Showing posts with label Bacteria. Show all posts
Showing posts with label Bacteria. Show all posts

Friday, 22 June 2018

Learning about Autism from the 3 Steps to Childhood Leukaemia

Special baby yoghurt to prevent childhood leukaemia, would quite likely also reduce the severity/incidence of some autism by permanently modulating the immune system.

Today’s post is about Leukaemia/Leukemia, another condition like autism, that is usually caused by "multiple hits".  It makes for surprisingly interesting reading for those interested in understanding autism.  
Leukaemia is a group of cancers that begin in the bone marrow and result in high numbers of abnormal white blood cells. Symptoms may include bleeding and bruising problems, feeling tired, fever, and an increased risk of infections. These symptoms occur due to a lack of normal blood cells.
Cancer research is making some great strides and, being English myself, I am pleased that some of the cleverest research is being carried out in England; the epicentre is the Royal Marsden Hospital/Institute of Cancer Research. Sadly, there is no such centre of excellence for autism research in England, or anywhere in Europe.  The best autism research usually comes from the US, Canada and increasingly China; the exception being bumetanide/NKCC1 research in France.  
Now straight to leukaemia and yoghurt.

Professor Mel Greaves from The Institute of Cancer Research, London, assessed the most comprehensive body of evidence ever collected on acute lymphoblastic leukemia (ALL) -- the most common type of childhood cancer.
His research concludes that the disease is caused through a two-step process of genetic mutation and exposure to infection that means it may be preventable with treatments to stimulate or 'prime' the immune system in infancy
The first step involves a genetic mutation that occurs before birth in the fetus and predisposes children to leukemia -- but only 1 per cent of children born with this genetic change go on to develop the disease.
The second step is also crucial. The disease is triggered later, in childhood, by exposure to one or more common infections, but primarily in children who experienced 'clean' childhoods in the first year of life, without much interaction with other infants or older children.
Acute lymphoblastic leukemia is particularly prevalent in advanced, affluent societies and is increasing in incidence at around 1 per cent per year.
Professor Greaves suggests childhood ALL is a paradox of progress in modern societies -- with lack of microbial exposure early in life resulting in immune system malfunction 

The same paradox applies to autism and is likely a big part of why medical autism is increasing in prevalence, once you adjust for some foolish doctors moving the goalposts of what is autism.

Here is another easy to read summary of what Professor Grieves is saying.

Our modern germ-free life is the cause of the most common type of cancer in children, according to one of Britain's most eminent scientists. 

Acute lymphoblastic leukaemia affects one in 2,000 children.
Prof Mel Greaves, from the Institute of Cancer Research, has amassed 30 years of evidence to show the immune system can become cancerous if it does not "see" enough bugs early in life. 
It means it may be possible to prevent the disease
Combined events
The type of blood cancer is more common in advanced, affluent societies, suggesting something about our modern lives might be causing the disease. 
There have been wild claims linking power cables, electromagnetic waves and chemicals to the cancer.  That has been dismissed in this work published in Nature Reviews Cancer
Instead, Prof Greaves - who has collaborated with researchers around the world - says there are three stages to the disease
§  The first is a seemingly unstoppable genetic mutation that happens inside the womb
§  Then a lack of exposure to microbes in the first year of life fails to teach the immune system to deal with threats correctly
§  This sets the stage for an infection to come along in childhood, cause an immune malfunction and leukaemia
This "unified theory" of leukaemia was not the result of a single study, rather a jigsaw puzzle of evidence that established the cause of the disease. 
Prof Greaves said: "The research strongly suggests that acute lymphoblastic leukaemia has a clear biological cause and is triggered by a variety of infections in predisposed children whose immune systems have not been properly primed."
Evidence that helped build the case included:
§  An outbreak of swine flu in Milan that led to seven children getting leukaemia
§  Studies showing children who went to nursery or had older siblings, which expose them to bacteria, had lower rates of leukaemia
§  Breastfeeding - which promotes good bacteria in the gut - protects against leukaemia
§  Lower rates in children born vaginally than by caesarean section, which transfers fewer microbes
§  Animals bred completely free of microbes developed leukaemia when exposed to an infection
This study is absolutely not about blaming parents for being too hygienic. 
Rather it shows there is a price being paid for the progress we are making in society and medicine. 
Coming into contact with beneficial bacteria is complicated; it's not just about embracing dirt. 
But Prof Greaves adds: "The most important implication is that most cases of childhood leukaemia are likely to be preventable." 
His vision is giving children a safe cocktail of bacteria - such as in a yoghurt drink - that will help train their immune system
This idea will still take further research. 
In the meantime, Prof Greaves said parents could "be less fussy about common or trivial infections and encourage social contact with other and older children".
Good germs
This study is part of a massive shift taking place in medicine. 
To date we have treated microbes as the bad guys. Yet recognising their important role for our health and wellbeing is revolutionising the understanding of diseases from allergies to Parkinson's and depression and now leukaemia.

Childhood Leukaemia Incidence is Rising

The overall prevalence of all types of leukaemia is about 1.5%.
Today we are just looking at one sub-type, acute lymphoblastic leukemia (ALL). It usually occurs in children aged 2 to 5 and if not treated promptly is fatal within a matter of months.
ALL is the most common type of childhood cancer. Approximately 3 of 4 children and teenagers who are diagnosed with leukemia are diagnosed with ALL. It is most common in children younger than 5, with most cases occurring between the ages of 2 and 4.
The prevalence of ALL is increasing while that of adult leukaemia is static.

While nobody ever talks much about it, ethnicity clearly is very relevant to autism incidence. It is not just about wealth and poverty; some ethnic groups are more prone to certain diseases than others. In the case of childhood leukaemia you have the most risk if you are a white Hispanic American.
In the case of autism, it looks to be parents who are Non-Hispanic White Americans who have the highest risk and if you are Jewish and high IQ the risk goes up further.

It is not all about genes
In about 10% of autism you can trace the cause back to a single miscreant gene, or entire chromosome, but for most autism it is much more complex.
For many genes, an error does not mean that a related dysfunction is guaranteed to occur it just makes you predisposed to that dysfunction. As we see with childhood leukaemia, most children with the miscreant gene never develop that cancer. Only 1% of all the children with the risk gene develop the cancer.  
This is one reason to be very careful opting to carry out Whole Exome Sequencing (WES), because you will likely discover genetic mutations that are associated with all kinds of possible conditions, but quite possibly none of the dysfunctions have, or will ever, occur in that person.
There are some genetic conditions that invariable do occur, but most often there are tell-tale physical signs. A short little finger (pinkie) is one I was discussing recently with someone, to help them narrow down a possible diagnosis.

Dr Grieves' full paper 
In this Review, I present evidence supporting a multifactorial causation of childhood acute lymphoblastic leukaemia (ALL), a major subtype of paediatric cancer. ALL evolves in two discrete steps. First, in utero initiation by fusion gene formation or hyperdiploidy generates a covert, pre-leukaemic clone. Second, in a small fraction of these cases, the postnatal acquisition of secondary genetic changes (primarily V(D)J recombination-activating protein (RAG) and activation-induced cytidine deaminase (AID)-driven copy number alterations in the case of ETS translocation variant 6 (ETV6)–runt-related transcription factor 1 (RUNX1)+ ALL) drives conversion to overt leukaemia. Epidemiological and modelling studies endorse a dual role for common infections. Microbial exposures earlier in life are protective but, in their absence, later infections trigger the critical secondary mutations. Risk is further modified by inherited genetics, chance and, probably, diet. Childhood ALL can be viewed as a paradoxical consequence of progress in modern societies, where behavioural changes have restrained early microbial exposure. This engenders an evolutionary mismatch between historical adaptations of the immune system and contemporary lifestyles. Childhood ALL may be a preventable cancer.  

Childhood acute leukaemia is the most common paediatric cancer in developed societies, accounting for  one- third of all cases, with a variable incidence rate of 10–45 per 106 children per year and a cumulative risk of ~1 in 2,000 up to the age of 15 years1. The most common paediatric leukaemia, acute lymphoblastic leukaemia (ALL), is an intrinsically lethal cancer, as evidenced by a universally adverse clinical outcome before effective therapy was developed. Currently, however, cure rates for ALL using combination chemotherapy are around 90%, making this one of the real success stories of oncology. While this is a cause for celebration, the current treatment remains toxic, traumatic for young patients and their families, and carries some long- term health consequences. It is unfortunate that we have remained ignorant as to the cause of ALL. The open question as to whether this cancer is potentially preventable is  therefore important.

Most cases of childhood ALL are potentially preventable. But how? Lifestyle changes including day care attendance or protracted breastfeeding in the first year of life can be advocated but would be difficult to achieve. A more realistic prospect might be to design a prophylactic vaccine that mimics the protective impact of natural infections in infancy, correcting the deficit in modern societies. Reconstitution or manipulation of the natural microbiome or helminth injections are strategies under consideration for early- life immune disorders in modern societies, including autoimmune and allergic conditions. Oral administration of benign synbiotics (bacteria species such as Lactobacillus spp. and oligosaccharides) can have profound and beneficial modulating effects on the developing immune system. The results of those endeavours might inform approaches for preventing BCP- ALL. Cross collaboration of scientists working in disparate fields of early- life immune dysfunction — allergy, autoimmune disease and ALL — would be beneficial.

Other modulators of risk in childhood aLL 
In addition to patterns of infectious exposure and inherited genetics, other factors are likely to contribute to multifactorial risk, including diet and chance. For acute lymphoblastic leukaemia (aLL) as well as acute myeloid leukaemia (aML) and most other paediatric cancers, risk is significantly and consistently elevated in association with higher birthweights or, possibly, accelerated fetal growth. a plausible interpretation of this link is that higher weight, possibly orchestrated via insulin-like growth factor 1 (iGF1) levels, may provide a greater number of cells at risk. iGF1 potentiates expansion of B cell lineage progenitors. Recently, evidence has been presented, using mouse models of aLL, that a restricted diet can have a risk- reducing impact. intermittent fasting was shown to block expansion of leukaemic cell populations and progression of disease. the effect operated via attenuation of leptin receptor expression on leukaemic cells, possibly enforcing differentiation. Diet or calorie intake may, therefore, have a modulating impact on risk of aLL, reinforcing the likely multifunctional nature of causation of aLL, as in cancer in general. random events or chance get short shrift in cancer epidemiology, but it has long been recognized that contingency and chance pervades all of biology. Some posit that a substantial number of cancers are due to chance alone, but this has been contentious. Chance is likely to be an ingredient in each and every cancer, including childhood aLL. this is because inheritance of risk alleles is a lottery at conception, because exposures including infections, at particular times, may or may not happen and because mutational mechanisms alter genes independently of their function.

Professor Grieves looks like my kind of academic/researcher. We came across another such one, Dr Peter Barnes, also English, who is known for translational research in asthma and COPD. What matters is applying/translating research, not making a good living publishing inconsequential research, editing a journal and being on the board of some charities. In the real world, results are what count.  
In the academic world it seems to be quantity of publications that matter.  I vote for quality over quantity.
Intestinal bacteria are clearly a fundamental part of human health, but to fully understand the implications will take many decades of research. Even today, we can see the critical importance of exposure to a wide range of bacteria very early on life and indeed during pregnancy.

Thursday, 17 August 2017

Viruses, Bacteria, Fungi, Parasites and Altered Gene Expression, Relevant to Autism

Today’s post started life as a review of how some viruses affect gene expression and may help cause, or just trigger flare-ups in, some neurological disorders ranging from autism to MS (multiple sclerosis). 
Some people with autism are treated with anti-viral drugs and, anecdotally, some do respond well.  This is not yet an area with hard facts and definitive clinical trials.  
It is actually better to first take a few steps back and consider how all microorganisms can play a role in human health by modifying the gene expression of the host (which is you).  There are four broad categories of microorganism.
Each type of microorganism can be countered by a matching category of pharmaceutical.

·        Antibacterials/antibiotics for bacteria

·        Antifungals to kill or prevent further growth of fungi

·        Antivirals to minimize (but often not eradicate) viruses

·        Antiparasitics to kill parasites  (protists)

All of the above categories of microorganism can affect the expression of multiple genes. By either up or down-regulating important genes at critical times during development, long lasting effects can be created, or there may be just transient effects.
Changes in gene expression likely play a role in many neurological conditions and in particular in what I call “flare-ups”, for example in autism, PANS, PANDAS and indeed schizophrenia.
Not all changes in gene expression are bad. The TSO parasites that do seem to help some people’s autism, by down regulating their immune response, very likely are modifying the host’s gene expression, which then reduces their immune response. This is the mechanism developed by the parasite to protect itself from the host (you) and ensure it is not eradicated.
Steroids affect the expression of multiple genes. When a bacteria of virus triggers PANDAS/PANS the positive effect of steroid therapy may well be by “resetting” the expression of certain important genes.  Here again, even though PANDAS/PANS is now treated clinically in the US, much remains unknown.
For those interested, earlier this summer revised treatment guidelines were published for PANDAS/PANS.

In "
Part I–Psychiatric and Behavioral Interventions," Margo Thienemann, MD, Stanford University and coauthors present consensus guidelines for treating the psychiatric and behavioral symptoms of children with PANS/PANDAS. Symptom improvement is aimed at decreasing suffering, improving functioning, and making it easier for the children to adhere to therapeutic interventions.

In "
Part II–Use of Immunomodulatory Therapies," Jennifer Frankovich, MD, and coauthors provide recommendations to help guide the use of therapies targeting the neuroinflammation and post-infectious autoimmunity that are common in PANS-PANDAS.

In “
Part III–Treatment and Prevention of Infections," Michael Cooperstock, MD, MPH, University of Missouri School of Medicine (Columbia) and coauthors representing the PANS PANDAS Consortium, present a consensus guideline for managing the infection components of these neuropsychiatric conditions.

There is research on what virus/bacteria affects which specific gene, but this area of science is in its infancy.
MS (Multiple Sclerosis) a condition that features faulty remyelination, is likely a much simpler condition than autism and yet nobody knows for sure what causes it. It has been suggested that a virus may be the trigger of at least some types of MS, but researchers are decades away from proving anything. So when it comes to microorganisms and autism, it is mainly a case of speculation and the odd N=1 case study. 

Viral triggers of multiple sclerosis 

The relationship between infections and autoimmune diseases is complex and the mechanisms by which infectious pathogens could trigger MS are likely dynamic, i.e., they might change over time and not be mutually exclusive. Epidemiological observations indicate that viral infections could contribute to MS development not only as triggers of disease exacerbations but also as etiological agents, i.e., long before the disease becomes clinically apparent. The two- to three-folds increased risk of developing MS among individuals with history of IM compared with subjects who acquired EBV without symptoms, the almost universal seropositivity for EBV in adults and children with MS, and the steep and monotonic increase in MS risk with increasing titers of antibodies to EBV in apparently healthy adults could suggest that EBV infection is causally linked to MS development. The mechanisms responsible for this association are far from understood. Moreover, the incidence of IM in Western countries (≥ 5%)  exceeds the prevalence of MS in comparable populations (0.1%) by far (more than 50-fold) suggesting that yet unidentified genetic and/or additional environmental factors determine whether symptomatic EBV infection indeed predisposes to MS.

Although one particular MS-causing agent might still be discovered, current data suggest that multiple infections along with noninfectious environmental factors trigger the development of MS. These factors are likely ubiquitous, i.e., highly prevalent in the general population, and they require a permissive genetic background that predisposes for MS development. Future studies investigating infectious pathogens in a complex and heterogenous disease such as MS will benefit from careful and detailed clinical, pathological, and neuroimaging-based patient characterizations and from reproducibility in different study populations. In addition, novel humanized animal models of autoimmune diseases that are simultaneously permissive for viral pathogens which usually infect only humans  should allow investigation of specific aspects of host–pathogen interactions during autoimmune CNS inflammation in vivo. The integration of these data might eventually allow us to better define the role of viruses in the etiology and pathogenesis of MS and how virus–host interactions could be targeted for MS therapy.  

The ubiquitous human herpesvirus 6 may play a critical role in impeding the brain's ability to repair itself in diseases like multiple sclerosis. These findings may help explain the differences in severity in symptoms that many people with the disease experience
What is still not fully understood is the relationship between the extent of the viral infection in the brain and the severity of diseases like multiple sclerosis and other demyelinating diseases such as leukodystrophies and Vanishing White Matter disease. For example, do the number of infected cells need to reach a certain threshold before OPC function is impeded? Are individuals who have congenital HHV6 more vulnerable to severe forms of these diseases?
"More research is needed to understand by which mechanisms the virus impedes the function of OPCs and what impact this has on the progression of these diseases," said Mayer-Proschel. "But it is clear that HHV6, while not necessarily the cause of demyelinating diseases, is limiting the ability of the brain to repair damage to myelin thereby potentially accelerating the progression of these diseases."  

Mainstream and “Alternative” Research  
Not all published research fits with the current mainstream scientific consensus. The mainstream is clearly moving towards the realization that all kinds of things can affect gene expression. One currently fashionable area is the gut microbiota, as in this article:-

Some researchers develop hypotheses that go much further, like this one regarding autism’s elder brother, schizophrenia.

Many genes have been implicated in schizophrenia as have viral prenatal or adult infections and toxoplasmosis or Lyme disease. Several autoantigens also target key pathology-related proteins. These factors are interrelated. Susceptibility genes encode for proteins homologous to those of the pathogens while the autoantigens are homologous to pathogens' proteins, suggesting that the risk-promoting effects of genes and risk factors are conditional upon each other, and dependent upon protein matching between pathogen and susceptibility gene products. Pathogens' proteins may act as dummy ligands, decoy receptors, or via interactome interference. Many such proteins are immunogenic suggesting that antibody mediated knockdown of multiple schizophrenia gene products could contribute to the disease, explaining the immune activation in the brain and lymphocytes in schizophrenia, and the preponderance of immune-related gene variants in the schizophrenia genome. Schizophrenia may thus be a “pathogenetic” autoimmune disorder, caused by pathogens, genes, and the immune system acting together, and perhaps preventable by pathogen elimination, or curable by the removal of culpable antibodies and antigens.

And this one by the same author:-

Herpes simplex virus 1 (HSV-1) can promote beta-amyloid deposition and tau phosphorylation, demyelination or cognitive deficits relevant to Alzheimer's disease or multiple sclerosis and to many neuropsychiatric disorders with which it has been implicated. A seroprevalence much higher than disease incidence has called into question any primary causal role. However, as also the case with risk-promoting polymorphisms (also present in control populations), any causal effects are likely to be conditional. During its life cycle, the virus binds to many proteins and modifies the expression of multiple genes creating a host/pathogen interactome involving 1347 host genes. This data set is heavily enriched in the susceptibility genes for multiple sclerosis (P = 1.3E-99) > Alzheimer's disease > schizophrenia > Parkinsonism > depression > bipolar disorder > childhood obesity > chronic fatigue > autism > and anorexia (P = 0.047) but not attention deficit hyperactivity disorder, a relationship maintained for genome-wide association study data sets in multiple sclerosis and Alzheimer's disease. Overlapping susceptibility gene/interactome data sets disrupt signalling networks relevant to each disease, suggesting that disease susceptibility genes may filter the attentions of the pathogen towards particular pathways and pathologies. In this way, the same pathogen could contribute to multiple diseases in a gene-dependent manner and condition the risk-promoting effects of the genes whose function it disrupts.

Back to Autism
As we have seen previously in this blog, autism is usually polygenic, meaning very many different genes are affected. This does not mean that anything is necessarily defective in those genes, it just means those genes are either over or under-expressed, this means you end up with either too much, or too little, of whatever that gene makes.
So for a polygenic condition, where in one person hundreds of your 22,000 individual genes are likely over or under-expressed, we really do not want anything to come along and further miss-express critical genes.
Many genes are inter-related and so miss-expression of one can trigger a wave of further effects. This can be either good or bad.
The science is still in its infancy, so it will be many decades before it is translated into medicine, but we can certainly already say what may be happening.
The interactome is a relatively new word to describe the whole set of molecular interactions in a particular cell.
 For example, the well-known bacteria H.pylori that can cause stomach ulcers:- 

Over 1,200 interactions were identified between H. pylori proteins, connecting 46.6% of the proteome.

Just this one common bacterium affects half of the entire set of proteins expressed by a genome (the so called proteome).
So we should not be surprised if some bacteria or viruses have a bad, or indeed good, effect on autism.
This also bring us back to the idea of the holobiont and hologenome, which was introduced in an earlier post. The idea is that what really matters in human health is not just your genome, but the totality of what surrounds you, so that means everything living in you, on you and around you. That includes bugs, bacteria and also those of your pet dog.
All of these factors influence how your genes are expressed. During evolution your body has got used to things and if you make rapid changes, you may indeed upset the balance. So while chlorinating water may have an overall good effect, by killing all those bacteria your body had been expecting, there may be some negative effects. Humans evolved living close to animals, be it dogs or farm animals. We saw earlier that pregnant mothers who live with pets produce children with a lower incidence of asthma.
We also reviewed the hygiene hypothesis, which basically says that a bit of dirt is good for you.
So this post, rather than narrowing things down, really broadens them out.  Everything affects everything.  If you rock the evolutionary boat, don’t be surprised if strange things happen.
Taking Somali refugees to live in Sweden increased their incidence of autism. Is that really a surprise? Recall the Somali autism clusters in Sweden and San Diego.
Apparently, the Amish in the US have a low prevalence of autism. Is that really a surprise?  One reader recently suggested sending autistic people to live with the Amish, as a therapy. The possibly effective therapy would have been to send the parents to live with the Amish for a couple of years before the child was born.
So perhaps we should consider much autism, and indeed conditions like asthma, as collateral damage from modern living?  Life expectancy has risen, infant mortality has been greatly reduced, but the downside is that we now have much more autoimmune disease and that includes autism.

Autism and Microorganisms
Now back to autism and the four categories of microorganism.
Can parasites cause autism? Actually we know they can; for example cerebral malaria can result in it. But how often is this case? Probably very rarely.
Can fungi cause autism? Perhaps, but we know from many examples (including in the comments on this blog) that some fungi can make autism worse.  Is the fungus candida albicans growing in the intestines really an issue in most autism? I seriously doubt it, but oral thrush/candidiasis caused by inhaled steroids does seem to make autism worse and is reversible by removing the fungus. The effect seems more likely to be from the candida than the steroid, since inhaled steroids only mildly enter the bloodstream.
Can bacteria cause autism? Well streptococcus bacteria can cause OCD and cognitive impairment (PANDAS).
Can a virus cause autism? Antonio Persico, one of the more serious autism researchers, has suggested that some autism may be caused by polyomaviruses transmitted at conception from father to mother.

Can the rubella virus cause autism? Some serious people do see a possibility, even in people who have been vaccinated.

These both remain controversial hypotheses; but can viruses cause flare ups in autism, later in life? This is also controversial, but I think quite plausible.  It all depends which genes the virus causes to get miss-expressed.
Enough is known to say that odd changes in autism may potentially be triggered by the appearance of specific types of microorganism, but quite possibly most microorganisms have little, or no, negative effect in most people. So it is not a case of all viruses/bacteria will make autism worse, but it is likely true that some may have the potential to do so.
In trying to figure out possible causes of autism flare-ups, due consideration should be given to microorganisms.  This is another case of personalized medicine, with all its potential pitfalls.
The big risk is potentially becoming obsessed with non-existing bacteria, viruses, fungi or parasites.  

Back to Antivirals and Autism 
Finally we come back to where the original idea for this post came from; is there any basis of the use of antiviral drugs to treat autism?
DAN-type doctors do prescribe the antiviral drugs Valtrex, Famvir or Acyclovir.

Antiviral drugs do not destroy their target virus they just inhibit its development.
Most of the antiviral drugs now available are designed to help deal with HIV, herpes viruses, the hepatitis B and C viruses, and influenza A and B viruses.
You identify a virus by looking for antibodies to that specific virus in the blood. You can test for antibodies that suggest if the infection is new and active, called IgM antibodies and you can test for antibodies that show the infection occurred sometime in the past, called IgG antibodies.
You would need to know which virus to test for, the common ones are:-

HSV 1:  Herpes Simplex Virus 1 causes canker sores in the mouth

HSV 2: Herpes Simplex Virus 2 causes genital herpes.

HHV 6: Human Herpes Virus 6 is commonly known as Roseola virus

EBV: Epstein-Barr Virus, causes the illness known as infectious mononucleosis



“We’re not saying that HSV-2 is responsible for infecting the [fetal] brain and causing autism,” stresses senior author Ian Lipkin, an infectious disease expert and epidemiologist at Columbia. Indeed, fetal infection with HSV-2 is so serious that it frequently leads to miscarriages or stillbirths. Rather, Lipkin suspects that HSV-2 is just one among many environmental insults that, when they arrive at a vulnerable point in fetal development in women predisposed to damaging reactions, may trigger ASD in the fetus.” 

Conclusion: Rate of contact with HSV1 and HSV2 assessed by the mean of detection of specific antibodies was similar between children with ASD and healthy controls.

Conclusion: Levels and seropositivity rate of antibodies to HHV-6 and HHV-8 do not differ between children with ASD and controls.
CONCLUSION: Titre and seropositivity rate of antibodies to CMV and EBV are similar between children with ASD and healthy controls.

Valtrex seems to be the antiviral most commonly prescribed in autism.  This is an off-label use, meaning Valtrex is not approved to treat autism.  Valtrex is active against most species in the herpesvirus family. In descending order of activity:

So we might assume the people with autism who respond to Valtrex might have one of the above, or similar, viruses. Unless Valtrex has some other modes of action, unrelated to being an anti-viral, which remains a possibility. 

Mitochondrial Disease and Viral Infections
Since this post is already full of speculation, I will add some more. Some people say that their child’s mitochondrial disease was preceded by a viral infection, so how likely is it that a virus can trigger mitochondrial disease and then autism?  Again, this is not something anyone can prove, one way or the other, but it does look like your mitochondria are particularly vulnerable to viruses.
The virus will exploit the mitochondria to further its own development, perhaps in doing so, in some people with a pre-disposition, this triggers a process to chronic mitochondrial dysfunction.  Read the papers below for more on this subject.


Mitochondrial dynamics influences mitochondrial and cellular functions.
Mitochondrial dynamics is affected during viral infections.
Viruses exploit mitochondrial dynamics and mitophagy to benefit infectious process.
Virus-altered mitochondrial dynamics determines the outcome of infection.
Disruption of mitochondrial dynamics promotes viral pathogenesis.

If a virus can trigger mitochondrial disease, as we have seen a vaccination can, is there any possible merit in using antivirals years later?
Is there merit treating regressive autism, which is likely to be mitochondrial disease, immediately with antiviral drugs?
Is there merit treating autism flare-ups, that do not respond to PANDAS/PANS therapies, with antiviral drugs?
Is there merit treating MS (multiple sclerosis) immediately on diagnosis with antiviral drugs? Would MS flare-ups respond to antivirals?

My take
If I was to develop MS tomorrow, given there is currently no cure, I think I might want to try an antiviral, just in case it might actually do some good.
My son with classic autism did have a PANDAS-like regression last year, with sudden onset OCD and strange verbalizations. It all went away after a couple of weeks, having been treated as a PANDAS flare-up, as documented in an old post on this blog. If after a viral infection he developed a sudden onset regression I would certainly reread this post.
Readers of this blog with a clear case of mitochondrial disease might want to check for the commonly implicated viruses, since if one was never suppressed this might be something to consider.
So do antivirals have a place in treating autism?  There is no hard evidence to support their use, but I would not at all be surprised if a minority do genuinely benefit. I think the most likely group might be those who have a sudden regression from near typical. As with PANDAS/PANS, the sooner the treatment commences, the better the likely outcome. 
Could antivirals help control flare-ups that can occur in those already with autism? They could well help; ideally you would confirm the presence of the virus first.   

I recently watched an expert clinician talking about irritable bowel syndrome (IBS); he was very open about his opinion that science likely only understands about 30% of the disorder. When it comes to autism I think science may be only at the 10% mark. As a result you have to be very careful about saying anything definitive.
We know that very many things contribute to the prevalence of autism.  It looks more than likely that viruses, bacteria, fungi and parasites may, on occasion, play a role in some people’s autism.
But, just like we know that in some people vaccination can trigger mitochondrial disease and result in an autism diagnosis, this does not mean it is a common cause of autism. Vaccinations have saved hundreds of millions of lives, but it has long been known that they can have side effects and that is why there is a large industry-funded compensation scheme in the US.
So while parasites can in some circumstances lead to autism, this does not mean feeding bleach to children with autism is a clever idea. Nor does filling them with antibiotics to treat a non-existing bacteria.
You can see why mainstream medicine is not eager to treat autism.
Nonetheless, applying that meagre sounding 10% of understanding can yield results, when applied with caution.