Infection of Human Neuronal Cells by Clamydia Pneumoniae and/or Herpes Simplex Virus Type 1 Infection Alters the Expression of Genes Related to Alzheimer\u27s Disease

Alzheimer\u27s disease (AD) is a severe, progressive neurodegenerative brain disorder that accounts for 80% of dementia cases and is the seventh leading cause of death in the United States of America (Bi, 2010). Cunently, there is no cure and the treatment options are minimal with only having effective results in the early stages of the disease. Research to discover the cause of this illness is ongoing and critical to finding effective medications. Several studies have suggested an infectious etiology for AD. We have been investigating a potential role for both Chlamydia pneumoniae (c. pneumoniae) and herpes simplex virus type 1 (HSV 1) in the initiation and progression of sporadic lateonset AD. The current study focuses on investigation of gene expression using Alzheimerspecific Real-Time PCR microanays on RNA derived from SKNMC human neuronal cells infected with C. pneumoniae and/or HSVI. There are distinct differences in the patterns of gene regulation by the two pathogens. For example, C. pneumoniae induces expression of genes involved in amyloid production and processing, while HSVI tends to down-regulate expression of many ofthose same genes. The co-infection with C.pneumoniae and HSV 1 produced an even greater down-regulation of gene expression than that seen with HSV 1 and a completely different regulation when compared to the genes up regulated with C. pneumoniae. Our data indicate that both C. pneumoniae and HSVI can modulate expression of genes associated with AD, and thus could contribute to AD pathology, however these two pathogens likely act via different pathways. Furthermore, for several genes, co-infection with both C. pneumoniae and HSVI appears to intensify the changes in gene expression seen with HSVI alone.