sero-convertion, the immune system would remain intact and capable of controlling HIV thus lowering viral loads by improving intercellular dendritic and T cells signaling during inflammatory processes and increase MIP-1α (Macrophage inflammatory protein-1 alpha) secretion.CCL3, also known as Macrophage inflammatory protein 1a (MIP-1α), is a cytokine belonging to the CC chemokine family that is involved in the acute inflammatory state in the recruitment and activation of polymorphonuclear leukocytes and defensins. The over expression of CCL3, can also down-regulate CCR-5 gene expression.

HIV can generate ROS (reactive oxygen species) free radicals, and can manipulate inflammatory cytokine patterns even with TNF-a, IFγ then induction of IL-10 and reduction of IL-2. This can cause a multi vitamin deficiency, by the generation more ROS. This vitamin deficiency then will cause an amino acid deficiency in two de novo synthesis pathways to suppress immune response protecting HIV then gaining control of CCR-5 expression. B-6 for example, has many tasks including dicarboxylatetion metabolism without this two de novo pathways will not work and become corrupted.

Vitamin B6 is well known in its bio chemically active form as pyridoxal 5'-phosphate, an essential cofactor of numerous metabolic enzymes. The vitamin is also implicated in numerous human body functions ranging from modulation of hormone function to its recent discovery as a potent antioxidant. B-6 is needed for both DOPA decarboxylase, for dopamine, and trytophan decarboxylation for Htp-5 serotonin and melatonin. With low amounts of B-6 we would have very little dopamine, trytophan would be lost by tryptophan catabolism along the kynurenine path-way with decreasedserotonin, and melatonin levels.

The De novo synthesis or pathways refers to the synthesis of complex molecules from simple molecules such as sugars or amino acids, as opposed to their being recycled after partial degradation.

STOPPING The HIV related loss of T cells and lymphocytes

I have found with 1/2 gallon of milk a day (containing 2.34% tryptophan) Whey protein, containing 300mg. L- tryptophan, 4 times a week, 300mg. niacinamide, 200mg. niacin and 200mg. of B-6 a day will correct this and will raise your T-cells with HIV. If this is not corrected, T-cell dysfunction due to essential amino acid depletion will lead to a domino like effect, the depletion of NAD+ via trytophan and niacin depletion, then the loss of NAD+ from PARP-1 induction, then NADH is lost because NAD+ has been lost, leaving little ATP to form in T cells and lymphocytes, these cells eventually compromise by energy loss, result in normal like cell death.