latent herpes fights bacteria

[Guest guest]

I have a better summary of this research on my office computer but

this study ended up suggesting that latent viral infections can help

kill off bacterial infections.

That said, my belief has been that our kids have a triangular

infection of virus, bacteria and fungus.

The only condition that kicks up underlying fungal infections after

antiviral treatment is AUTISM. I sometimes see it in chronic

fatigue and really sick adults but for the most part it is a unique

footprint of autism. This article supports that an underlying

smoldering virus might be holding bacteria and fungus at a lower

level... even though there could be a MAJOR infection.

This is why, in my opinion, we need to visualize these kids as

having several infections at the same time and treat them so. We

have way too many case reports of fungal flares from Valtrex when

used all by itself in autism and I have NEVER seen a recovery from

Valtrex all by itself. Only when used properly in a combination

strategy that includes antifungals (very specifically the ones I

mentioned) AND a bacterial and dietary (so critical) strategy

(typicaly I lean towards SCD).

I will be adding this study the conclusions to the antiviral

document.

Basically folks, in many cases, we need to kill off all the

infections to get these kids back.

And don't be suprised if we have more information on the topic than

the typical autism focused doctor. I see this mistake time and

again.

My best,

Stan

Herpes Infection May Help To Fight Off Some Bacteria

Main Category: Infectious Diseases / Bacteria / Viruses News

Article Date: 22 May 2007 - 12:00 PDT

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Mice with chronic herpes virus infections can better resist the

bacterium that

causes plague and a bacterium that causes one kind of food poisoning,

researchers report in this week's Nature.

Scientists at Washington University School of Medicine in St. Louis

attributed

the surprising finding to changes in the immune system triggered by

the

long-term presence of a latent herpes virus infection. In latent

viral

infections, the virus is present for the lifetime of the host in a

relatively

quiescent form that does not cause overt symptoms.

While presenting their results, researchers stressed that they did

not want to

minimize or in any way disregard the human suffering and health

risks caused by

disease-causing herpes infections. But they noted that several

strains of herpes

viruses found in much of the human population remain symptom-free

throughout the

host's lifetime.

" Our results suggest that we should look at whether humans receive

similar

advantages from these and other chronic infections that do not cause

active

disease, " says senior author Herbert W. " Skip " Virgin, M.D., Ph.D.,

head of the

Department of Pathology and Immunology. " If so, that has public

health

implications because we would want to very carefully weigh the risks

and

benefits of eliminating a virus that our bodies have established a

symbiotic

relationship with. "

Scientists previously used vaccination to eliminate the deadly and

highly

contagious smallpox virus. Vaccines are currently in use or in

clinical trials

for several disease-causing strains of herpes.

Human herpes viruses include oral and genital herpes, the chickenpox

virus,

cytomegalovirus, Epstein-Barr virus and Kaposi's sarcoma-associated

herpes

virus. During an initial period of acute infection, many of these

viruses cause

symptoms, such as fever, cold sores or blisters. They then enter

periods of

latency. Sometimes symptoms never recur; sometimes they flare up

periodically

before becoming quiescent again. In addition, less infamous herpes

viruses like

HHV6 and HHV7 permanently infect most humans without ever producing

any

significant symptoms.

The results have potentially wide-reaching implications for immune

research.

Humans and other mammals have spent millions of years living and

evolving with

latent viral infections, Virgin notes, and the new results imply

that infections

may have altered our immune systems at a fundamental level. This

could mean the

virus-free animal models scientists use to study vaccines,

autoimmune diseases,

and other immune system issues have the potential to produce

misleading results.

" Chronic virus infections may in part define what a normal human

immune response

is, " says Virgin, who is the Mallinckrodt Professor of

Pathology and

Immunology. " We may need to think about that as we consider the

implications

animal model results hold for human diseases. "

Scientists have recognized for years that many types of bacteria and

other

microorganisms live in the human gut to the advantage of both the

microbes and

their human hosts. The results from the Virgin lab are among the

first to

suggest the potential for symbiotic benefits from viral infections

that live in

areas beyond epithelial surfaces like the skin, throat or intestines.

For the new research, Virgin's group worked with strains of mouse

herpes virus

closely related to human Epstein-Barr virus, Kaposi's sarcoma-

associated herpes

virus and cytomegalovirus. During studies of how mouse herpes

viruses transition

from acute to latent infections, Virgin made a discovery that piqued

his

interest in the possibility that latent infections might confer

unrecognized

benefits.

" We found evidence that the mouse immune system controls latent

herpes

infections in part by increasing production of a protein hormone

called

interferon gamma, " Virgin says. " This is a signaling hormone that in

effect puts

some immune system soldiers on yellow alert, causing them to patrol

for invaders

with their eyes wide open and defense weapons ready. "

Other scientists previously had shown that interferon gamma helps

the immune

system fight off some strains of bacteria. This led Virgin and his

colleagues to

test herpes-infected mice with exposure to the bacteria Yersinia

pestis, which

causes plague, and Listeria monocytogenes, which is a minor cause of

food

poisoning and can infect the central nervous system. Many aspects of

Listeria

infection in mice are also similar to those that occur in humans

infected with

tuberculsis. They found that when mice had a latent herpes

infection, the

bacteria replicated more slowly and were less likely to kill the

mice.

When herpes was still in the acute phase of infection, no protective

effect was

present. When scientists exposed the mice to a mutant herpes virus

that can

infect but cannot establish latency, the herpes infection did not

confer

resistance. The protective effect could be produced by two different

mouse

herpes viruses.

" We have a good feel for who the main players are in this protective

effect, but

we need further research to better understand the exact mechanisms

that underlie

the process, " Virgin says.

He suspects that the virus may be prompting the immune system to

produce more

interferon gamma to keep itself from emerging from latency. If the

virus stays

latent, it prevents itself from seriously endangering the host and

can continue

to spread to new hosts from its current perch.

" We need to explore whether there are additional costs and benefits

to the host

from this, " Virgin says. " Are there additional pathogens that find

it harder to

come in as a secondary infection after herpes becomes latent " Do

other latent

infections convey similar protective effects " These are not the

kinds of

questions we're accustomed to asking about such infections, but our

findings

suggest that we need to start. "

Virgin notes that human and mouse herpes viruses are genetically

very closely

related. The similarity strongly suggests that modern herpes viruses

are likely

descended from herpes viruses that infected evolutionary ancestors

common to

both mice and humans.

" That means that for as long as we've been human, these viruses have

been with

us, " he says. " In that respect - given the millions and millions of

years that

mammalian immune systems have had to adapt to these viruses -

perhaps these

results are not as surprising as they might seem at first. "

----------------------------

Article adapted by Medical News Today from original press release.

----------------------------

Barton ES, White DW, Cathelyn JS, Brett-McClellan KA, Engle M,

Diamond MS,

VL, Virgin IV HW. Herpesvirus latency protects the host from

bacterial

infection: latency as mutualistic symbiosis. Nature, May 17, 2007.

Funding from the National Institutes of Health supported this

research.

Washington University School of Medicine's full-time and volunteer

faculty

physicians also are the medical staff of -Jewish and St. Louis

Children's

hospitals. The School of Medicine is one of the leading medical

research,

teaching and patient care institutions in the nation, currently

ranked fourth in

the nation by U.S. News & World Report. Through its affiliations with

-Jewish and St. Louis Children's hospitals, the School of

Medicine is

linked to BJC HealthCare.

Contact: C. Purdy

Washington University School of Medicine