• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

nk function increased 5 months after immunovir use stopped

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
Immunesupressed males used isoprinosine/immunovir at 3 grams a day for 28 days with effects last 5 months after treatment stopped.
Maybe it could be used like this one month on and one month off as an alternative to other dosing schedules.
http://ukpmc.ac.uk/abstract/MED/2452254/reload=0;jsessionid=JibJlLGwEw0Tkmt10qME.24
We have evaluated the immunomodulatory effects of isoprinosine in a double blind randomized clinical study on 63 immunosuppressed male homosexuals with persistent generalized lymphadenopathy (PGL) or ARC. The subjects received either placebo or isoprinosine at 1 or 3 g/day for 28 days. All subjects were monitored for performance for a one year period. In the 3 g/day treatment group clinical improvement was reported by 52% of the patients in contrast to 15% in the placebo group. Patients receiving 3 g/day isoprinosine showed significant increase in NK cells, a major subset of which bears the Leu 7 surface antigen, and in NK cell function as early as at the termination of treatment. This normalized NK cell property was still evident 5 months after cessation of therapy. Total T lymphocytes and T helper cells also increased in this group and a concomitant reduction was observed in activated T lymphocytes (HLA-DR+). As a direct result of the therapy an increase was found in the Th regulatory (Leu 3+ Leu 8+) cell population resulting in normalization of Th inducer/Th regulatory cell ratio. A concomitant reduction to normal range occurred in Ts effector (Leu 2+ Leu :cool: and functionally activated Ts (Leu 2+ HLA-DR+) cell populations. The kinetics of these effects suggest that isoprinosine stimulates the production of precursor lymphocytes and initiates a process of cell differentiation capable of producing long-term restoration of host immunity.

cheers!!!
 

currer

Senior Member
Messages
1,409
My ME consultant used to use immunovir for ME as he said there was clear evidence of immune abnormality.

It was used as an immunomodulator, not as and antiviral.
The medical information on this drug is here.
http://www.rivexpharma.com/pdf/Physician information package.pdf

Heapsreal you should look at this information, it explains in detail the pharmacological actions of this drug. It has widespread effects on the immune system. I cannot copy the relevant sections to thos thread, can someone else do this?
 

currer

Senior Member
Messages
1,409
I passed this information on to Dr Fluge who did the rituximab research, as I thought there may be a link between the underlying reasons for the effectiveness of both rituximab and immunovir in ME.

They both have an effect on the immune system and their effect in the body may cast a light on some of the pathological processes going on in this disorder.

In addition immunovir is much safer than rituximab.
 

currer

Senior Member
Messages
1,409
Interestingly immunovir inhibits viral RNA synthesis as well as having immunostimulatory effects.
It evokes a th1 response.
 

Seven7

Seven
Messages
3,444
Location
USA
I am on immunovir. The drug is very much use by Dr Klimas and Dr Ray, is used to raise NK cell. Not sure but she told me to raise my Tcell too. But for Sure NK cell.

You can build resistance to the drug so it has to be pulsed. Weekends off and take one month off very 6 months.
It does have its side effect. I get burning in all cavities if I do not drink A LOT of water (Bowel, eyes, vagina..). Also on days off, I get very sad ( I do not suffer from depression). The drug says you can develop Gout.So you should not use if you have gout or predisposition for gout.
 

Marg

Senior Member
Messages
343
Location
Wetumpka Alabama
I have not had any trouble with it. I take 500 twice a day and off weekends. I have noticed that some take a lot more. What is your dose Inester 7, just curious.
 

Seven7

Seven
Messages
3,444
Location
USA
week1 and 3 = 3 pills a day (500mg each)
Week 2 and 4 = 6 pills a day

weekends off. Take one month off every 6 months.
 

Marg

Senior Member
Messages
343
Location
Wetumpka Alabama
I think I will ask about taking more time off..The dose of two has never changed and stayed when we went over everything last May. I did not think to ask at the time. Unless becasue it is just 500 2x. It worked that way so I guess there must be a reason,I will want to know what it is the next chance I get.
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
Hi:It seems like there are many variations in how doctors prescribe this drug for CFS. I take six pills a day on odd weeks and 3 pills a day on even ones. But I have a month off every two months.

you spread your dosage throughout the day? on the 6 pills a day do u dose twice or 3 times ?
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
Heapsreal, you seem to be every experienced with this. Have you tried AHCC? If so, how would you rate that for effectiveness in increasing NK function as compared to any pharmaceuticals?
 

Rooney

Senior Member
Messages
185
Location
SE USA
Inosine, part of isoprinosine, was used by several doctors. Is it still considered equal or almost equal to this?
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
Heapsreal, you seem to be every experienced with this. Have you tried AHCC? If so, how would you rate that for effectiveness in increasing NK function as compared to any pharmaceuticals?
No to ahcc, on my list to try but is expensive to use the dosages used in studies 2000-3000mg aday?? but i am looking forward to using isoprinosine/immunovir.
I have only found one thing good for nk function that i can actually say worked but i was in a study on nk cell activity and not suppose to try and treatments like this but u know how it is. I used a russian interferon inducer(cycloferon) and this greatly increased my nk activity but not my bright cell activity that is shown to be the dysfunction they find in cfs/me. I had some partial good response from this and may add it soon in alternating cycles with immunovir, when my bank account looks healthy enough once more.
http://www.ncbi.nlm.nih.gov/pubmed/11220949
http://www.arbidol.org/27390604.pdf
http://portal1.democms.ru/resources/files/INSTRUCTION-for-Cycloferon-ampoules.pdf
http://portal1.democms.ru/resources/files/INSTRUCTION-for-Cycloferon-ampoules.pdf
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
Pharmacodynamics.
Cycloferon is a low-molecular-weight inducer of interferon, which defines
a wide range of its biological activities (antiviral, immunomodulating, anti-inflammatory,
antiproliferative, antineoplastic etc.) The medicine induces high titers of α- and β-interferon in
organs and tissues, containing lymphoid elements (mucous of small intestine, spleen, liver, and
lungs), and crosses the blood-brain barrier. Cycloferon is very competent at curing diseases
caused by viruses of tick-borne encephalitis, influenza, hepatitis, herpes, cytomegalovirus,
human immunodeficiency virus (HIV), and various enteroviruses. It amplifies the antibacterial
action of antibiotics used in therapy of acute enteric infection. The medicine acts as
anticarcinogenic and anti-metastatic drug, thus preventing the formation of tumors through the
activation of immune response in organism. Immunomodulating action of Cycloferon is
manifested both as activation of phagocytosis, of cytotoxic T-cells and natural-killer-cells and as
organism immune status correction at immunodeficiency disorders of different genesis.

INDICATIONS
In adults Cycloferon is recommended during combined therapy of:
-
herpes infections,

-
acute enteric infection,

-
chronic viral hepatitis B and C,

-
influenza and acute respiratory infections,

-
neural infections (aseptic (serous) meningitis, Lyme disease),

-
HIV infection (stages 2A-3B),

-
secondary immunodeficiency, associated with chronic bacterial and fungal

infections.

In children over 4 years old Cycloferon is recommended during combined therapy of:
-
acute and chronic hepatitis B and C,

-
herpes infections,

-
preventive treatment and therapy of influenza and acute viral respiratory

infections,
-
acute enteric infections,

-
combined therapy of HIV infection (stages 2-3B)


 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
cycloferon is used in a similar way to immunovir, to increase immune function.

Interferons (IFNs) are proteins made and released by host cells in response to the presence of pathogens such as viruses, bacteria, parasites or tumor cells. They allow for communication between cells to trigger the protective defenses of the immune system that eradicate pathogens or tumors.
IFNs belong to the large class of glycoproteins known as cytokines. Interferons are named after their ability to "interfere" with viral replication within host cells. IFNs have other functions: they activate immune cells, such as natural killer cells and macrophages; they increase recognition of infection or tumor cells by up-regulating antigen presentation to T lymphocytes; and they increase the ability of uninfected host cells to resist new infection by virus. Certain host symptoms, such as aching muscles and fever, are related to the production of IFNs during infection.
About ten distinct IFNs have been identified in mammals; seven of these have been described for humans. They are typically divided among three IFN classes: Type I IFN, Type II IFN, and Type III IFN. IFNs belonging to all IFN classes are very important for fighting viral infections.

Function
All interferons share several common effects; they are antiviral agents and can fight tumors.
As an infected cell dies from a cytolytic virus, viral particles are released that can infect nearby cells. However, the infected cell can warn neighboring cells of a viral presence by releasing interferon. The neighboring cells, in response to interferon, produce large amounts of an enzyme known as protein kinase R (PKR). This enzyme phosphorylates a protein known as eIF-2 in response to new viral infections; eIF-2 is a eukaryotic translation initiation factor that forms an inactive complex with another protein, called eIF2B, to reduce protein synthesis within the cell. Another cellular enzyme, RNAse L—also induced following PKR activation—destroys RNA within the cells to further reduce protein synthesis of both viral and host genes. Inhibited protein synthesis destroys both the virus and infected host cells. In addition, interferons induce production of hundreds of other proteins—known collectively as interferon-stimulated genes (ISGs)—that have roles in combating viruses.[4][5] They also limit viral spread by increasing p53 activity, which kills virus-infected cells by promoting apoptosis.[6][7] The effect of IFN on p53 is also linked to its protective role against certain cancers.[6]
Another function of interferons is to upregulate major histocompatibility complex molecules, MHC I and MHC II, and increase immunoproteasome activity. Higher MHC I expression increases presentation of viral peptides to cytotoxic T cells and natural killer cells, while the immunoproteasome processes viral peptides for loading onto the MHC I molecule, thereby increasing the recognition and killing of infected cells. Higher MHC II expression increases presentation of viral peptides to helper T cells; these cells release cytokines (such as more interferons and interleukins, among others) that signal to and co-ordinate the activity of other immune cells.
Interferons, such as interferon gamma, directly activate other immune cells, such as macrophages and natural killer cells.
Interferons can inflame the tongue and cause dysfunction in taste bud cells, restructuring or killing taste buds entirely

Virus resistance to interferons
Many viruses have evolved mechanisms to resist interferon activity.[11] They circumvent the IFN response by blocking downstream signaling events that occur after the cytokine binds to its receptor, by preventing further IFN production, and by inhibiting the functions of proteins that are induced by IFN.[12] Viruses that inhibit IFN signaling include Japanese Encephalitis Virus (JEV), dengue type 2 virus (DEN-2) and viruses of the herpesvirus family, such as human cytomegalovirus (HCMV) and Kaposi's sarcoma-associated herpesvirus (KSHV or HHV8).[12][13] Viral proteins proven to affect IFN signaling include EBV nuclear antigen 1 (EBNA1) and EBV nuclear antigen 2 (EBNA-2) from Epstein-Barr virus, the large T antigen of Polyomavirus, the E7 protein of Human papillomavirus (HPV), and the B18R protein of vaccinia virus.[13][14] Reducing IFN-α activity may prevent signaling via STAT1, STAT2, or IRF9 (as with JEV infection) or through the JAK-STAT pathway (as with DEN-2 infection).[12] Several poxviruses encode soluble IFN receptor homologs—like the B18R protein of the vaccinia virus—that bind to and prevent IFN interacting with its cellular receptor, impeding communication between this cytokine and its target cells.[14] Some viruses can encode proteins that bind to double-stranded RNA (dsRNA) to prevent the activity of RNA-dependent protein kinases; this is the mechanism reovirus adopts using its sigma 3 (σ3) protein, and vaccinia virus employs using the gene product of its E3L gene, p25.[15][16][17] The ability of interferon to induce protein production from interferon stimulated genes (ISGs) can also be affected. Production of protein kinase R, for example, can be disrupted in cells infected with JEV or flaviviruses.[12] Some viruses escape the anti-viral activities of interferons by gene (and thus protein) mutation. The H5N1 influenza virus, also known as bird flu, has resistance to interferon and other anti-viral cytokines that is attributed to a single amino acid change in its Non-Structural Protein 1 (NS1), although the precise mechanism of how this confers immunity is unclear.[18]
http://en.wikipedia.org/wiki/Interferon I know its a wiki link but still good info and stuff to look uo.
 

Seven7

Seven
Messages
3,444
Location
USA
Just as a side note, how much inosine and imunovir is used on CFS and we don't have more formal studies on it.
 
you spread your dosage throughout the day? on the 6 pills a day do u dose twice or 3 times ?
Hi Heapsreal:

Yes I do try to spread my dose out and take 2 pills with breakfast, 2 with lunch and 2 with dinner. Sometimes I forget my lunchtime dose and when this happens I try to take it as soon as possible and move my dinnertime dose to bedtime.

I did feel really bad on this medication for the first couple of months and was ready to give up on it because I thought it was making me worse not better. But my doctor persuaded me to keep going. I needed a lot of extra rest and days in bed because of flu-like symptoms and increased fatigue. But now after being on it for just over a year there has been such a huge improvement that I feel it has been one of the most effective treatments for my CFS.




you spread your dosage throughout the day? on the 6 pills a day do d

ose twice or 3 times ?
real, post: 295236, member: 187"]you spread your dosage throughout the day? on the 6 pills a day do u dose twice or 3 times ?[/quote]
 
Messages
43
Location
southwest USA
Just wondering if there are any other meds that can't be taken with this. I read that there are few interactions, so were the restrictions that were listed from the ME/CFS study just for control purposes? My main question would be antibiotics, plaquenil, or natural (very low dose) hydrocortisone (Isocort).