Tenofovir (Viread) / Raltegravir (Isentress) Cures ME/CFS Patient Sick for 20 Yrs + Tenofovir Poll

[IThinkImTurningJapanese]

Can you be more precise in your question. What is the "it" you are talking about?

"It" would be the beneficial effect.

Antiretroviral effects are antiviral effects. Antiretroviral means an antiviral effect against retroviruses.

That clears it up for me. I have been considering that ARV's may be inhibiting viruses rather than their benefit suggesting a retrovirus problem.

 

[Chugi]

Th2 to Th1 shifters listed in this post.

Sorry my english isnt very good...the products as listed are good for our condition?

 

[Hip]

the products as listed are good for our condition?

Only oxymatrine and azithromycin have been demonstrated to help ME/CFS. The others may theoretically help, but this is not proven.

 

[fingers2022]

Can you be more precise in your question. What is the "it" you are talking about?

Antiretroviral effects are antiviral effects. Antiretroviral means an antiviral effect against retroviruses.

Sorry, Hip, that's really confusing...sure retroviruses are a subset of viruses. I understand why ITITJ was asking the question - I think you've often posted to say that the beneficial effects of ARV's might be (specifically) due to their AV (i.e. not ARV) properties.

 

[fingers2022]

"It" would be the beneficial effect.



That clears it up for me. I have been considering that ARV's may be inhibiting viruses rather than their benefit suggesting a retrovirus problem.

I'm glad it clears it up for you! Not for me
Semantically, anything which is retroviral is also viral (by definition). BUT not vice-versa.
I thought you were on track asking for clarity on ARV or AV effect, and that Hip's response didn't clarify it.
In relation to HERV-K18 in previous post I think Hip was referring to a ARV effect, but in previous posts (not related to HERVs) the reference has been specifically to AV (NOT ARV effects).
Semantics for sure, but an important point.

 

[Hip]

@fingers
OK, I see what the question is getting at. But before I answer, let's just clarify some terms:

Antiviral is a general term for any drug or compound that directly inhibits viruses.

If you want to be specific and mention the particular type of viruses inhibited, then you might say anti-enteroviral (= an antiviral that inhibits virus from the enterovirus genus), anti-herpesviridae (= an antiviral that inhibits viruses from the herpes virus family) or antiretroviral (= an antiviral that inhibits viruses from the retrovirus family), etc.

Antiviral drugs or compounds will often have antiviral effects for a range of different viruses, rather than one virus. For example, the drug Epivir is antiviral for hepatitis B virus, as well as being antiviral for HIV.

Antiviral drugs and compounds can work by various mechanisms of action, such as for example preventing viruses from entering cells (viral entry inhibitions), or preventing them from replicating once they have entered a cell (viral replication inhibitors). You can see a list of the various mechanisms of action that antiviral may work by here.

In the case of antiretrovirals, different antiretroviral drugs work by different mechanisms of action. Tenofovir is a NRTI (nucleoside reverse transcriptase inhibitor), raltegravir is a INSTI (integrase strand transfer inhibitor). The different mechanisms of action that various antiretroviral drugs work are summarized here.



To complicate things further, antiviral drugs may also fight viruses not just by an antiviral mechanism of action, but also at the same time by an immunomodulatory mechanism of action. Immunomodulation means altering (= modulating) the functioning of the immune system. Some antiviral drugs, as well as being antiviral, also modulate the immune system in a way that increases the immune response against viruses, and this also serves to fight viral infections.

So if we take tenofovir, we know this has antiviral effects against HIV, against feline leukemia virus, and hepatitis B virus. An it is possible that tenofovir will also be antiviral for HERVs.

But tenofovir is also a potent immunomodulator (it potently inhibits the immune signaling molecule IL-10), and it is theoretically possible (though not proven) that this inhibition of IL-10 may stimulate the immune system to more fiercely fight enteroviruses (see this post for more info).

Raltegravir we know is antiviral for HIV, feline leukemia virus, murine leukemia virus, probably antiviral for HERVs, and has some antiviral effects against the some herpes family viruses.


So when we observe an ME/CFS patient improve while taking these tenofovir and/or raltegravir, it's not clear why. It could be because there is an unknown retrovirus in ME/CFS (perhaps in the murine leukemia virus family), or it could be because these drugs are suppressing HERVs in the body, or it could be because the immunomodulatory effects of tenofovir are fighting enteroviruses, or it might be because raltegravir has some antiviral effects against herpes family viruses.

Or it could be due to a combination of these factors (ie, these drugs may be fighting more than one virus at the same time in ME/CFS patients).
tenofovir anti-inflammatory

It's often the case that when a drug shows benefit for ME/CFS (or any other disease for that matter), it is not always easy to figure out why it works, because most drugs have multiple simultaneous mechanisms in the body, and more than one mechanism might be responsible for the beneficial effect of a drug.

 

[fingers2022]

@fingers
OK, I see what the question is getting at. But before I answer, let's just clarify some terms:

Antiviral is a general term for any drug or compound that directly inhibits viruses.

If you want to be specific and mention the particular type of viruses inhibited, then you might say anti-enteroviral (= an antiviral that inhibits virus from the enterovirus genus), anti-herpesviridae (= an antiviral that inhibits viruses from the herpes virus family) or antiretroviral (= an antiviral that inhibits viruses from the retrovirus family), etc.

Antiviral drugs or compounds will often have antiviral effects for a range of different viruses, rather than one virus. For example, the drug Epivir is antiviral for hepatitis B virus, as well as being antiviral for HIV.

Antiviral drugs and compounds can work by various mechanisms of action, such as for example preventing viruses from entering cells (viral entry inhibitions), or preventing them from replicating once they have entered a cell (viral replication inhibitors). You can see a list of the various mechanisms of action that antiviral may work by here.

In the case of antiretrovirals, different antiretroviral drugs work by different mechanisms of action. Tenofovir is a NRTI (nucleoside reverse transcriptase inhibitor), raltegravir is a INSTI (integrase strand transfer inhibitor). The different mechanisms of action that various antiretroviral drugs work are summarized here.



To complicate things further, antiviral drugs may also fight viruses not just by an antiviral mechanism of action, but also at the same time by an immunomodulatory mechanism of action. Immunomodulation means altering (= modulating) the functioning of the immune system. Some antiviral drugs, as well as being antiviral, also modulate the immune system in a way that increases the immune response against viruses, and this also serves to fight viral infections.

So if we take tenofovir, we know this has antiviral effects against HIV, against feline leukemia virus, and hepatitis B virus. An it is possible that tenofovir will also be antiviral for HERVs.

But tenofovir is also a potent immunomodulator (it potently inhibits the immune signaling molecule IL-10), and it is theoretically possible (though not proven) that this inhibition of IL-10 may stimulate the immune system to more fiercely fight enteroviruses (see this post for more info).

Raltegravir we know is antiviral for HIV, feline leukemia virus, murine leukemia virus, probably antiviral for HERVs, and has some antiviral effects against the some herpes family viruses.


So when we observe an ME/CFS patient improve while taking these tenofovir and/or raltegravir, it's not clear why. It could be because there is an unknown retrovirus in ME/CFS (perhaps in the murine leukemia virus family), or it could be because these drugs are suppressing HERVs in the body, or it could be because the immunomodulatory effects of tenofovir are fighting enteroviruses, or it might be because raltegravir has some antiviral effects against herpes family viruses.

Or it could be due to a combination of these factors (ie, these drugs may be fighting more than one virus at the same time in ME/CFS patients).
tenofovir anti-inflammatory

It's often the case that when a drug shows benefit for ME/CFS (or any other disease for that matter), it is not always easy to figure out why it works, because most drugs have multiple simultaneous mechanisms in the body, and more than one mechanism might be responsible for the beneficial effect of a drug.

Nope.
You are trying to obfuscate the discussion here.
Folk (like me) are taking ARVs because we think that ME may be caused by a retrovirus.
A retrovirus is a particular type of virus which, in my layman's terms integrates with RNA.
Enteroviruses don't do that. HHV variants don't do it either.
So, we have viruses and retroviruses, two main types, based on their lifecycle and replication processes.
ARVs specifically disrupt the RV replication cycle - yes, at different points.
Sure, ARV's may be effective against non-RV viruses, I get that, but a common or garden AV is unlikely to be effective against a RV.
Further, none of us really cares too much how this shit works, as long as we improve, and as long as side effects aren't too severe in terms of symptoms or collateral damage. However, it's important to get to the best understanding of what is really going on so that, as you have said, we make informed decisions. We can't make informed decisions if the communication is obfuscated like this my friend.

 

[Hip]

You are trying to obfuscate the discussion here.

You think that presenting various different possible explanations of why tenofovir may work for ME/CFS is obfuscation?

Folk (like me) are taking ARVs because we think that ME may be caused by a retrovirus.

That's the reason you are taking antiretrovirals, yes. But it may not necessarily be the reason antiretrovirals work for ME/CFS. Nothing wrong with what you are doing, nothing wrong with working on your assumption that an unknown retrovirus causes ME/CFS.

However, you retrovirus-theory people are not the only ME/CFS patients who are interested in using tenofovir or raltegravir. Patients with enterovirus infections might also find tenofovir interesting. And patients who believe that HERVs may play a role in ME/CFS may be interested in trying antiretrovirals for their ability to inhibit HERVs.

Or as you point out, there may be patients that have simply heard that tenofovir or raltegravir can help, and they are not too worried about why they help, but are more interested it seeing what these drugs can do for them.

That's my case: I am interested if tenofovir or raltegravir would work for me and other ME/CFS patients. But I would not put my eggs into just one basket in terms of how tenofovir or raltegravir work. At this stage, any of the explanations — retrovirus, HERVs, immunomodulatory effects against enteroviruses — all seem possible. Why would I choose just one theory and disregard the rest?

HHV variants don't do it either.

Actually HHV-6 does chromosomally integrate itself into human DNA. Hepatitis B virus also integrates into human chromosomes. It's not just retroviruses that insert their genes into human DNA. In any case, it does not really make much difference. Chromosomal integration is just one of several mechanisms that viruses use to set up long term latency states in human cells. But other viruses have just as effective techniques of turning a human cell into their permanent home.

 

[fingers2022]

You think that presenting various different possible explanations of why tenofovir may work for ME/CFS is obfuscation?





That's the reason you are taking antiretrovirals, yes. But it may not necessarily be the reason antiretrovirals work for ME/CFS. Nothing wrong with what you are doing, nothing wrong with working on your assumption that an unknown retrovirus causes ME/CFS.

However, you retrovirus-theory people are not the only ME/CFS patients who are interested in using tenofovir or raltegravir. Patients with enterovirus infections might also find tenofovir interesting. And patients who believe that HERVs may play a role in ME/CFS may be interested in trying antiretrovirals for their ability to inhibit HERVs.

Or as you point out, there may be patients that have simply heard that tenofovir or raltegravir can help, and they are not too worried about why they help, but are more interested it seeing what these drugs can do for them.

That's my case: I am interested if tenofovir or raltegravir would work for me and other ME/CFS patients. But I would not put my eggs into just one basket in terms of how tenofovir or raltegravir work. At this stage, any of the explanations — retrovirus, HERVs, immunomodulatory effects against enteroviruses — all seem possible. Why would I choose just one theory and disregard the rest?





Actually HHV-6 does chromosomally integrate itself into human DNA. Hepatitis B virus also integrates into human chromosomes. It's not just retroviruses that insert their genes into human DNA. In any case, it does not really make much difference. Chromosomal integration is just one of several mechanisms that viruses use to set up long term latency states in human cells. But other viruses have just as effective techniques of turning a human cell into their permanent home.

The way you talk about it seems to suggest that the whole concept of retroviruses is a red herring. Whatever disease we are talking about.
Is that the case with HIV?
OK I will stand down, as I'm out of my depth. Are you a (retro)virologist?
Think we need some input, but I'd still like some clarity on the communication. Is there no point differentiating retroviruses? Should we simply be talking about viruses? There is nothing special about a retrovirus then, because viruses not designated as retro still do the same things?
Now I'm TOTALLY confused.

 

[Hip]

The way you talk about it seems to suggest that the whole concept of retroviruses is a red herring.

I am not against a retrovirus theory, but I tend to look at things scientifically, and so at present, because there is little evidence of retroviral involvement in ME/CFS, my views reflect that. But let's say in one years time Ian Lipkin publishes new a study which finds stronger evidence of retroviruses, then I would update my opinions, and would be more prepared to agree that tenofovir likely helps ME/CFS by targeting retroviruses.

It would be the same if you were a detective in a criminal investigation: a detective will think the culprit is most likely the person with the highest amount of damning evidence that links them to the crime, not the person who is only vaguely and circumstantially linked to that crime.


I certainly would not want to put off or discourage anyone who was thinking of trying tenofovir or raltegravir from doing so. So if anyone thinks that ME/CFS might be caused by a retrovirus, and wants to try these antiretroviral drugs, I think that is well and good. Likewise, if they think tenofovir might help them fight enterovirus infections, that's another reason to try this drug. My view is that is that the more ME/CFS treatment you try, the more likely it will be that you find one that works for you.

Even if it turns out that ME/CFS is not caused by any retrovirus involvement, we would still be in debt to and grateful for the people that have pioneered the use of antiretrovirals in ME/CFS, as these people discovered that drugs like tenofovir can have a beneficial effect in ME/CFS.

 

[fingers2022]

I am not against a retrovirus theory, but I tend to look at things scientifically, and so at present, because there is little evidence of retroviral involvement in ME/CFS, my views reflect that. But let's say in one years time Ian Lipkin publishes new a study which finds stronger evidence of retroviruses, then I would update my opinions, and would be more prepared to agree that tenofovir likely helps ME/CFS by targeting retroviruses.

It would be the same if you were a detective in a criminal investigation: a detective will think the culprit is most likely the person with the highest amount of damning evidence that links them to the crime, not the person who is only vaguely and circumstantially linked to that crime.


I certainly would not want to put off or discourage anyone who was thinking of trying tenofovir or raltegravir from doing so. So if anyone thinks that ME/CFS might be caused by a retrovirus, and wants to try these antiretroviral drugs, I think that is well and good. Likewise, if they think tenofovir might help them fight enterovirus infections, that's another reason to try this drug. My view is that is that the more ME/CFS treatment you try, the more likely it will be that you find one that works for you.

Even if it turns out that ME/CFS is not caused by any retrovirus involvement, we would still be in debt to and grateful for the people that have pioneered the use of antiretrovirals in ME/CFS, as these people discovered that drugs like tenofovir can have a beneficial effect in ME/CFS.

Nice. But you conveniently ignored my point about whether retroviruses are anything special.

 

[fingers2022]

Poll results so far - summary:

33% chance of benefit
16% chance of regression
Big chance that folk don't think these odds are good enough.
WTF do you want people? A slow death?
Try ampligen or rituximab then...much better odds huh?
Alternatively, wait for Lipkin...he can milk the funding until he dies...you trust him?

 

[Hip]

But you conveniently ignored my point about whether retroviruses are anything special.

You edited your post, and I did not see that additional question. But to answer it:

OK I will stand down, as I'm out of my depth. Are you a (retro)virologist?
Think we need some input, but I'd still like some clarity on the communication. Is there no point differentiating retroviruses? Should we simply be talking about viruses? There is nothing special about a retrovirus then, because viruses not designated as retro still do the same things?
Now I'm TOTALLY confused.

I've no background in biology or medicine, and before I developed ME/CFS, I'd never even heard of HHV-6, Epstein-Barr virus, cytomegalovirus or coxsackievirus B. But not working for many years gave me a lot of time to read about this stuff, all in the hope of trying to find some answers and treatments for my ME/CFS. I don't claim to understand very much about biology or medicine, I've just picked up a few ME/CFS-related facts here and there.

There is nothing particularly special about retroviruses. I sometimes get the impression that all those AIDS public education adverts we saw in the 1980s put the fear of God into people about retroviruses, so that people think a retrovirus is something very sinister.

OK, HIV was a nasty virus (in the days before it could be treated with antiretrovirals), but if we take the closest relatives to HIV, a couple of retroviruses called HTLV-I and HTLV-II, these are endemic in certain countries (eg, Caribbean and Japan), but 99% of people who have HTLV in their body remain healthy throughout their lives, and never manifest any of the diseases HTLV can cause (one of the illnesses HTLV can cause is a ME/CFS-like disease, but it usually takes decades to slowly appear).

Whereas if you take enterovirus, this may be killing 90,000 people per year in the US alone through triggering heart attacks (see this post).

 

[Jenny]

Poll results so far - summary:

33% chance of benefit
16% chance of regression
Big chance that folk don't think these odds are good enough.
WTF do you want people? A slow death?
Try ampligen or rituximab then...much better odds huh?
Alternatively, wait for Lipkin...he can milk the funding until he dies...you trust him?

N=6 only.

 

[Jesse2233]

N=6 only.

Agreed we need more data. Would be good to get some patients of Drs Chia, Weir, and Deckoff-Jones to vote

 

[heapsreal]

Deckoff-Jones

I was in contact with her briefly about 12 months ago. From her experience and first hand she has heard from other drs and patients, she estimated 50% of cfsers improved on arvs, tenofovir was most used drug. The other 50% had no response. I think it shows that a proper diagnosis is hard to define.

 

[Jesse2233]

I was in contact with her briefly about 12 months ago. From her experience and first hand she has heard from other drs and patients, she estimated 50% of cfsers improved on arvs, tenofovir was most used drug. The other 50% had no response. I think it shows that a proper diagnosis is hard to define.

interesting, 50% is certainly a significant number

 

[heapsreal]

interesting, 50% is certainly a significant number

Yes and its possible it could be higher with a combination of arvs maybe?

Id really like to know more about Dr Montoya's patient research group that showed 85% had a retrovirus and why the specific retroviruses werent mentioned?

 

[Jesse2233]

Yes and its possible it could be higher with a combination of arvs maybe?

Id really like to know more about Dr Montoya's patient research group that showed 85% had a retrovirus and why the specific retroviruses werent mentioned?

Yea he was asked about that in an interview recently and I believe he mentioned he didn't think the findings were significant

Still, since Valcyte doesn't work for a large subset of patients, I wonder why he doesn't at least try ARVs on them (given his ID background)

 

[heapsreal]

Yea he was asked about that in an interview recently and I believe he mentioned he didn't think the findings were significant

Still, since Valcyte doesn't work for a large subset of patients, I wonder why he doesn't at least try ARVs on them (given his ID background)

I think he's been muzzled.