They have also been shown to protect mice from a lethal challenge with several TBE-virus isolates obtained over a period of more than 30 years from all over Europe and the Asian part of the former Soviet Union. In addition, it has been demonstrated that antibodies induced by vaccination of human volunteers neutralized all tested isolates. Pregnancy and breastfeeding
The vaccine appears to be safe during pregnancy, but because of insufficient data the vaccine is only recommended during pregnancy and breastfeeding when it is considered urgent to achieve protection against TBE infection and after careful consideration of risks versus benefits. Schedule
Two to three doses are recommended depending on the formulation. Typically one to three months should occur between the first doses followed by five to twelve months before the final dose. Additional doses are then recommended every three to five years. A study from 2006 suggests that the FSME-Immun/Ticovac and Encepur are interchangeable for booster vaccination, but cautions against change during the primary immunization course. History
The first vaccine against TBE was prepared in 1937 in the brains of mice. Some 20 years later TBE vaccines derived from cell cultures (chicken embryo fibroblast cells) were developed and used for active immunization in humans in the former Soviet Union. Later, a purified, inactivated virus vaccine was developed which proved to be more immunogenic than previous TBE vaccines. Society and culture
Economics
Per dose it costs between £50 and £70 in the United Kingdom. Brand names
Brand names of the vaccines include Encepur N, FSME-Immun CC and Ticovac, Encevir-Neo, Klesh-E-Vak.
This gene is responsible for the potassium channel beta subunit MiRP1 which generates the potassium current IKr, and variant that decrease this current have been associated with prolongation of the QT interval. However, subsequent evidence such as the relatively common finding of variants in the gene in those without long QT syndrome, and the general need for a second stressor such as hypokalaemia to be present to reveal the QT prolongation, has suggested that this gene instead represents a modifier to susceptibility to QT prolongation. Some, therefore, dispute whether variants in the gene are sufficient to cause Romano–Ward syndrome by themselves.LQT9 is caused by variants in the membrane structural protein, caveolin-3. Caveolins form specific membrane domains called caveolae in which voltage-gated sodium channels sit. Similar to LQT3, these caveolin variants increase the late sustained sodium current, which impairs cellular repolarization.LQT10 is an extremely rare subtype, caused by variants in the SCN4B gene. The product of this gene is an auxiliary beta-subunit (NaVβ4) forming cardiac sodium channels, variants in which increase the late sustained sodium current. LQT13 is caused by variants in GIRK4, a protein involved in the parasympathetic modulation of the heart. Clinically, the patients are characterized by only modest QT prolongation, but an increased propensity for atrial arrhythmias. LQT14, LQT15 and LQT16 are caused by variants in the genes responsible for calmodulin (CALM1, CALM2, and CALM3 respectively).