Re: ARBs & ACE inhibitors - INCREASES certain virus suseptibility

[Guest guest]

Barb, I'm replying because I think this could be very important. I

have not one but two chronic-active viral infections, and am certain

that many others who have had high-dose ARB therapy recommended to

them can say the same.

This is a good opportunity to demonstrate the principles that guide

me in evaluationg such information:

No, it doesn't cause me to tell Penny or others who are happy with

ARB treatment that they're making a misguided choice.

Yes, I do regard this as CRITICAL information for anyone

contemplating following their example.

The priniciple being: we don't question how individual patients

choose to relieve their suffering, but we insist on asking hard

questions when someone's chosen remedy is being promoted as

appropriate for others.

Cheers,

>

>

>

> I know that previously I posted that Losartan kept the herpes

simplex

> virus lock in the cells.. and posted the reference... SEE REF #1

> And we all thought that was a good thing...

>

> Well know it looks like the BO meds are selevtive in how they

handel

> INF alpga, beta and gamma.. and these drugs can cause a LATENT

virus

> (depending on the type of virus) to come OUT of Latency and cause

> disease and (death in the immunocompromised). ....SEE REF 2

>

> SEE REF for:

> Latency/Cytomeglovirus and INF gamma:

>

> http://mstp.wustl.edu/alumni/rachel_presti.html

>

> IT LOOKS TO ME LIKE IF YOU ARE TAKING HIGH DOSE ARBS or ACE

> (and experiencing what you think are viral infections) you may

want

> to read these and make your own conclusions.

>

> Barb

>

>

>

>

> Ref #1 ........................

> Life Sci. 1994;55(4):283-9.

> Effects of the angiotensin II receptor antagonist losartan on

herpes

> simplex virus-type 2 infection of cultured vero and cardiac

neonatal

> myocytes.

>

> Gardner PL, Mbuy GN, Knabb MT.

>

> Department of Biology, West Chester University, PA 19383.

>

> Previous studies indicate that captopril, an angiotensin II

> converting enzyme inhibitor, attenuates cardiomyopathy in a murine

> viral myocarditis model. Accordingly, we investigated the ability

of

> captopril as well as angiotensin II (AII) and losartan, a

nonpeptide

> AII receptor antagonist, to alter infection or replication of

herpes

> simplex virus- type 2 (HSV-2) in cultured cardiac and vero cells.

> Neither captopril nor AII influenced the ability of HSV-2 to

> replicate in either cell type. Losartan, however, caused a dose

> dependent decrease in pfu ability on vero cells with an ED50 of

1.35

> mM. In cultured myocytes, losartan (400 microM) reduced

significantly

> %LDH released (54.9 +/- 7.5 vs 29.1 +/- 4.2 in infected controls)

and

> % pfu released (40.9 +/- 8.4 vs 14.8 +/- 3.8 in infected controls)

> into the media.

>

> REF # 2 .........................................

>

> J Virol. 2002 Sep;76(18):9060-8.

> The antiviral response to gamma interferon.

>

> Costa-Pereira AP, TM, Strobl B, Watling D, Briscoe J, Kerr

> IM.

>

> Cancer Research UK London Research Institute, London WC2A 3PX,

United

> Kingdom.

>

> A role for alpha/beta interferon (IFN-alpha/beta) in the IFN-gamma

> antiviral response has long been suggested. Accordingly, possible

> roles for autocrine or double-stranded-RNA (dsRNA)-induced IFN-

> alpha/beta in the IFN-gamma response were investigated. Use was

made

> of wild-type and a variety of mutant human fibrosarcoma cell lines,

> including mutant U5A cells, which lack a functional IFN-alpha/beta

> receptor and hence an IFN-alpha/beta response. IFN-gamma did not

> induce detectable levels of IFN-alpha/beta in any of the cell

lines,

> nor was the IFN-gamma response per se dependent on autocrine IFN-

> alpha/beta. On the other hand, a number of responses to dsRNA [poly

> (I). poly©] and encephalomyocarditis virus were greatly enhanced

by

> IFN-gamma pretreatment (priming) of wild-type cells or of mutant

> cells lacking an IFN-alpha/beta response; these include the primary

> induction of dsRNA-inducible mRNAs, including IFN-beta mRNA, and,

to

> a lesser extent, the dsRNA-mediated activation of the p38 mitogen-

> activated protein (MAP) kinase(s). IFN-gamma priming of mRNA

> induction by dsRNA is dependent on JAK1 and shows biphasic

kinetics,

> with an initial rapid (<30-min) response being followed by a more

> substantial effect on overnight incubation. The IFN-gamma-primed

> dsRNA responses appear to be subject to modulation through the p38,

> phosphatidylinositol 3-kinase, and ERK1/ERK2 MAP kinase pathways.

It

> can be concluded that despite efficient priming of IFN-beta

> production, the IFN-alpha/beta pathways play no significant role in

> the primary IFN-gamma antiviral response in these cell-virus

systems.

> The observed IFN-gamma priming of dsRNA responses, on the other

hand,

> will likely play a significant role in combating virus infection in

> vivo.

>

>

>

>

>

>

> Pharmaceuticals

> The Virus That Took Down Tysabri

> Herper, 03.02.05, 6:00 AM ET

>

http://www.forbes.com/business/healthcare/2005/03/02/cx_mh_0301jcviru

s

> .html

[Guest guest]

I don't see this as a big deal. High dose ARBs do not eliminate inf-g.

They reduce high inflammatory levels down to near normal levels. Most

immune system pathways are still open and inf-g production can still

be stimulated from these other pathways. I saw nothing in the studies

to indicate that high levels are healthy, or that decreasing to normal

levels would increase viral infections.

Ken

[Guest guest]

I appreciate your perspective on this Ken, and it's something I've

been thinking about.

I most definitely have found myself much more susceptible to the

common cold virus (but no others) since Benicar therapy. Prior to

that, I hadn't had a cold in 10 years, which is pretty strange in

itself because Prior to THAT, before the CFS really took me down, I

had a cold at least every other month.

So what I've been wondering is if I'm unnecessarily worrying about the

possibility of viral susceptibility having increased with the Benicar,

or if perhaps my immune system is just working more like it would

normally. So I've had two colds in the last year. That's still a lot

better than I ever did before CFS.

These are important issues, IMO, and should be researched in much more

depth if ARBs are perhaps to become the future anti-inflammatories of

choice. My guess right now is the ARB manufacturers are just

scrambling to find out if they've got the same issues as the 2

inhibitors (which are all being pulled from the shelves due to heart

risks).

penny

> I don't see this as a big deal. High dose ARBs do not eliminate inf-

g.

> They reduce high inflammatory levels down to near normal levels.

Most

> immune system pathways are still open and inf-g production can still

> be stimulated from these other pathways. I saw nothing in the

studies

> to indicate that high levels are healthy, or that decreasing to

normal

> levels would increase viral infections.

>

> Ken