| Backgrounds:The childhood autism is a pervasive developmental disorder. It wasreported that the morbidity rate was 0.2‰~1.3‰. Most children withautism are likely to occur at less than 30 months of age. And theincidence in boys are 2.6~7.5 times more than that in girls. Many studieson clinic semeiology had summed up that there are three nuclearsymptoms, including impairments in language, social communication,and behavior, such as strict interest and stiff or repeated action. As theresearch on cognitive function related to children with autism, thebehavioral training intervention had been accepted by clinicians. It haslong been a hotspot to explore the special pathogenesis of autism. And ithas been also a focus of attention for the role of virus infection andimmunodeficiency in the pathogenesis of autism. Stubbs (1976) reportedthat autism children presented autoimmune deficiency, as 5 of 13 autismchildren did not produce the antibodies after inoculate with measlesvaccine. Both Ivarsson (1990) and Yamashita (2003) proposed that autismmight be correlated with infection of human cytomegalovirus (HCMV),which might affect the neurodevelopment. Other risk factors such asinfection of virus in pregnancy, perinatal, early infants might play roles inthe cerebral dysfunction, developmental delay, and cognitive impairments.Although autism has been shown to aggregate significantly withinfamilies, there were still no pervasive accepted conclusions of geneticmode or susceptibility genes of autism. Klauck (1997) reported that thepolymorphism of 5-HTT-VNTR associated with autism. Therefore, weevaluated the cytoimmunological function and the HCMV IgG antibody,HCMV gene examination, the 5-HTT-VNTR polymorphism and therelationship with clinical symptoms, developmental index, and adaptivebehavior to explore the pathogenesis of autism.Objectives:To explore the adaptive behavioral characteristics of autism, relatedmateral high risk factors and immunological function. To evaluate therelationship between infection of HCMV, the immunological function andclinical characteristics. Furthermore, to identify the role of virus andimmunologyical factors or 5-HTT transporter gene polymorphism mightplay in the pathogenesis of children autism. To find out the susceptibilityfactors of autism.Methods:With the general status questionnaire, CARS, ABC, and adaptivebehavior scale (ABS), we examined the clinical and developmentalcharacteristics, and the high risk factors in 43 children with autism.Forty-three autism children and 43 healthy control children were alsoexamined the T lymphocyte subpopulation, and CD4+/CD8+. With theELISA and PCR-ELISA technology, the HCMV IgG OD value andHCMV DNA were examined, and analyzed with clinical symptoms. Thenwe explored the possible relationship between HCMV and autism and therole of viroimmunological abnormality in neurodevelopment. With thePCR technology, the frequencies of the different forms of the genotypesand alleles of 5-HTT genes were analyzed in 63 autism children and 90healthy controls. With the multi-factorial statistic analyses, we exploredthe relationship among the clinical symptoms and immunological orgenetic factors.Results:1. Compared with healthy children, autism children and theirmothers during pregnancy suffered higher maternal virus infective ratebut more retarded neurodevelopmental index (P<0.05).2. The quotient of ABS in autism group was much less than that inhealth control group, so did the factors, such as taking care of oneself,speech development, individual tropism, social duty, time and spacedirection, working skill, economic activities, sense and movement, et al(P<0.05).3. The percentages of CD4 + , CD8 + in autism group weresignificantly lower than those in control group, so did the ratio of CD4+/CD8+(P<0.05).4. The positive rate of HCMV IgG antibodies and DNA detectionin autism group were significantly higher than those in healthy controlgroup (P<0.05). However, there were no significantly differencesbetween the results of the two methods (P>0.05).5. Pearson correlation analysis showed that in autism group, theCD4+, CD8+, CD4+/CD8+, OD value of HCMV IgG antibody werecorrelated with severity of autism or some factors of ABC (r>0.3, P<0.05).And the relationship between the CD4+,CD8+, CD4+/CD8+ and OD ofHCMV IgG antibody were also significant (r>0.3, P<0.05).6. Stepwise regression analysis showed that in autism group, thepositive rate of HCMV IgG OD value, CD4+ counting, and CD4+/CD8+et al,were the possible etiology of autism.7. With genetic epidemiology analysis, autism showes kindredaggregation. The frequencies of the 10 or 12 alleles and the genotypes10/10, 10/12, 12/12 in 2 intron of 5-HTT-VNTR were not significantlydfferent from those in healthy control group (P>0.05). No significantdifference in clinical symptoms, adaptive behavior, immunological indexand viroimmonological index between the patients with 12/12 and 10/10or 12/10 genotype of 5-HTT-VNTR (P>0.05).Conclusions:1. Compared with healthy control children, autism children suffereddistinct environmental high risk factors such as maternal infection ofvirus, which might result in retardant neurodevelopment.2. Compared with healthy children, autism children displayed fullinferior adapted and behavioral capacity.3. Autism children might suffer defection in cytoimmunologicalfunction, such as autoimmunological defection.4. The Compared with healthy children, autism children sufferedhigh HCMV infective rates.5. The autoimmonological deficiency and infection of HCMV mightplay a role in the pathogenesis of autism. The capacity of immonologymay be correlated with the infection of virus.6. The 5-HTT-VNTR polymorphism might not be the susceptibilityloci for autism. Autism showes kindred aggregation.7. The etiology of autism perhaps has heterogenous character.
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