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ВОЗ о клещевом энцефалите

Tick-borne encephalitis.

Disease Burden

The endemic area for tick-borne encephalitis (TBE) spreads from Alsace-Lorraine in the west to Vladivostok and north-eastern regions of China in the east, and from Scandanavia to Italy, Greece and Crimea in the south. TBE also is endemic in North Japan, where the virus has repeatedly been isolated from blood samples of sentinel dogs, ticks, and rodent spleens. TBE is a serious acute central nervous system infection which may result in death or long-term neurological sequelae in 35–58% of patients. The fatality rate associated with clinical infection is 0.5–20%. The proportion of cases involving subclinical infection varies between 70% and 98%. Symptomatic infection occurs in all age groups.

The agent is the TBE virus (TBEV), a flavivirus that is transmitted to humans by the bite of a tick. Eight species of ticks have been identified that can transmit TBEV. The chief vectors are Ixodes ricinus in Europe and the western part of the Russian Federation, and Ixodes persulcatus in the eastern part of the Russian Federation. Occasionally, transmission also can occur through consumption of raw milk from an infected cow, goat or sheep. There are two subtypes of TBEV: eastern and western that show slight differences in the structure of the viral proteins. In the past, diseases caused by the two variants were referred to as “Russian spring/summer encephalitis” and “central European encephalitis”, respectively. The virus subtype largely determines the clinical course of the disease. The eastern variant has proven to be more virulent and to more often lead to severe illness. Transmission of the disease is seasonal and occurs in spring and summer, particularly in rural areas, where two seasonal peaks of the disease are typically seen, one in June–July and the other in September–October, corresponding to two waves of feeding of tick larvae and nymphae. A rise in incidence of TBE has been observed in recent decades in some regions – presumably linked to global warming – as milder winters lead to proliferation of rodent populations (voles and field mice) which are the main hosts and reservoirs of the virus and, as a consequence, also of ticks.

Vaccine

At least four formalin-inactivated TBE vaccines are available, made of virus grown on chick embryo fibroblasts, inactivated by formaldehyde and purified by continuous flow-density centrifugation. These vaccines are administered along a two-dose schedule followed by a booster immunization at one year and recommended booster injections every 3–5 years. They are produced in Austria (Baxter Vaccine, previously Immuno), Germany (Chiron, previously Beringwerke) and the Russian Federation (Institute of Poliomyelitis and Viral Encephalitidis and Virion Company). Active surveillance in Austria has demonstrated a dramatic decline in the incidence of TBE in vaccinated groups, with a reported vaccine efficacy of 95%. The main reported side effect with currently available vaccines is postvaccination fever and allergic reactions in children. A series of improvements to the available vaccines were introduced to reduce their reactogenicity. In Germany, the vaccine is widely used to immunize children in high-risk areas. The Russian vaccine induces high seroconversion rates and is believed to be highly effective. So far, attempts to develop a live attenuated TBE vaccine have been unsuccessful, although promising preliminary results have been obtained in a mouse model using deletion mutants of the 3’ noncoding region of the TBEV genome combined with a mutation (Thr 310) in the putative receptor-binding site in the E glycoprotein. The development of a live attenuated vaccine would provide major advantages with respect to generating long-lasting immunity without the need of frequent booster injections. Other approaches to develop TBE vaccines are based on the use of DNA or RNA vaccines.

http://www.who.int/vaccine_research/diseases/vector/en/index2.html

 


   
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