Re: Question for Dr. Goldberg and Elyse (microglial activation and antivirals)

[Guest guest]

,

I have recently been wondering the same thing about targeting microglial

inflammation!

There are several interesting studies on the subject:

1. www.medicalnewstoday.com/articles/123027.php

2. www.webmd.com/brain/news/20080519/can-celery-help-cut-brain-inflammation

3.

http://hmb300neurowiki.intodit.com/page/neuroinflammation-of-neurodegenerative-d\

iseases

4. http://www.bioquestinnovations.com/node/9/print

Amber S.

________________________________

From: <jrodrig6605@...>

nids

Sent: Wed, August 11, 2010 12:13:37 PM

Subject: Question for Dr. Goldberg and Elyse (microglial activation and

antivirals)

Dear Elyse and Dr. Goldberg,

I have a question that I believe it is very important regarding brain

inflammation, microglial activation and antiviral treatments.

We all know at least in this list that the herpesvirus 6 shows preference for

the temporal lobes. This can be seen in brain SPECT scans in children with

autism.

We also know that this kind of infections can cause microglial immune cell

activation as described by the study #2 below. We know the differences

between HSV encephalitis and HHV6 encephalopathy as described in the study #3

below. Now, the s Hopkins Medicine's

Brain's Immune System Triggered In Autism study (#7) provides evidence of

microglial activation and inflammation in the brains of individuals with autism.

The question that I have for you and I don't think it has been ever asked in

this list is the following. What medical approach do you follow

to reduce microglial activation in the brains of your patients during or after

antiviral treatment, see item 5 below? There are studies that provides

clear evidence that the microglial cells stay activated inducing inflammation

for years after the viral infection has been treated (See #5 and #6 below).

Regards,

1. Prolonged Microglial Cell Activation and Lymphocyte Infiltration following

Experimental Herpes Encephalitis

http://www.jimmunol.org/cgi/content/abstract/181/9/6417

2. Experimental murine herpes simplex virus (HSV)-1 brain infection stimulates

microglial cell-driven proinflammatory chemokine production which precedes the

presence of brain-infiltrating systemic immune cells.

The Journal of Immunology, 2008, 181, 6417 -6426

3. CT and MRI findings of human herpesvirus 6-associated encephalopathy:

comparison with findings of herpes simplex virus encephalitis.

http://www.ncbi.nlm.nih.gov/pubmed/20173155

CONCLUSION: Serial MRI showed transient abnormal signal intensity in the mesial

temporal lobes in patients with HHV-6 encephalopathy but persistent abnormal

signal intensity in both the mesial temporal lobes and the extratemporal regions

in patients with HSE. CT in the early period showed no abnormality in patients

with HHV-6 encephalopathy but definite abnormal findings in patients with HSE.

These differences may be useful in the differential diagnosis of the two

conditions.

4. http://en.wikipedia.org/wiki/Microglia

Herpes simplex virus (HSV) can cause herpes encephalitis in babies and

immunocompetent adults. Studies have shown that long-term neuroimmune activation

persists after the herpes infection in patients.[23] Microglia produce cytokines

that are toxic to neurons; this may be a mechanism underlying HSV-related CNS

damage. It has been found that " active microglial cells in HSV encephalitis

patients do persist for more than 12 months after antiviral treatment. " [23]

5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614272/

Prolonged Microglial Cell Activation and Lymphocyte Infiltration Following

Experimental Herpes Encephalitis

6. Microglia

http://en.wikipedia.org/wiki/Microglia

It has been found that " active microglial cells in HSV encephalitis patients do

persist for more than 12 months after antiviral treatment. "

7. Brain' Immune System Triggered in Autism by s Hopkins Medicine

http://www.hopkinsmedicine.org/Press_releases/2004/11_15a_04.html

[Guest guest]

,

There is a flaw in this line of questioning. HHV 6 , and HSV are only part

of this puzzle. Some kids do NOT have activation to HHV 6, or HSV 1 or 2 -

but do show reactivity to IGG tests for CMV and EBV (not IgM) which are not

included in the preface in your discussion. My son is one of these cases and

are profoundly difficult to treat. This does not mean that they have had or

been exposed to CMV or EBV. My son had very extensive viral studies for EBV

at UCLA's Dept of Pediatric Immunology at Dr G's suggestion and there was no

evidence ever of an EBV infection found - yet his EBV IgG and CMV IgG

levels remain high. While the references you cite are vital in our

understanding of this process, my experience suggests the issue is far more

complex than being about HHV 6 or HSV, and that we are dealing with

retroviruses and genetic viral mutations that have yet to be properly

studied.

_____

From: [mailto: ] On Behalf Of

Sent: Wednesday, August 11, 2010 12:14 PM

nids

Subject: Question for Dr. Goldberg and Elyse (microglial activation

and antivirals)

Dear Elyse and Dr. Goldberg,

I have a question that I believe it is very important regarding brain

inflammation, microglial activation and antiviral treatments.

We all know at least in this list that the herpesvirus 6 shows preference

for the temporal lobes. This can be seen in brain SPECT scans in children

with autism.

We also know that this kind of infections can cause microglial immune cell

activation as described by the study #2 below. We know the differences

between HSV encephalitis and HHV6 encephalopathy as described in the study

#3 below. Now, the s Hopkins Medicine's

Brain's Immune System Triggered In Autism study (#7) provides evidence of

microglial activation and inflammation in the brains of individuals with

autism.

The question that I have for you and I don't think it has been ever asked in

this list is the following. What medical approach do you follow

to reduce microglial activation in the brains of your patients during or

after antiviral treatment, see item 5 below? There are studies that provides

clear evidence that the microglial cells stay activated inducing

inflammation for years after the viral infection has been treated (See #5

and #6 below).

Regards,

1. Prolonged Microglial Cell Activation and Lymphocyte Infiltration

following Experimental Herpes Encephalitis

http://www.jimmunol.org/cgi/content/abstract/181/9/6417

2. Experimental murine herpes simplex virus (HSV)-1 brain infection

stimulates microglial cell-driven proinflammatory chemokine production which

precedes the presence of brain-infiltrating systemic immune cells.

The Journal of Immunology, 2008, 181, 6417 -6426

3. CT and MRI findings of human herpesvirus 6-associated encephalopathy:

comparison with findings of herpes simplex virus encephalitis.

http://www.ncbi.nlm.nih.gov/pubmed/20173155

CONCLUSION: Serial MRI showed transient abnormal signal intensity in the

mesial temporal lobes in patients with HHV-6 encephalopathy but persistent

abnormal signal intensity in both the mesial temporal lobes and the

extratemporal regions in patients with HSE. CT in the early period showed no

abnormality in patients with HHV-6 encephalopathy but definite abnormal

findings in patients with HSE. These differences may be useful in the

differential diagnosis of the two conditions.

4. http://en.wikipedia.org/wiki/Microglia

Herpes simplex virus (HSV) can cause herpes encephalitis in babies and

immunocompetent adults. Studies have shown that long-term neuroimmune

activation persists after the herpes infection in patients.[23] Microglia

produce cytokines that are toxic to neurons; this may be a mechanism

underlying HSV-related CNS damage. It has been found that " active microglial

cells in HSV encephalitis patients do persist for more than 12 months after

antiviral treatment. " [23]

5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614272/

Prolonged Microglial Cell Activation and Lymphocyte Infiltration Following

Experimental Herpes Encephalitis

6. Microglia

http://en.wikipedia.org/wiki/Microglia

It has been found that " active microglial cells in HSV encephalitis patients

do persist for more than 12 months after antiviral treatment. "

7. Brain' Immune System Triggered in Autism by s Hopkins Medicine

http://www.hopkinsmedicine.org/Press_releases/2004/11_15a_04.html

[Guest guest]

Hey ,

It is nice to hear from you, give me a call, we haven't chatted in a while.

I know there are several pathogens that can cause microglial activation that can

lead to brain inflammation (see #1 below). I used the HHV6 example, because

that is the one the viruses that Dr. Goldberg talks the most about.

My question was that regardless of what causes the microglial activation. What

medical approach do Dr. Goldberg follow to reduce microglial activation in the

brains of your patients during or

after antiviral treatment? There are studies that provide

clear evidence that the microglial cells stay activated inducing

inflammation for years after the viral infection has been treated.

I hope we get an answer to this question for the benefit of the children of

everybody in this list.

#1. In the link below read the following sections that lists the different kind

of pathogens that can cause microglial activation

http://en.wikipedia.org/wiki/Microglia#Role_in_viral_infections

a. Role in viral infections (including retroviruses like HIV)

b. Role in bacterial infections

c. Role in parasitic infections

Talk to you soon,

>

> ,

>

> There is a flaw in this line of questioning. HHV 6 , and HSV are only part

> of this puzzle. Some kids do NOT have activation to HHV 6, or HSV 1 or 2 -

> but do show reactivity to IGG tests for CMV and EBV (not IgM) which are not

> included in the preface in your discussion. My son is one of these cases and

> are profoundly difficult to treat. This does not mean that they have had or

> been exposed to CMV or EBV. My son had very extensive viral studies for EBV

> at UCLA's Dept of Pediatric Immunology at Dr G's suggestion and there was no

> evidence ever of an EBV infection found - yet his EBV IgG and CMV IgG

> levels remain high. While the references you cite are vital in our

> understanding of this process, my experience suggests the issue is far more

> complex than being about HHV 6 or HSV, and that we are dealing with

> retroviruses and genetic viral mutations that have yet to be properly

> studied.

>

>

>

>

>

>

>

> _____

>

> From: [mailto: ] On Behalf Of

>

> Sent: Wednesday, August 11, 2010 12:14 PM

> nids

> Subject: Question for Dr. Goldberg and Elyse (microglial activation

> and antivirals)

>

>

>

>

>

>

>

> Dear Elyse and Dr. Goldberg,

> I have a question that I believe it is very important regarding brain

> inflammation, microglial activation and antiviral treatments.

>

> We all know at least in this list that the herpesvirus 6 shows preference

> for the temporal lobes. This can be seen in brain SPECT scans in children

> with autism.

> We also know that this kind of infections can cause microglial immune cell

> activation as described by the study #2 below. We know the differences

> between HSV encephalitis and HHV6 encephalopathy as described in the study

> #3 below. Now, the s Hopkins Medicine's

> Brain's Immune System Triggered In Autism study (#7) provides evidence of

> microglial activation and inflammation in the brains of individuals with

> autism.

>

> The question that I have for you and I don't think it has been ever asked in

> this list is the following. What medical approach do you follow

> to reduce microglial activation in the brains of your patients during or

> after antiviral treatment, see item 5 below? There are studies that provides

> clear evidence that the microglial cells stay activated inducing

> inflammation for years after the viral infection has been treated (See #5

> and #6 below).

>

> Regards,

>

>

> 1. Prolonged Microglial Cell Activation and Lymphocyte Infiltration

> following Experimental Herpes Encephalitis

> http://www.jimmunol.org/cgi/content/abstract/181/9/6417

>

> 2. Experimental murine herpes simplex virus (HSV)-1 brain infection

> stimulates microglial cell-driven proinflammatory chemokine production which

> precedes the presence of brain-infiltrating systemic immune cells.

> The Journal of Immunology, 2008, 181, 6417 -6426

>

> 3. CT and MRI findings of human herpesvirus 6-associated encephalopathy:

> comparison with findings of herpes simplex virus encephalitis.

> http://www.ncbi.nlm.nih.gov/pubmed/20173155

> CONCLUSION: Serial MRI showed transient abnormal signal intensity in the

> mesial temporal lobes in patients with HHV-6 encephalopathy but persistent

> abnormal signal intensity in both the mesial temporal lobes and the

> extratemporal regions in patients with HSE. CT in the early period showed no

> abnormality in patients with HHV-6 encephalopathy but definite abnormal

> findings in patients with HSE. These differences may be useful in the

> differential diagnosis of the two conditions.

>

> 4. http://en.wikipedia.org/wiki/Microglia

> Herpes simplex virus (HSV) can cause herpes encephalitis in babies and

> immunocompetent adults. Studies have shown that long-term neuroimmune

> activation persists after the herpes infection in patients.[23] Microglia

> produce cytokines that are toxic to neurons; this may be a mechanism

> underlying HSV-related CNS damage. It has been found that " active microglial

> cells in HSV encephalitis patients do persist for more than 12 months after

> antiviral treatment. " [23]

>

> 5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614272/

> Prolonged Microglial Cell Activation and Lymphocyte Infiltration Following

> Experimental Herpes Encephalitis

>

> 6. Microglia

> http://en.wikipedia.org/wiki/Microglia

> It has been found that " active microglial cells in HSV encephalitis patients

> do persist for more than 12 months after antiviral treatment. "

>

> 7. Brain' Immune System Triggered in Autism by s Hopkins Medicine

> http://www.hopkinsmedicine.org/Press_releases/2004/11_15a_04.html

>

>

>

[Guest guest]

Yes , we learned via the Whittermore- institute several years ago

that the virus leaves a imprinto the brain after it is gone but the continuation

of treatment or change of meds is dependant on many variables NK cells, CD

counts, titers,lymps etc. It is different for each patient. It would be wrong

to tell you a general treatment.

Elyse

>

>

>

> Dear Elyse and Dr. Goldberg,

> I have a question that I believe it is very important regarding brain

inflammation, microglial activation and antiviral treatments.

>

> We all know at least in this list that the herpesvirus 6 shows preference for

the temporal lobes. This can be seen in brain SPECT scans in children with

autism.

> We also know that this kind of infections can cause microglial immune cell

activation as described by the study #2 below. We know the differences

> between HSV encephalitis and HHV6 encephalopathy as described in the study #3

below. Now, the s Hopkins Medicine's

> Brain's Immune System Triggered In Autism study (#7) provides evidence of

microglial activation and inflammation in the brains of individuals with autism.

>

> The question that I have for you and I don't think it has been ever asked in

this list is the following. What medical approach do you follow

> to reduce microglial activation in the brains of your patients during or after

antiviral treatment, see item 5 below? There are studies that provides

> clear evidence that the microglial cells stay activated inducing inflammation

for years after the viral infection has been treated (See #5 and #6 below).

>

> Regards,

>

>

> 1. Prolonged Microglial Cell Activation and Lymphocyte Infiltration following

Experimental Herpes Encephalitis

> http://www.jimmunol.org/cgi/content/abstract/181/9/6417

>

> 2. Experimental murine herpes simplex virus (HSV)-1 brain infection stimulates

microglial cell-driven proinflammatory chemokine production which precedes the

presence of brain-infiltrating systemic immune cells.

> The Journal of Immunology, 2008, 181, 6417 -6426

>

> 3. CT and MRI findings of human herpesvirus 6-associated encephalopathy:

comparison with findings of herpes simplex virus encephalitis.

> http://www.ncbi.nlm.nih.gov/pubmed/20173155

> CONCLUSION: Serial MRI showed transient abnormal signal intensity in the

mesial temporal lobes in patients with HHV-6 encephalopathy but persistent

abnormal signal intensity in both the mesial temporal lobes and the

extratemporal regions in patients with HSE. CT in the early period showed no

abnormality in patients with HHV-6 encephalopathy but definite abnormal findings

in patients with HSE. These differences may be useful in the differential

diagnosis of the two conditions.

>

> 4. http://en.wikipedia.org/wiki/Microglia

> Herpes simplex virus (HSV) can cause herpes encephalitis in babies and

immunocompetent adults. Studies have shown that long-term neuroimmune activation

persists after the herpes infection in patients.[23] Microglia produce cytokines

that are toxic to neurons; this may be a mechanism underlying HSV-related CNS

damage. It has been found that " active microglial cells in HSV encephalitis

patients do persist for more than 12 months after antiviral treatment. " [23]

>

> 5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614272/

> Prolonged Microglial Cell Activation and Lymphocyte Infiltration Following

Experimental Herpes Encephalitis

>

> 6. Microglia

> http://en.wikipedia.org/wiki/Microglia

> It has been found that " active microglial cells in HSV encephalitis patients

do persist for more than 12 months after antiviral treatment. "

>

> 7. Brain' Immune System Triggered in Autism by s Hopkins Medicine

> http://www.hopkinsmedicine.org/Press_releases/2004/11_15a_04.html

>

>

>