Virus-Induced Encephalitis and Innate Immune Responses – A Focus on Emerging or Re-Emerging Viruses

A wide variety of emerging and re-emerging viruses (e.g. arboviruses, ‘arthropod-borne viruses’) contributes to neurological diseases. Infections can be associated with new viral variants that are more efficiently transmitted and lead to massive outbreak and increased reports of complicated cases involving the CNS (Tsetsarkin et al., 2007; Vazeille et al., 2007). It is also possible that viruses may have acquired increased neurovirulence by a previously non-neurotropic virus. Viruses that appear to have recently become more neurovirulent include for example the West Nile flavivirus (WNV), Chikungunya alphavirus (CHIKV) and the enterovirus 71 (ENV71) (Griffin, 2010). In addition to these newer challenges, Japanese encephalitis flavivirus (JEV), rabies, polio, measles virus (MV), human immunodeficiency virus (HIV) and human herpes virus (HHV) remain important causes of neurologic diseases. Focusing on CHIKV, this is an alphavirus of the Togaviridae family transmitted by mosquitoes of the Aedes (Ae) genus. The alphavirus group comprises 29 viruses, six of which of the ‘Old World, ie Africa’ can cause human joint disorders (arthralgia evolving to arthritis), namely CHIKV, O’nyong-nyong virus (ONNV), Semliki forest virus (SFV), Ross River (RRV), Sindbis virus (SINV), Mayaro virus (MAYV) while the so-called ‘New World’ such as Eastern equine encephalitis virus (EEEV) and Venezuelan equine encephalitis virus (VEEV) can cause severe brain damage (Das et al., 2010; Jaffar-Bandjee et al., 2009). Interestingly, CHIKV-associated neuropathology was first described in the 1960s but it is the unprecedented incidence rate in the Indian Ocean with efficient clinical facilities that allowed a better description of cases with severe encephalitis, meningoencephalitis, peripheral neuropathies and deaths among newborns (mother-to-child infection), infants and elderly patients (Das et al., 2010; Jaffar-Bandjee et al., 2009). The follow-up of the neonates contaminated by CHIKV clearly indicates poor outcomes and neurodevelopment defects (Jaffar-Bandjee et al., 2011). Neurological manifestations described in adults requiring hospitalization involved cases of encephalopathy frequently associated