Once in the CNS, the virus will attach to a host cell by binding with a cell surface receptor. The host cell surface receptor is a glycoprotein that has been recently identified as CD155. Once the virus has bound to the host cell, it will penetrate the host cell membrane and begin the replication of its genome. Many cells contain the surface receptor CD155; however, manifestation of this disease does not occur in all cells. The reason for incidence of the disease in only certain areas of the brain such as the brainstem is unknown. Once areas of the brain have been invaded by the virus, inflammation will occur. During inflammation, the brain’s tissues become swollen due to the body’s immune system response to the infection. Fluid, white blood cells, dead cellular debris and inactivated viruses resulting from the actions of the immune response can significantly alter the fluid surrounding healthy neurons. The function of these healthy neurons can decline due to disruptions in the cell membrane affecting electrical properties of the neuron or by interfering with the blood supply causing anoxic cellular damage. Depending on which neurons are damaged will result in a variety of different symptoms. Diagnosis
If someone is suspected of having polioencephalitis a sample of throat secretions, stool or cerebrospinal fluid is checked for the virus. Blood tests can be done to detect antibodies against viral antigens and foreign proteins. Virus isolation is the most sensitive method and it is most likely to be isolated from stool samples.
Experiments on transgenic mice are investigating the initial sites of viral replication in the host and how the virus moves from the bloodstream into the central nervous system. Research into the host range of the virus has also been of interest. The host range of a virus is determined by the interaction of the virus with host cellular receptors such as CD155. Comparison of the amino acid sequence in the binding domain of the host cell receptor is highly variable among mammalian species. Rapid changes in the sequence of the binding domain have restricted the host range of the poliovirus. Targeting of the brain and spinal cord have also come under investigation. The restricted tropism maybe due to organ specific differences in the initiation of translation by the virus internal ribosome entry site. == References ==