Human cytomegalovirus (HCMV), a member of the Herpesvirus family, is the most common etiologic agent of congenital anomalies of the central nervous system (CNS) caused by intrauterine infection in humans, with an average incidence of approximately 1.0% among live births (20). It is estimated that 5%-10% of embryos with congenital HCMV infection will have severe neurologic damage at birth, such as microcephaly and perivascular calcification (16). To date, the mechanism concerning the injuries induced by this kind of viral infection remains uncertain.
Nerve growth factor (NGF) is a metabolically active peptide, which was first isolated in nerve tissue. NGF plays a key role in differentiation, development and survival of sympathetic and sensory nerve cells, neural stem cells and cholinergic neurons of the central nervous system (CNS) (2, 12). Apoptosis and cell death may be induced by NGF withdrawal from culture medium of several nerve cells (6, 15, 17). During the embryonic stage, NGF is mainly secreted by neuroglia cells, which are more susceptible to HCMV infection than other nerve cells (2). In this study we analyzed the gene expression of normal and infected human glioma cell lines by RT-PCR and Western Blotting. We found that HCMV infection was associated with alterations in expression of NGF genes.
HCMV Infection Depress NGF Expression in Human Glioma Cells
- Received Date: 11 December 2008
- Accepted Date: 08 April 2009
Abstract: Human cytomegalovirus (HCMV) is the most common cause of congenital infection, resulting in birth defects such as microcephaly. In this study, RT-PCR and Western Blotting were performed to quantify the regulation of endogenic nerve growth factor expression in neuroglia cells by HCMV infection. The results showed that basal, endogenous NGF expression in U251 was unchanged during early HCMV infection. NGF expression is strongly down-regulated during the latent phase of infection. These results suggest that HCMV can depress the NGF expression in U251 cells.