Updated: Nov 12, 2021
In other articles, I have already discussed some of the infectious origins of mental illness as the result of persistent viral infections and accumulation of vaccine antigen with an affinity for brain and nerve tissue, causing a marked neurotropic effect on the brain and central nervous system.  This results in a chronic low-level neuroinflammation that is oftentimes missed on conventional scans (CT, MRI, etc.) and diagnostics.  The invasive effect on the brain affects the emotional states, behavior, and well-being of the individual, who is oftentimes misdiagnosed or told there is nothing wrong, after the conventional scans and diagnostics fail to pick up on it.  Virus, vaccine antigen, along with additional or concurrent microbial infections, are able to easily invade the brain and central nervous system when injected into tissue and the bloodstream, to actively destroy it in the slow, infectious process. 
This would be somewhat akin to a slow-acting, chronic wasting disease. Antigen alone, without having to be considered "infectious particles," can accumulate in the brain and nerves to cause chronic inflammation of the central nervous system, and thus symptoms of mental illness and neurological problems will inevitably result when the brain is inflamed. A research publication from 2010, Bacterial lipoproteins can disseminate from the periphery to inflame the brain, reviews this process in strains of relapsing fever spirochetes (Borrelia turicatae), as the spirochetes invade the brain and central nervous system. 
Speaking of spirochetes and mental illness, a late German psychologist who headed the psychology department at the Kaiser-Wilhelm Institute, Franz Jahnel (1885-1951), was also a spirochete researcher and scientist, and those stricken with syphilis and other infections of a similar nature were sent to him at the psychology department to deal with the complications of their disease.  This was because back in those days, infectious diseases like syphilis and relapsing fever were known to cause mental illness and psychosis. They rightfully classed the two subjects together, but since that time, this reality has been obscured or ignored in Western science and medicine.
Other publications have been forthcoming on the reality of infectious antigen and para-infectious stimuli disseminating to the brain to cause neuro-inflammation, such as the 2018 publication, In vivo evidence for the contribution of peripheral circulating inflammatory exosomes to neuroinflammation, it states:
Background: Neuroinflammation is implicated in the development and progression of many neurodegenerative diseases. Conditions that lead to a peripheral immune response are often associated with inflammation in the central nervous system (CNS), suggesting a communication between the peripheral immune system and the neuroimmune system. The underlying mechanism of this relationship remains largely unknown; however, experimental studies have demonstrated that exposure to infectious stimuli, such as lipopolysaccharide (LPS) or high-fat diet (HFD) feeding, result in profound peripheral- and neuro-inflammation. 
The results of this research concluded:
Conclusions: The experimental results suggest that circulating exosomes may act as a neuroinflammatory mediator in systemic inflammation. 
Hundreds if not thousands of research papers in virology, bacteriology, and immunology have rightfully linked infections of the brain and central nervous system to psychiatric disorders. However, what links the similar presentation between these viruses and infectious agents are the similar lipoproteins or antigen,  sometimes referred to as 3C Protease, or Pam-3-Cys,  which has a specific affinity for the brain and nerve tissue.  This would indicate that so-called non-infectious vaccine antigen, injected into the tissue and bloodstream, has much greater potential to cause neurotropic disease than those naturally picked up in the environment.
Some of the following research publications demonstrate the presentation of diverse symptoms of mental illness in relation to such antigenic stimuli:
Chronic hepatitis C virus infection and neurological and psychiatric disorders: an overview
Main HCV-associated neurological conditions include cerebrovascular events, encephalopathy, myelitis, encephalomyelitis, and cognitive impairment, whereas "brain fog", depression, anxiety, and fatigue are at the top of the list of psychiatric disorders. 
Chronic Viral Neuroinflammation: Speculation on Underlying Mechanisms
Viral infection in the brain can be acute or chronic, with the responses often producing foci of increasingly cytotoxic inflammation. This can lead to effects beyond the central nervous system (CNS). 
Psychiatric disorders and functioning in hepatitis B virus carriers
The authors compared asymptomatic hepatitis B virus carriers and healthy subjects in terms of their psychological state. Participants (43 asymptomatic hepatitis B virus carriers and 43 healthy comparison subjects) completed self-report questionnaires. Psychiatric disorders and psychosocial functioning were evaluated with structured clinical interviews and the Global Assessment of Functioning scale. Hepatitis B virus carriers were more likely to have psychiatric disorders than comparison subjects (30.2% vs. 11.6%). Also, carriers had significantly higher depression and anxiety scores and lower Global Assessment of Functioning scores than did comparison subjects... 
Herpes Simplex Virus Type 1 infection is associated with suicidal behavior and first registered psychiatric diagnosis in a healthy population
Increasing evidence shows that latent infections and inflammation is associated with cognitive and behavioral changes in humans. This case-control study investigates the association between Herpes Simplex Virus Type 1 (HSV-1) infection and C-reactive Protein (CRP) levels, and psychiatric disorders and suicidal behavior. Public health register data from 81,912 participants in the Danish Blood Donor Study, were reviewed to identify individuals registered with an ICD-10 code of any psychiatric diagnosis, or who had attempted or committed suicide. 
Post-influenzal psychiatric disorder in adolescents
The association between influenza and psychiatric disorder in adolescents was studied at a time when both were highly prevalent concurrently. First 505 secondary school pupils aged 15-18 completed questionnaires, including a symptom inventory derived from the SCL-90-R. Subsequently, 113 blood samples were examined for influenza antibody titers of five virus strains. Statistical analysis showed that adolescents who had been ill with influenza in the previous six months had significantly more psychiatric disorder than those who had not been ill with influenza in that period. 
Large-scale study of Toxoplasma and Cytomegalovirus shows an association between infection and serious psychiatric disorders
This large-scale serological study is the first study to examine temporality of pathogen exposure and to provide evidence of a causal relationship between T. gondii and schizophrenia, and between CMV and any psychiatric disorder. 
Neuroinflammation During RNA Viral Infections
Neurotropic RNA viruses continue to emerge and are increasingly linked to diseases of the central nervous system (CNS) despite viral clearance. Indeed, the overall mortality of viral encephalitis in immunocompetent individuals is low, suggesting efficient mechanisms of virologic control within the CNS. Both immune and neural cells participate in this process, which requires extensive innate immune signaling between resident and infiltrating cells, including microglia and monocytes, that regulate the effector functions of antiviral T and B cells as they gain access to CNS compartments. While these interactions promote viral clearance via mainly neuroprotective mechanisms, they may also promote neuropathology and, in some cases, induce persistent alterations in CNS physiology and function that manifest as neurologic and psychiatric diseases. 
Anger, rage, violence, depression, manic depression, bi-polar depression, obsessive-compulsive disorders, eating disorders, psychoses, depersonalization/dissociation, confusion, hallucinations, criminal behaviors, and just about any other symptom one can read about in the DSM-V, are all symptoms that can and do present themselves in active infections or accumulation of vaccine antigen in the brain and central nervous system. This can be mirrored in the discussion from a research paper from 2003, Behavioral consequences of infections of the central nervous system: with emphasis on viral infections, it states:
Infections of the central nervous system can damage the brain and cause abnormal behavior. In this article, the authors examine how behavior is affected by damage to different parts of the brain. They then focus on damage caused by specific infections of the brain and how these can result in abnormal behavior with legal consequences. Examples of such infections include neurosyphilis, encephalitis lethargica, herpes simplex encephalitis, and various other viral encephalitides, both acute and chronic. The AIDS dementia complex, which results from HIV infection of the brain, causes behavioral abnormalities in addition to motor and cognitive impairments. In some cases of violence and other criminal behavior, this can be a consequence of central nervous system infection, and the authors suggest that criminal sanctions in such events are inappropriate in the absence of volitional criminal intent. 
Now that this has been pointed out, it would be helpful to also point out the common, underlying thread that links these infections together, is once again, the P3C antigen/lipoprotein mentioned earlier, made of a lipid-like moeiety that is immunosuppressive in nature and has been known to cause immune tolerance. It can be found in such infectious agents as the HIV virus, LCM virus, Lyme disease (Borrelia burgdorferi), Malaria (Plasmodium vivax), Tuberculosis (Mycobacterium tuberculosis), Mycoplasma pneumoniae, Influenza virus, polio virus, it is oftentimes found in broad range of arthropod-borne diseases like bartonellosis, babesiosis, ehrliciosis, and many other pathogens contain these constituents. 
This class of antigenic material has been used in many vaccines which have resulted in adverse reactions like immune tolerance,  reactivation of latent herpesvirus,  neurological and psychiatric problems, as well as permanent progressive neurodegenerative diseases.  It is this common denominator that has linked these outcomes with this particular antigen of the viral and other pathogenic agents, it was in the 1970's known as Braun's Lipoprotein, viral proteins that were expressed in E. coli bacteria,  but had immunosuppressive qualities that resulted in immune tolerance, also called endotoxin tolerance,  and immune paralyisis.  This is the harmful component of such infections causing these neurotropic effects, and yet it is this component of the infectious agent they are injecting into the general population as viable and safe vaccines, but caused immunosuppression, which they erroneously considered a form of protective immunization.  Such perceived "protection" is based on a flawed or incomplete pitcure immunology, because Western science covered up and buried the aspects of immune tolerance in 1960, when they gave the Nobel Prize to Burnet and Medawar for immune tolerance but only attributed it to organ transplants instead of infectious disease.  It was actually discovered and configured by German virologist Erich Traub in 1935,  who noted not just the slow-virus disease it produced, but also the manner it which it transmitted down generations congenitally from mother to newborn,  and led to a dramatic increase in lymphomatosis and leukemia. 
Immune Tolerance is defined as
“a state of unresponsiveness to a specific antigen or group of antigens to which a person is normally responsive. Immune tolerance is achieved under conditions that suppress the immune reaction and is not just the absence of an immune response.” 
When there is a lack of response, the antigen or group of antigens will accumulate and colonize tissues, and the immune system will not fight back. Put two and two together. When that happens, the antigen will find its way to the tissues which it finds affinity for, and will actively degrade that tissue, which in this case, will be tissue of the brain and central nervous system.
Long before the term autism came into effect, before the more rigorous attempts to coverup the neurotropic effects of vaccination, these effects were called post-vaccinal encephalitis, which I have described in other articles at length.  However, I would like to reiterate the quote from a key paper I often cite, Para-Infectious and Post-Vaccinal Encaphalomyelitis, published in 1969:
Similarly, although the encephalitis following vaccination against smallpox (post-vaccinal encephalitis) is the typical example of encephalitis as a sequel to prophylactic inoculations, the term post-vaccinal should be used for the range of neurological disorders following vaccinations of all kinds (deVries,1960). 
To further show the link between mental illness and infectious neurotropic material invading the brain and CNS relevant to compulsory vaccine practices and the stacking of vaccines on children already dealing with immunosuppression from subclinical infections, I will pull out some material from an earlier paper I put together called Neurotropic Viral Infections: the Darker Side of Immune Tolerance, which laid out the sinister effects of immune tolerance on the brain and mental health. That is to say, when the immune system is suppressed into a state of non-responsiveness, the brain is significantly affected. It throws the biology of the body into disarray and the reactivated viruses start actively invading and destroying the brain and central nervous system. 
A major complication in compulsory vaccinations is the reactivation of latent herpesvirus infections.  The herpesvirus family can be highly neurotropic and greatly contribute to the neurological disorders commonly seen today,  as they reactivate in the face of the induced immunosuppression following vaccination.  This is hinted at in a publication, Herpesvirus Infections of the Nervous System, by two researchers of neurological diseases in human beings:
RECENT FINDINGS: As more patients are becoming therapeutically immunosuppressed, human herpesvirus infections are increasingly common. Historically, infections with human herpesviruses were described as temporal lobe encephalitis caused by herpes simplex virus type 1 or type 2. More recently, however, additional pathogens, such as varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6 have been identified to cause serious neurologic infections. As literature emerges, clinical presentations of herpesvirus infections have taken on many new forms, becoming heterogeneous and involving nearly every location along the neuraxis. Advanced diagnostic methods are now available for each specific pathogen in the herpesvirus family. As data emerge on viral resistance to conventional therapies, newer antiviral medications must be considered.
SUMMARY: Infections from the herpesvirus family can have devastating neurologic outcomes without prompt and appropriate treatment. Clinical recognition of symptoms and appropriate advanced testing are necessary to correctly identify the infectious etiology. Knowledge of secondary neurologic complications of disease is equally important to prevent additional morbidity and mortality. This article discusses infections of the central and peripheral nervous systems caused by herpes simplex virus type 1 and type 2, varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6. The pathophysiology, epidemiology, clinical presentations of disease, diagnostic investigations, imaging characteristics, and treatment for each infectious etiology are discussed in detail. 
The action of systemic viral infections like the reactivated herpesvirus have a profound effect on psychological process. Mental illness would be the inevitable expression of these viral infections and antigen, as German researcher Karl Bechter pointed out in his 2013 paper, Virus Infection as a Cause of Inflammation in Psychiatric Disorders. Inflammation of the brain does not always present with the acute forms typically seen in acute or fatal cases of encephalitis or meningitis. Chronic, low-level neuroinflammation allows the problem to go undiagnosed and unrecognized by conventional diagnostics:
Many neurotropic viruses exist and may cause classical inflammation but also low-level neuroinflammation. However, viruses may be dormant within the CNS and become active later. The role of neurotropic virus infections in the causation of psychiatric disorders may be underestimated, because the diagnostic approach to the CNS is difficult and to dormant infections in general, but especially within the CNS. Evidence is increasing that infections increase the risk of psychiatric disorders, not only prenatal infections but also infections during the lifetime. The question how low level neuroinflammation may be involved in severe psychiatric disorders like affective and schizophrenic spectrum disorders is intriguing but remains to be studied. Experimental data clearly show that low-level neuroinflammation can be induced by viruses, but the definitions of inflammation and low level neuroinflammation appear to be blurred and apparently the previous classical definition of inflammation has to be widened. Virus infection itself or virus-related products or virus-induced autoimmunity may play a role in disease pathogenesis. More sensitive diagnostic approaches from neuroimaging and CSF investigations may hold the key to a better understanding and definition of CNS viral infections as an etiopathogenetic sub-group of severe psychiatric disorders. 
Western science and public health set up psychiatry to deal with symptoms of mental illness only, ignoring the neurotropic effects caused by stealth infections and adverse reactions to vaccination and other infectious etiologies. This inconvenient truth is likely the reason they never publicly spend much time seeking or funding considerable research to find the reason why mental illness occurs in the first place.
Bechter also studied this further with notable German virologist Rudolf Rott, published MRI in psychiatric patients with serum antibodies against Borna Disease virus regarding the findings of Borna Disease Virus antibodies in psychiatric patients, as evidence of infection among the mentally ill, but not in the healthy controls:
Investigations in the FRG and the USA revealed the presence of serum antibodies against the [Borna Disease (BD)] virus in psychiatric patients with affective psychoses, but not in healthy controls. We demonstrated the occurrence of BD virus-specific antibodies in sera of about 7% of the psychiatric inpatients at our hospital, not only in patients with affective psychoses but also in those with other psychiatric disorders. By comparison, in surgical patients from an endemic region, only 3% were found to be seropositive, some of whom had psychiatric or neurological disturbances. The question was whether the BD virus-positive seroreaction was a coincidental and harmless finding or whether it could represent the cause of psychiatric disorders.