Tick-borne encephalitis vaccine is a vaccine used to prevent tick-borne encephalitis (TBE). The disease is most common in Central and Eastern Europe, and Northern Asia. More than 87% of people who receive the vaccine develop immunity. It is not useful following the bite of an infected tick. It is given by injection into a muscle.The World Health Organization (WHO) recommends immunizing all people in areas where the disease is common. Otherwise the vaccine is just recommended for those who are at high risk. Three doses are recommended followed by additional doses every three to five years. The vaccines can be used in people more than one or three years of age depending on the formulation. The vaccine appears to be safe during pregnancy.Serious side effects are very uncommon. Minor side effects may include fever, and redness and pain at the site of injection. Older formulations were more commonly associated with side effects.The first vaccine against TBE was developed in 1937. It is on the World Health Organizations List of Essential Medicines. The vaccine was approved for medical use in the United States in August 2021. Medical uses
In the United States, tick-borne encephalitis vaccine is indicated for active immunization to prevent tick-borne encephalitis (TBE) in individuals one year of age and older.The efficacy of these vaccines has been well documented.
If either the ERCC6 or the ERCC8 gene is altered (as in Cockayne Syndrome), DNA damage encountered during transcription isnt repaired, causing RNA polymerase to stall at that location, interfering with gene expression. As the unrepaired DNA damage accumulates, progressively more active gene expression is impeded, leading to malfunctioning cells or cell death, which likely contributes to the signs of Cockayne Syndrome such as premature aging and neuronal hypomyelination. Mechanism
In contrast to cells with normal repair capability, CSA and CSB deficient cells are unable to preferentially repair cyclobutane pyrimidine dimers induced by the action of ultraviolet (UV) light on the template strand of actively transcribed genes. This deficiency reflects the loss of ability to perform the DNA repair process known as transcription coupled nucleotide excision repair (TC-NER).Within the damaged cell, the CSA protein normally localizes to sites of DNA damage, particularly inter-strand cross-links, double-strand breaks and some monoadducts. CSB protein is also normally recruited to DNA damaged sites, and its recruitment is most rapid and robust as follows: interstrand crosslinks > double-strand breaks > monoadducts > oxidative damage. CSB protein forms a complex with another DNA repair protein, SNM1A (DCLRE1A), a 5 – 3 exonuclease, that localizes to inter-strand cross-links in a transcription dependent manner. The accumulation of CSB protein at sites of DNA double-strand breaks occurs in a transcription dependent manner and facilitates homologous recombinational repair of the breaks.