Overall, this study will help to strengthen and guide health policy implementation of primary and secondary cervical cancer prevention strategies in Kazakhstan.

Autism spectrum disorders (ASD) are a range of neurodevelopmental conditions that are clinically present early in childhood with the symptoms of social withdrawal and repetitive behavior. Despite an extensive research on ASD, no commonly accepted theory on the disease etiology exists. Hence, we reviewed several scientific publications, including reviews, preclinical and clinical investigations, and published hypotheses to analyze various opinions on the nature and cause of the disorder. Many studies suggest that infections and inflammation during pregnancy play a significant role in genetic and epigenetic changes in the developing fetus, resulting in an autistic phenotype in a child. Still, there is a lack of comprehensive literature about the multitude of autism inducing factors. Therefore, this article reviews and discusses available scientific evidence on the roles of viral, bacterial, fungal, and parasitic infections, overactivation of the immune system, and intestinal microflora in the pathogenesis and clinical manifestation of ASD. The overview of the scientific publications, including our own studies, suggests that TORCH infections, imbalanced microbiome, and persistent inflammation are significantly associated with the disruption of the social domain in ASD children. The ASD-related changes begin prenatally as maternal-to-fetal immune activation triggered by infection. It results in continuous low-grade inflammation and oxidative stress in a fetus, causing germline and somatic genetic changes in the developing brain and the establishment of the dysregulated immune system. These changes and dysregulations result in central  and peripheral nervous systems dysfunctions as well as other comorbid conditions found in autistic children.

The most recent studies and publications demonstrate the enormous role of infectious agents and chronic inflammation not only in various comorbid conditions in autistic patients but also in the dysregulation of the immune system, which in turn leads to the accumulation of immunodeficiency states and to a worsening of the autistic phenotype. Therefore, the focus of this article is on how congenital and early postnatal infections found in children with autism spectrum disorders may trigger the chain of pathological events found in autism. We discuss how some infectious agents such as Toxoplasma gondii, measles, rubella, cytomegalovirus, Epstein-Barr virus, and herpes-simplex virus-1 and 2 are involved in the dysregulation of immunity and nervous system abnormalities. Furthermore, we want to provide recommendations for potential combined treatment methods for patients with autism with concomitant immune dysfunction.

Autism spectrum disorders (ASD) are a range of neurodevelopmental conditions that are clinically present early in childhood with the symptoms of social withdrawal and repetitive behavior. Despite an extensive research on ASD, no commonly accepted theory on the disease etiology exists. Hence, we reviewed several scientific publications, including reviews, preclinical and clinical investigations, and published hypotheses to analyze various opinions on the nature and cause of the disorder. Many studies suggest that infections and inflammation during pregnancy play a significant role in genetic and epigenetic changes in the developing fetus, resulting in an autistic phenotype in a child. Still, there is a lack of comprehensive literature about the multitude of autism inducing factors. Therefore, this article reviews and discusses available scientific evidence on the roles of viral, bacterial, fungal, and parasitic infections, overactivation of the immune system, and intestinal microflora in the pathogenesis and clinical manifestation of ASD. The overview of the scientific publications, including our own studies, suggests that TORCH infections, imbalanced microbiome, and persistent inflammation are significantly associated with the disruption of the social domain in ASD children. The ASD-related changes begin prenatally as maternal-to-fetal immune activation triggered by infection. It results in continuous low-grade inflammation and oxidative stress in a fetus, causing germline and somatic genetic changes in the developing brain and the establishment of the dysregulated immune system. These changes and dysregulations result in central and peripheral nervous systems dysfunctions as well as other comorbid conditions found in autistic children.