Experiments in M. rhesus showed persistence to be a typical property of West Nile virus. This property was exhibited by strains belonging to different antigenic types, and varying in virulence and in the isolation area (U.S.S.R., Uganda, India). The duration of persistence was at least 5 1/2 months in asymptomatic infection and in convalescence after encephalitis or a febrile disease. The virus isolated within the first 2 weeks after inoculation of monkeys has the standard properties. The virus persisting for 2 months retains its cytopathic and antigenic activity, however, is non-pathogenic for white mice. After 5 1/2 months of persistence the virus has no neurovirulence or cytopathic properties but is capable of infecting the susceptible cells and induces in them the synthesis of virus-specific antigen detectable by immunofluorescence. The persisting virus has been isolated by cocultivation of trypsinized monkey organ cells and cells of the indicator culture. This virus was located mostly in the cerebellum, cerebral subcortical ganglia, lymph nodes, and kidneys. The monkeys experiencing encephalitis, febrile, or asymptomatic infection showed in morphological examinations a subacute inflammatory-degenerative process in the central nervous system. The results suggest that West Nile virus, one of the most widely spread arboviruses in Africa, Asia, and Europe, may be implicated in the etiology of subacute diseases of the CNS.

Tick-borne encephalitis virus (TBEV) causes human epidemics across Eurasia. Clinical manifestations range from inapparent infections and fevers to fatal encephalitis but the factors that determine disease severity are currently undefined. TBEV is characteristically a hemagglutinating (HA) virus; the ability to agglutinate erythrocytes tentatively reflects virion receptor/fusion activity. However, for the past few years many atypical HA-deficient strains have been isolated from patients and also from the natural European host tick, Ixodes persulcatus. By analysing the sequences of HA-deficient strains we have identified 3 unique amino acid substitutions (D67G, E122G or D277A) in the envelope protein, each of which increases the net charge and hydrophobicity of the virion surface. Therefore, we genetically engineered virus mutants each containing one of these 3 substitutions; they all exhibited HA-deficiency. Unexpectedly, each genetically modified non-HA virus demonstrated increased TBEV reproduction in feeding Ixodes ricinus, not the recognised tick host for these strains. Moreover, virus transmission efficiency between infected and uninfected ticks co-feeding on mice was also intensified by each substitution. Retrospectively, the mutation D67G was identified in viruses isolated from patients with encephalitis. We propose that the emergence of atypical Siberian HA-deficient TBEV strains in Europe is linked to their molecular adaptation to local ticks. This process appears to be driven by the selection of single mutations that change the virion surface thus enhancing receptor/fusion function essential for TBEV entry into the unfamiliar tick species. As the consequence of this adaptive mutagenesis, some of these mutations also appear to enhance the ability of TBEV to cross the human blood-brain barrier, a likely explanation for fatal encephalitis. Future research will reveal if these emerging Siberian TBEV strains continue to disperse westwards across Europe by adaptation to the indigenous tick species and if they are associated with severe forms of TBE.

Relevance.Modern inactivated culture vaccines against tick-borne encephalitis (TBE) with at least 70% of the population living in the  natural foci of the FE give a high epidemiological effect. Unresolved  issues are the simplification of the cumbersome vaccination scheme,  the optimal number of revaccinations, the protective titer of  antibodies against the Siberian subtype of the TBE virus dominant in Russia.Goalof this work is to study the state of postvaccinal immunity in the population of the highly endemic area of the Trans-Urals.Materials and methods. 1381 blood serum of the population vaccinated from 3 to 13 times with vaccines was studied: unconcentrated culture inactivated from strain No. 205 of the TBE  virus produced by «Virion», Tomsk, «EnceVir» produced by  «Microgen», Tomsk, produced by Chumakov Federal Scientific Center for Research and Development of Immuneand-Biological Products of  Russian.To identify specific antibodies – IgG, IgM, antigen of TBE  virus, sets of reagents of ELISA from «Vector-Best» were used.  Neutralizing activity of sera was determined by the index of  neutralization index with 4 strains of the Siberian subtype of TBE  virus.Results.The immune layer among the vaccinated population in 10 districts of the Kurgan region, which differ in epidemiological tension, ranges from 69.9% to 94.6%. The intensity of humoral immunity  varied according to IgG titers in ELISA from 1: 100 – 1: 200 to 1:  3200 (rarely 1: 6400). The duration and intensity of immunity  depends on the number of vaccinations and the number of missed  remote revaccinations. Preservation and intensity of immunity with  reliability P = 95%, higher in persons vaccinated 6–10 times  compared with the group of vaccinated 3 times. In persons who had 4–8 booster dose of vaccine, the immunity persisted for 15–19–36 years with an IgG titer of not more than 1: 100. The neutralizing  activity of the sera of vaccinated individuals with antibody titers from 1:100 to 1: 6400 was studied for the Siberian subtype of BCE. The  degree of protection of the vaccinated population against the doses  of the virus found in individual mites is determined. From the doses  of the virus, 57% of the vaccinated population are most often found  in mites, and from the dose of 105– 8%. Recommendations are  proposed on the tactics of revaccination of the population, depending on the level of immunity.

Background: December 2007, some cases of dengue hemorrhagic fever were diagnosed in clildren in Rio de Janeiro, Brazil. Along the following months, the has ravaged the state, infecting more than 150,000 people with 232 suspected deaths. 42% of fatal cases were in children. The deaths showed us that the plasma leakage and shock are more common than hemorrhagic phenomena. In many cases, the presence of pleural, pericardial and peritoneal effusions were associated with a severe disease. The emergency rooms in the state were not capableto absorb the extra demand and causing the collapse of the healthcare system. The last outbreak in Rio de Janeiro was happen in 2002 with the serotype 3 and now the serotype 2 e 3 has been reported.Methods: On February 2008, a hundred of new dengue cases were being reported/ hour, so the health department of Rio the Janeiro State, the Mylitary Fire Corps and the Armed Forces assembled 7 field hospitals to support the emergency rooms, working with more 1000 health care providers. The average field hospital was equipped with an electronic blood cell counting machine, 30 beds for hydratation and 1 advanced ambulance. This intervention was based in the cocept of disaster medicine. The patients were triaged in the hospitals, had their blood taken for diagnosis, kept in observation and hydratated. The caes with deterioration were admitted to the hospital and if the patient got better, he was sent home.Results: The intravenous fluid administration during 12 hour observation period was associated with a decreased risk for the death and complications. On April, 29,000 cases were treated in the field hospitals and less than 2% of the patients were admitted to the emergency hospitals. Conclusion:The Field hospitals were a practical solution to reduce the mortality and morbility in this outbreak.