MAINTENANCE


WHY TREATMENT IS A MUST

If there is one thing virtually all experts agree on, it is that untreated HIV or FIV infection results in the progressive loss of CD4+ cells from the circulation as well as depletion of CD4+ cells from total body stores.

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UNTREATED FIV CAT

Eight-year observation and comparative study of specific pathogen-free cats experimentally infected with feline immunodeficiency virus (FIV) subtypes A and B: terminal acquired immunodeficiency syndrome in a cat infected with FIV petaluma strain.

J Vet Med Sci 1998 Mar;60(3):315-21 (ISSN: 0916-7250)

Kohmoto M; Uetsuka K; Ikeda Y; Inoshima Y; Shimojima M; Sato E; Inada G; Toyosaki T; Miyazawa T; Doi K; Mikami R...Department of Veterinary Microbiology, Graduate School of Agriculture and Life Sciences, University of Tokyo

Three specific pathogen-free cats experimentally infected with feline immunodeficiency virus (FIV) strains Petaluma, TM1 and TM2, respectively were observed for over 8 years. Without showing any significant clinical signs of immunodeficiency syndrome(AIDS) for 8 years and 4 months of asymptomatic phase, the Petaluma-infected cat exhibited severe stomatitis/gingivitis, anorexia, emaciation, hematological and immunological disorders such as severe anemia, lymphopenia, thrombocytopenia, and decrease of CD4/CD8 ratio to 0.075, and finally died with hemoperitoneum at 8 years and 8 months post-infection. Histopathological studies revealed that the cat had systemic lymphoid atrophy and bone marrow disorders indicating acute myelocytic leukemia (aleukemic type). etc etc

WHAT CAUSES CD4+ LOSS

In a recent article stated CD4+ primary loss is caused by continuous hyperactivation of the immune system as reflected by increase cell division.....Alternatively, it may be that the intrinsically low thymic output cannot compensate for the continuous loss of naive cells incurred by the increased priming of naive cells due to persistent immune activation, resulting in gradual depletion of CD4+ T cells without in fact exhaustion of thymic output.

Researchers discovered a portion of lymph nodes called the T cell zone is significantly damaged by chronic inflammation, which causes fibrosis.

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IMMUNE COMPLEX

AIDS is in part an autoimmune disease. The difference is FIV destroys the immune system. In FIV B-cells that produce antibodies don't work well because they go against a virus covered with (self) normal membrane which breaks self tolerance and induces autoantibodies. Dendritic cell APC creates immune complex between antigen and antibody which creates autoantibodies and inflammation. This increases diabetes, cancer and infections. WOBENZYM an enzyme supplement has been used against immune compexes which arise from combination of an antigen with an antibody from an antigen that was formed from the body itself.

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Collagen deposition in HIV-1 infected lymphatic tissues and T cell homestasis

Timothy W. Schacker, Phuong L, etc

....This procss of fibrosis leading to loss of tissue function is analogous to the parthogenesis of cirrhosis in chronic active hepatitis B and C infection, wherein ongoing viral replication in hepatocytes leads to a state of chronic inflammation and fibrosis. Over time, functional liver tissue is replaced by collagen, and the patient develops cirrhosis with all of its sequelae. In HIV-1 infection, secondary Lymphatic tissue (LT) become gradually replaced by collagen, leading to a gradual inability to maintain a population of CD4+ T cells.

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Neural-immune interactions in health and disease

Ann N Y Acad Sci 2002 Jun;966:20-7 (ISSN: 0077-8923

Eskandari F; Steinberg EM etc

Neuroendocrine regulation of immune function is essential for survival during stress or infection and to modulate immune responses in inflammatory disease. Glucocorticoids are the main effector endpoint of the neuroendocrine response system.

"The hypothalamus-pituitary-adrenal axis constitutes the most powerful circuit regulating the immune system...neuropeptides have a direct regulatory effect on lymphoid cells, regulating immune reactions by the stimulation of immunoregulatory hormones(glucocorticoids)."

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PET THEORY

Wall Street Joural article on Sepsis May 17, 2002 on Dr. Meduri use of steroids.

How Sepsis Can Occur

What happens when an infection invades the body and how it can lead to sepsis, using the example of a respiratory infection.

1. Bacterial products or other inflammatory agents enter the lungs, activating a protein called NFkB, NFkB stimulates the production of "fighting" proteins called cytokines.

2. These cytokines are sent into the bloodstream to organs. The resulting inflammation can kill bacteria, but if unabated, inflammation can turn into sepsis and threaten vital organs.

3. When cytokines reach the brain's pituitary gland, it releases a hormone called ACTH.

4. ACTH flows through the bloodstream and stimulates adrenal glands to produce a steroid called cortisol.

5. Cortisol attaches to cell proteins called glucocorticoid receptors, regulating the ability of NFkB to stimulate cytokine production. When the regulation doesn't occur properly, inflammation can spread, leading to sepsis. Dr. Meduri contends additional cortisol-like steroids can restart the normal process.

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For HIV and FIV disease: The HIV or FIV virus blocks the glucocorticoid receptor. The more receptors blocked, the more there is a short fall of cortisol for normal process, and the more steroid is needed to restart the normal process.

At some point with high viral load only a HIV drug can bring down viral load where steroid(Prednisolone) can again be used as long as there are enough receptors in T-cells. Which is why the needed low viral load and CD4 count greater than 200.

FIV gp120 causes release of CRH and AVP which causes adrenal insufficiency. Licorice root has shown to extend survival because it stimulates the bodies own glucocorticoid on infected HIV or FIV that have both good CD4 counts and low viral load.

NFkB is what decides whether to replicate the virus. In normal process it does not.

At the 9th Conference on Retroviruses and Opportunistic Infection Session 17 Symposium... T-Cell Turnover and Thymic Function... abtract S9, S10, S11, S12, S24.

HIV infection appears to result in hyperactivation, which results in increased rate of destruction of T cells. The lower T cell counts trigger feedback mechanisms which themselves become damaged by HIV infection and supply of new T cells dwindles resulting in overall decline of T cell counts over time.

Both Prednisolone and licorice root stimulate glucocorticosteroid which is immunosuppressive creates latency. It protects bone marrow by inhibiting cytokines which destroy stromal cells supporting the bone marrow. And protects the thymus tissue from damaging inflammation. This prevents the progression of FIV to AIDS.

END OF PET THEORY ___

ENDOCRINE INFO

"Unrecognized Endocrine-Immune Defects in Multiple Disease: An Effective Veterinary Model May Offer Therapentic Promise for Human Conidtions" by Alfred J. Plechner, 2002

For nearly three decades, the author has located multiple serious diseases of cats and dogs by correcting an unrecognized endocorine-immune imbalance originating with a deficiency or defect of cortisol. The cortisol abnormality creates a domino effect on feedback loops involving the hypothalamus-pituitary-adrenal axis. In this scenario estrogen becomes elevated, thyroid hormone becomes bound, and B and T cells become deregulated....Successful treatment and control, even in critical cases, have been consistently achieved with a long-term physiological (not pharmacological) replacement with cortisone.

Note: That excess estrogen (or testosterone) can decrease thyroid hormones because of imbalance originating with defect of cortisol. Ten percent of cats may require both thyroid and cortisol replacement. Therapy does not cure, but restores normalcy to a dysfunctional immune system. Comprehensive tests are not utilized routinely by veterinarians. They tend not to measure (cortisol, total estrogen, T-3, T-3, IgA, IgM, IgG) these levels and often prescribe steroids that may be too strong or not appropriate. This practice results frequently in side effects.

Reference: Cortisol and Immunity by William M. Jefferies...Medical Hypothese, 1991

Book, "Pets At Risk" Plechner

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Depletion of circulating natural type 1 interferon-producing cells in HIV-infected AIDS patients

Vassili Soumelis, Iain Scott, Fordous Gheyas, etc

Natural interferon-a producing cells (IPCs) are a newly characterized blood cell type, which is the major source of type I interferons in antiviral innate immune responses. The relationship between the number of circulating IPCs, HIV disease progression, and the occurrence of HIV-related complications was investigated. The study of 25 healthy donors and 54 HIV-infected subjects demonstrated a direct correlation between blood IPC number, interferon-a production, and clinical state of HIV-infected subjects. Asymptomatic long-term survivors had increased IPC number and function relative to uninfected controls and infected individuals with progressive disease. IPC numbers were markedly reduced in AIDS patients developing opportunistic infections and cancer. A negative correlation was found between the IPC number in the blood and HIV viral load, suggesting that IPCs are important in controlling HIV replication. This study provides the first evidence that IPCs are being affected during the course of HIV infection and suggests that these cells can play a vital role in the protection against opportunistic pathogens and cancer (Blood.2001;98:906-912)

An important part of the innate defense against virus is the production of the type I IFNs, IFN-a, and IFN-B. IFN-a/B not only directly inhibit HIV replication, but also have important adjuvant effects on a variety of immune cell types, such as monocytes, natural killer cells, and T cells. The in vitro type I IFN production by total peripheral blood mononuclear cells (PMBCs) was shown to be impaired during the course of HIV infection and this impairment was associated with the occurrence of opportunistic infections.

Reconstitution of Immune responses in patients with HIV-1 infection

Following effective ART, infected persons generally experience an increase in total CD4 cell count. The initial rise in circulating CD4 cells consists of an increased number of memory CD4 T cells, which is probably due to redistribution of cells previously trapped by the large amount of viral antigen in lymphoid tissue. Subsequently, there is a gradual increase in the number of circulating naive CD4 T cells, which may result from a combination of peripheral expansion as well as continued thymic production of T cells. In addition, ART decreases virus-induced immune activation. Diminished immune activation may lead to decreased activation-induced cell death of T lymphocytes. By reducing immunologic activation, ART may promote immune recovery.

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The Thymus and Immunologic Reconstitution

JAMA partial article

The extent to which the immune system can reconstitute itself during highly active antiretroviral therapy, or HAART, has profound implications for future HIV therapy. The immune system certainly recovers to some extent; the number of CD4 T cells begins to increase slowly as virus is suppressed. Whether the system can recover fully, even if only in some patients, perhaps with the aid of immunity-enhancing agents, is as yet unknown. But what is clear is that the degree of immunologic recovery achieved will largely, if not entirely, depend on the vitality and functional capacity of a patient's thymus, a most important component of the lymphoid system.

As they mature and undergo selection in the thymus many of the developing T cells display the CD4 molecule on their surfaces, which makes them targets for HIV. Like lymph nodes and other lymphoid tissues, the structure and function of the thymus can be disrupted by HIV infection, which impairs the capacity of the body to replace the CD4 cells killed by the virus.

However, strong evidence has emerged from both animals studies and clinical observations showing that this damage to the thymus is reversible, and that the organ recovers when HIV is suppressed by HAART. In fact, the slow upward creep in the numbers of naive T cells that is seen in patients who have been on HAART for a period of months almost certainly represents new emigrants from the thymus. Clearly, the thymus can begin to restore the T-cell repertoire when freed from the burden of HIV.

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RECONSTRUCTION

Dendritic cells can be infected by HIV-1, FIV and can result in depletion. DC from HIV-1 patients were reported to be functionally impaired with respect to T cell stimulation and cytokine production. Article "Dendritic cells and their role in HIV pathogenesis" explains dendritic cells. Since inhibition of DC also inhibits IL-12 this following article will be of interest

Restroation of HIV-specific cell-mediated immune responses by interleukin-12 in vitro

By M Clerici etc etc

Peripheral blood mononuclear cells (PBMCs) from many asymptomatic individuals infected with HIV-1 are unresponsive as measured by in vitro T cell proliferation and IL-2 production to influenza virus and synthetic peptides of HIV envelope. Strong influenza virus- and ENV-stimulated IL-2 responses and T cell proliferation were restored when cultures were stimulated in the presence of IL-12. Interferon-gamma production by PBMCs from HIV seropositive (HIV+) patients was also restored with IL-12. Furthermore, in vitro antigen-specific production of IL-2 and proliferation of PBMCs from HIV-donors were suppressed by antibody to IL-12, but were not enhanced by addition of exogenous IL-12. Thus, IL-12 may be limiting in PBMCs from HIV+ but not HIV- individuals. These findings demonstrate that IL-12 can restore HIV-specific cell-mediated immunity in vitro in HIV-infected individuals and suggest a potential use of IL-12 in augmenting the diminished immunologic functions associated with HIV infection

Agaricus and some other mushrooms stimulate IL-12. This should help the problem of poor functioning of T-cells.

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Medline Abstract: Med Hypotheses 1992 Aug;38(4):315-21 (ISSN: 036-9877)

Energy transformations in the biosynthesis of the immune system: their relevance to the progression and treatment of AIDS.

Tanner HA

Dysfunction of the immune system is observed in diseases where metabolic respiration is inhibited. Anabolites that enhance oxidative phosphorylation will provide the ATP essential for the biosynthesis of the cellular components and antibodies of the immune system. The induction of Coenzyme Q10 has been observed to protect against tumor growth and to enhance viral immunity in experimental animals. In a pilot study in AIDS patients the energy mediating catalyst elicited remarkable improvement. Additional cellular respiratory stimulants are considered as palliative synergists designed to enhance immunity in HIV infection. Competing antagonists to metabolic respiration acting to negate the effect of F delta in mediating optimal immune response to HIV are evaluated.

Biochem Biophys Res Commun 1991 Apr 30;176(2):786-91 (ISSN: 0006-291X)

Coenzyme Q10 increases T4/T8 ratios of lymphocytes in ordinary subjects and relevance to patients having the AIDS related complex.

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My vet uses a PET TAB which is new to me called "Felo-Form". I have seen it on the internet. Each tablet contains:

Amino Acids: Taurine - Min.4.5% 60mg

Minerals: Calcium 100mg, Phosphrus 50mg, Potassium 20mg, Iron 3mg, Zinc 1.25mg, Manganese 0.5mg, Copper 0.18mg, Cobalt 0.06mg, Iodine 0.05mg, Selenium 2mcg

Vitamins: Choline chloride 10mg, Niacin 5mg, Vitamin E 1IU, Thiamine mononitrate 0.5mg, Riboflavin 0.5mg, Vitamin A 750IU, D-Pantothenic acid 0.25mg, Vitamin B6 0.05mg, Folic acid 25mcg Vitamin D3 75IU, Vitamin B12 1.5mcg

Essential Fatty Acid: Vegetable oil Min. 1.0% 14mg

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LICORICE ROOT

Int Conf AIDS 1993 jun 6-11;9(1):234 (abstract no. PO-A25-0596)

Prophylactic effect of long-term oral administration of glycyrrhizin on AIDS development of asymptomatic patients.

Ikegami N; Akatani K; Imai M; Yosthioka K; Yano S

Clin Res. Inst., Osaka Nat. Hospital, Japan

Clinical effectiveness of glycyrrhizin (GL) by long-term oral administration to 16 asymptomatic HIV-1 carrier (AC) patients of hemophilia was studied. Glycyrrhizin is one of the biologically active compounds extracted from licorice roots. The immunomodulatory activity of GL has been already known. In this clinical study, asymptomatic patients of the treated group have received daily dose of 150-225mg of GL for 3 to 7 years. CD4+ and CD8+ T lymphocyte numbers, p24, p17 and Nef antibody levels, GL and glycyrrhetinic acid (GA) levels in sera were monitered. RESULTS: In the treated group neither progression of immunologic abnormalities nor development to AIDS has been seen. Orally administered GL was converted into GA which was detected in sera, without manifesting any side effect. Whereas, untreated patients showed the decreases in CD4+ and CD8+ cell counts and antibody levels. Two of them developed AIDS. It is concluded at present that long-term oral administration of GL to AC patients may be effective to delay or prevent their immunologic deterioration, and that an active component of GL in vivo appears to be GA.

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VITAMIN C, E

Effects of vitamin E and C supplementation on oxidative stress and viral load in HIV-infected subjects

AIDS 1998 Sep 10;12(13):1653-9 (ISSN: 0269-9370)

Allard JP; Aghdassi E; Chau J; Tam C; Kovacs CM; Salit IE; Walmsley SL

Department of Medicine, University of Toronto, Ontario, Canada.

OBJECTIVES: The HIV-infected population is known to be oxidatively stressed and deficient in antioxidant micronutrients. Since in vitro replication of HIV is increased with oxidative stress, this study assessed the effect of antioxidant vitamin supplementation on lipid peroxidation, a measure of oxidative stress, and viral load in humans. DESIGN: A randomized placebo-controlled, double-blind study. METHODS: Forty-nine HIV-positive patients were randomized to receive supplements of both DL-alpha-tocopherol acetate (800 IU daily) and vitamin C (1000 mg daily), or matched placebo, for 3 months. Plasma antioxidant micronutrient status, breath pentane output, plasma lipid peroxides, malondialdehyde and viral load were measured at baseline and at 3 months. New or recurrent infections for the 6-month period after study entry were also recorded. RESULTS: The vitamin group (n=26) had an increase in plasma concentratation of alpha-tocopherol (P greater 0.0005) and vitamin C (P greater 0.005) and a reduction in lipid peroxidation measured by breath pentane (P greater 0.025), plasma lipid peroxides (P greater 0.01) and malondialdehyde (P greater 0.0005) when compared with controls (n=23). There was also a trend towards a reduction in viral load (mean +/-SL) changes over 3 months, -45 +/-0.39 versus +0.50+/-0.40 log10 copies/ml; P=0.1;95% confidence interval, -0.21 to - 2.14) The number of infections reported was nine in the vitamin group and seven in the placebo group. CONCLUSION: Supplements of vitamin E and C reduce oxidataive stress in HIV and produce a trend towards a reduction in viral load. This is worthy of larger clinical trials, especially in HIV-infected persons who cannot afford new combination therapies.

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Inhibition of NF-kappaB-dependent transcription of human immunodeficiency virus 1 promoter by a phosphodiester compound of vitamin C and vitamin E, EPC-K1.

Immunopharmacology 1998 Mar39(1):31-8 (ISSN: 0162-3109)

Hirano F; Tanaka H; Miura T; Hirano Y; Okamoto K; Makino Y; Makino I

Second Department of Internal Medicine, Asahikawa Medical College, Nishikagura, Japan.

We investigated the effect of EPC-K1, which is a phosphodiester compound of vitamin E and vitamin C, on NF-kappaB activity in human cultured astrocytoma cells T98G. In TNFalpha-stimulated T98G cells, treatment with EPC-K1 nhibited oth DNA binding activity and transactivation of NF-kappaB in a dose-dependent manner, and the suppressive effect of EPC-K1 was stronger than either that of vitamin E or vitamin C. Moreover, we showed that in TNFalpha-stumlated T98G cells treatment with EPC-K1 repressed NF-kappaB-induced activation of the human immunodeficiency virus 1 promoter In contrast, THFalpha-induced activation of the human immunodeficiency virus 1 promoter was not completely inhibited by either treatment with vitamin E or vitamin C. We, thus suggest that EPC-K1 is considered to be one of the inhibitory agents of NF-kappaB.

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COLOSTRUM

Clin Investig 1992 Jul;70(7):588-94

Treatment of diarrhoea in human immunodeficiency virus-infected patients with immunoglobulins from bovine colostrum.

Rump JA, Arndt R, Bendick C, Dichtelmuller H, Franke M, Helm FB, Jager H, Kampmann B, Kolb P, et al

Abteilung Rheumatologic, Medizinische Universitats-Klinik Freiburg.

Diarrhoea and weight loss are found in more than 50% of patients with the acquired immunodeficiency syndrome (AIDS). In some patients the symptoms can be very severe, leading to death even in the absence of opportunistic infections. In 30% of these patients, enteric pathogens cannot be identified, and approximately only half of the identifiable aetiologic agents of diarrhoea in patients infected with the human immunodefiency virus (HIV) were treatable with antibiotics. Immunoglobulins from bovine colostrum (Lactobin, Biotest, Dreieich, FRG) contain high titers of antibodies against a wide range of bacterial, viral and protozoal pathogens as well as against various bacterial toxins. Lactobin (LIG) is quite resistant to 25-h incubation with gastric juice. In a multi-center pilot study 37 immunodeficiency patients with chronic diarrhoea [29 HIV-infected patients, 2 patients with common variable immunodeficiency (CVID), one unidentified immunodeficiency in five patients with graft versus host disease (GvHD) following bone marrow transplantation] were treated with oral LIG (10 g/day for 10 days). Good therapeutic effects were observed. Out of 31 treatment periods in 29 HIV-infected patients 21 gave good results leading to transient (10 days) or long-lasting (more than 4 weeks) normalisation of the stool frequency. The mean daily stool frequency decreased from 7.4 to 2.2 at the end of the treatment. Eight HIV-infected patients showed no response. The diarrhoea recurred in 12 patients within 4 weeks (32.4%), while 19 patients were free of diarrhoea for at least 4 weeks (51.3%). In 5 patients intestinal cryptosporidiosis disappeared following oral LIG treatment. LIG treatment was also beneficial in 4 out of 5 GvHD patients.

E-MAIL

Could you please tell me what I can do for my cat with FIV. He has had diarrhea with every movement that I can remember. Within recent months I have been giving him a diet supplement with garlic and brewers yeast and he has been wormed. Is there anything else I can add to his diet to help with diarrhea?

Thank you! ....

Have you taken the cat to the vet?

He may have Toxoplasmosis gondii. Tests are given by Colorado University 303 481-1274. This is treated using Antirobe Aquadrops (clindamycin hydrochloride liquid) manufactured by Upjohn-give 25mg orally twice daily until gone from bottle.

There will be a vitamin B12 deficiency. Colostrum has been used to treat Cryposporida. It will do away with the inflammation that is in the intestine. Diarrhea's most dangerous side effects are dehydration and the loss of essential minerals. Conventional veterinarians recommend electolyte replacement products. You can make your own with 2 cups water, 1 tablespoon unrefined sea salt, quarter teaspoon liquid colloidal trace minerals and half cup raw honey Use bottled water. Give this solution from a bowl, spoon or eyedropper, 1 tablespoon solution per five pounds of body weight every two or three hours.

Acidophilus supplements are important in restoring intestinal health and they help prevent and control diarrhea.

Get a copy of book "The Encylopedia of Natural PETCARE" by CJ Puotinen-Keats Publishing $19.95

Start treating the cat on instractions using PATENT NO. US5846961. One of the cats(Missy) had bloody diarrhea and dental problems.

For chronic diarrhea-A noninvasive evalution, including stooltest results (bacterial culture, parasite examination), should be initially performed.

You will have to work with your vet on FIV problem.

Printout PATENT NO. US5846961 and also my essay on the patent and give it to your vet.

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NALTREXONE

Naltrexone low dose that is used by Dr Bihari elevates endorphin in blood. But the trial done 15 years ago showed inconlusive results. Melatonin also increases endorphin.

Dr Bihari considers naltrexone as immune enhancing agent, endorphins the key hormones involved in the body's regulation of the immune system that regulate communication between the brain and the immune system.

Low dose naltrexone reduced alpha IFN, increased CRF production and beta-endorphin release in trial. Human dose is 4.5mg

COMMENT: Drug is likely to have similar results as Methinone Enkephalin

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Methinone Enkephalin Increases Immune cell Count by Nicholas P. Plotnikoff

Vaccine injection increases numbers of T cells and natural killer cells while reducing viral load in patients

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E-mail

August, received from pet owner that her cat Mary gained a pound and recently was retested. Cat is now FIV negative.

FIV not developing antibody suggests that the immune system is not seeing replicating virus. Treatment suggest a potent barrier to viral replication

My notes showed that I told her in February to use: Alpha Lipoic 50mg, Viola Clear Fire..one tablet, Melatonin 3mg, Vitamin E 400IU, Laktoferrin with colostrum one capsule, Milk thistle 75mg, Resveratrol synergy(Jarrow forumla) one tablet.

I was told mainly Resveratrol and Viola Clear Fire was used

Later CBC-Diff showed low WBC.

Told her to try to add alternating Prednisolone and Glycyrrhizinate Forte, also Coriolus to increase WBC

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COUNTS OF CD4+

From an experiment: Mean number of circulating CD4+ T lymphocytes in unvaccinated cats that became infected following cell-free challenge.

1200 0 months

1000 4

800 8 months

600 12

500 16

400 22

Once the cat has a CD4+ count of 200 or less opportunistic infections may show up. It is a good idea to keep track of CD4+ counts.

It is not enough to just inhibit the FIV, but also there is the need for a recovery of CD4+ counts.

Interleukin 2 (IL-2) boosts CD4 cell counts.

Korean Red Ginseng, Shiitake mushroom and Melatonin cause an increase of IL-2.


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