**1. Introduction**

[47] Velandia, M. L., Perez-Castro, R., Hurtado, H., & Castellanos, J. E. (2007). Ultrastruc‐ tural description of rabies virus infection in cultured sensory neurons. Mem. Inst. Os‐

[48] Warrell, M. J., & Warrell, D. A. (2004). Rabies and other lyssavirus diseases. Lancet ,

[49] Weekley, B. (1975). Electron Microscopy for Beginners [Russian translation], Mos‐

[50] WHO Expert Consulation on Rabies: first report.(2004). WHO technical report series,

[51] Whitby, J. E., Heaton, P. R., Black, E. M., Wooldridge, M., Mc Elhinney, L. M., & Johnstone, P. (2000). First isolation of a rabies-related virus from a Daubenton's bat in

[52] World Health Organization.(1987). Bat rabies in the USSR. Rabies Bulletin Europe, ,

waldo Cruz., Rio de Janeiro, , 102(4), 441-447.

the United Kingdom. Vet Rec., , 147, 385-8.

363, 959-969.

250 Encephalitis

N 931: 18.

4, 12-4.

cow: "Mir", 320 p.

Demyelinating encephalitis is a type of encephalitis in which the insulating myelin sheath sur‐ rounding nerve fibers is damaged. Most types of demyelinating encephalitis are known to be caused by viral infection, and therefore the nature of viral persistence in the central nervous sys‐ tem (CNS) has become crucial to understanding the pathogenesis of associated diseases. Suba‐ cute sclerosing panencephalitis (SSPE) is a progressive fatal demyelinating disease caused by infection with high levels of neuronal measles virus (MV) in the CNS. Thus, MV infection pro‐ vides one of the main paradigms of persistent viral infection that causes encephalitis. Many re‐ views have been published explaining how MV establishes a persistent infection in the CNS [1, 2, 3]. A number of studies on SSPE using cDNA cloning and sequencing techniques have re‐ vealed that MV genomes are present in samples obtained from SSPE patients. This demon‐ strates the presence of mutations that may lead to MV persistence in the CNS. However, no study has been able to explain how persistent MV is reactivated and results in subsequent pathogenesis of the CNS. In this review, we describe a brief overview of MV and SSPE. We will attempt to focus on host cell modifications related to MV persistence, and on reactivation mech‐ anisms of MV during persistent infections. We will then discuss the pathogenesis of persistent MV infections in patients to highlight molecular events that lead to the manifestation of SSPE symptoms. These key advances in the understanding of MV persistence will provide novel in‐ sights into the elucidation of SSPE pathogenesis.
