This study, Association of autism with polyomavirus infection in postmortem brains,
found that three viruses were significantly more prevalent in the brains of people with autism than in the controls "BKV, JCV, and SV40 combined are significantly more frequent among autistic patients compared to controls (67% versus 23%, respectively; P < .05). " SV40 is Simian Virus 40, a monkey virus that was a contaminant in polio vaccines used between 1955 and 1963. BK and JC viruses are closely related to each other, and are part of the family of polyomaviruses (which is a subgroup of papovaviruses). SV40 is also a papovavirus.
SV40 has long been suspected of causing cancer in humans, but evidence has been mixed and inconclusive. The Immunization Safety Review Committee of the Institute of Medicine put out a report on this question that can be viewed here, which essentially says that the epidemiological evidence that has been used to deny a connection between SV40 and cancer is too flawed to rule out a possible connection, that the idea that SV40 could contribute to human cancers is plausible, and that ongoing investigation is required.
The paper "BK Virus: A Clinical Review" provides more information about BK virus:
-the etiologic agent of progressive multifocal leukoencephalopathy (PML).
-The kidney, lung, eye, liver, and brain are sites of BK virus-associated disease, both primary and reactivated.
From Understanding the JC VIrus and the Risks for MS Patients:
-The JC Virus is the cause of Progressive Multifocal Leukoencephalopathy (PML), in which "it infects the white matter of the brain and attacks the cells responsible for making myelin, the protective coating that covers and protects nerve cells.".
-PML manifests as focal neurological deficits, usually with insidious onset and steady progression. Because the demyelinating lesions can involve different brain regions, specific deficits vary from patient to patient. Any region of the CNS can be involved, although some areas seem to be more favored, including the occipital lobes (with hemianopsia), frontal and parietal lobes (aphasia, hemiparesis, and hemisensory deficits), and cerebellar peduncles and deep white matter (dysmetria and ataxia).
-Spinal cord involvement is rare.
-Although lesions can be multiple, one often is clinically predominant.
-Initial symptoms and signs often begin as partial deficits (e.g., weakness in one leg) that worsen over time and involve a larger territory (e.g., evolution to hemiparesis) as individual lesions expand concentrically or along white matter tracts. The focal or multifocal nature of the pathology is responsible for the consistency of clinical presentations with distinct focal symptoms and signs, rather than as a more diffuse encephalopathy, or isolated dementia or behavioral syndrome, all of which are uncommon without concomitant focal findings.
-Although AIDS is the most common predisposing factor for JCV reactivation, there is increasing incidence of brain manifestations of JCV reactivation in non-HIV settings, including different rheumatologic, hematologic, and oncologic conditions; monoclonal antibody therapy; transplant recipients; primary immunodeficiency syndromes; and even in patients without any recognizable immune deficiency.
-It has become evident that PML has outgrown its name. JCV infection is no longer a 1-dimensional opportunistic infection, limited to HIV and lymphoproliferative disorders. Although HIV accounts for approximately 80% of the PML cases, there is increasing incidence of the disease in non-HIV settings.
-JCV is a ubiquitous human pathogen, and both inhalation and ingestion of contaminated water have been suggested as major modes of transmission of the virus.
-Usually, severe deficiency of T-cell immunity (cellular immunity) is necessary for reactivation of JCV.
-Calabrese et al18 recently reviewed 37 cases of PML in the setting of rheumatic diseases. All patients in this series were treated with some form of immunosuppressant before PML manifestation. Of all the rheumatologic conditions SLE was most commonly associated (65%) with PML. Other associated rheumatic diseases were rheumatoid arthritis, Wegener granulomatosis, dermatomyositis, polymyositis, and scleroderma. There are also reports of PML in patients with Sjogren syndrome19 and sarcoidosis20 with no prior immunomodulator therapy. In both of these cases, there was associated lymphocytopenia. It is unclear whether the rheumatologic condition or the lymphocytopenia was responsible for PML.
-PML has also been described in patients with primary immunodeficiency disorders, ICL being the most common condition to be associated with PML.28–30 PML has also been described in patients with common variable immune deficiency.
-Until recently, severe depletion of cellular immunity was considered an absolute requirement for the development of PML. However, there are now case reports of PML with less overt immunodeficiency, such as cirrhosis, renal failure, psoriasis, dermatomyositis, and even pregnancy.6 Furthermore, there are multiple reports in the literature of PML without any documented immunodeficiency.6 It is very important that neuroradiologists be aware of this expanding demography of PML, JCE, JCVGCN, and JCM.
-The pathogenesis of PML is divided into 3 phases. The first phase is a primary clinically unapparent infection. In the second phase, the virus maintains a persistent latent peripheral infection in the urinary tract, bone marrow, and probably the spleen.35 The presence of JCV in the bone marrow and shedding of the virus in urine are well documented in asymptomatic immunocompetent carriers.36,37 The CNS has also been suggested as a potential site for JCV persistence. The third or final phase is that of reactivation and dissemination of the virus with presumed hematogenous spread to the CNS.
-The authors concluded that tests for BK virus and JCV should be included in the investigative program for patients with meningitis or encephalitis.
-PML may involve gray matter as well. The thalamus is the most common area, followed by the basal ganglia.49,88 Usually gray matter lesions are associated with white matter involvement in almost all cases. Vary rarely, PML lesions can be isolated to the gray matter.
-As briefly mentioned previously, PML can occur in MS patients treated with natalizumab. It is very difficult to differentiate a new PML lesion from an MS plaque in patients treated with natalizumab.