The Role of Infections in Autism
Inflammation can damage DNA, the brain, and immune regulation. In many children, inflammation does not occur without a trigger. One of the most important triggers considered by AN is infection.
Infections may include prenatal, early-life, latent, chronic, bacterial, viral, and mixed microbial processes. Their effects may involve immune activation, neuroinflammation, gene-expression changes, and gastrointestinal dysfunction.
01
Immune Activation
Maternal or childhood infections may activate inflammatory pathways that affect the developing nervous system.
02
Brain and Gene Effects
Viral and bacterial triggers may influence gene expression, neuronal signaling, immune balance, and brain development.
03
Treatable Factors
AN focuses on identifying biological contributors that may be clinically evaluated and, when appropriate, addressed.
KEY INFECTIOUS AGENTS
Agents discussed in ASD-related publications
The AN model does not reduce autism to infection alone. It considers infection as one possible driver within a larger inflammatory, immune, metabolic, and microbiome-related process.
SCIENTIFIC RATIONALE
The Role of Infections in Autism
In a Swedish study of 2019, involving 1.8 million children, it was proved that any viral infection during pregnancy significantly increases the likelihood of autism in a child.
In a Danish study that analyzed all children born in Denmark from 1980 to 2005, it was found that hospitalization due to viral infection in the mother in the first trimester and bacterial infection in the mother in the second trimester were associated with a subsequent diagnosis of ASD in a child.
In another large Israel study of 1996, it was found that there is a positive correlation between the birth of autistic children and the epidemics of measles and viral meningitis in the mother.
Apart from this, genetic changes in mouse brain cells, similar to those in ASD and schizophrenia, have been shown to be a result of maternal immune activation (mIA) due to inflammation caused by a viral infection. In a study involving monkeys, monkeys manifested autistic behavior if their mothers experienced immune activation during pregnancy.
In another study, it was shown that newborn rats inoculated with a disease virus inside the brain showed an autistic phenotype and had similar changes in blood levels with elevated levels of TNF-alpha, IL-1 alpha and IL-1 beta.
Moreover, viral infections have the ability to directly damage DNA.
In one study, a mechanism, that showed the direct effect of viral infection on enhancing the activity of 21 genes and suppressing the activity of 18 genes in the brain, was shown. According to this study, these gene changes led to patterns of autism and schizophrenia.
Due to the fact that their genome is similar to the human one, DNA viruses (such as herpesviruses) are able to embed fragments of their DNA into the carrier’s DNA, thereby disrupting the immune system, so that it does not react to the presence of the virus.
However, such micro changes, in turn, affect the expression of genes responsible for other functions. In particular, if the virus infected the brain, then by inserting its DNA into the brain cells DNA, the virus directly affects brain formation and functioning.
Some viruses, such as herpesviruses or rubella virus cannot be completely treated, they only can be suppressed. Since not much attention is paid to these viruses in children with autism, they are not controlled.
Clinical implication
Children with autism may benefit from structured evaluation of immune, infectious, inflammatory, metabolic, and gastrointestinal markers.
AN direction
The goal is to identify treatable biological factors and support the child's development through a more complete medical framework.