**6. Conclusion**

Despite the vast genetic diversity among viruses, these pathogens face similar obstacles on the way into the CNS with the dual role of a physical and molecular barriers of the innate immune system to restrict and protect from infection. However, upon entry whether they are hidden in leukocytes or in apoptotic blebs, they will be free to interact with neurons in a rather 'immunopriviliged' environnement allowing viral persistence. However, this paradigm has been reconsidered with the observation that resident cells possess several of the key innate immune receptors involved in the recognition of the intruders and to engage a salutary antiviral response (IFN). It is now clear that other molecular interactions between the viruses and these host cells expressing primary and secondary signaling receptors will determine the outcome of the infection. Some receptors may control apoptosis or cell differentiation which in turn may have an impact on the capacity to resist viral infection and spreading. Our understanding of the molecular mechanisms of CNS diseases is still in its infancy. Increasingly, identification of virulence factors and host receptors will provide solutions for this complex puzzle. Understanding these interactions will increase our ability to control neuroinvasion and encephalitis. Moreover, it will also teach how to use these entry routes for therapeutic benefit, for example, for gene delivery of therapy of cancer and neurodegeneration.
