Prevention
Vaccination is the only known method to prevent the development of tumors when chickens are infected with the virus. However, administration of the vaccine does not prevent an infected bird from shedding the virus, though it does reduce the amount of virus shed in the dander, hence reducing horizontal spread of the disease. Mareks disease does not spread vertically. Before the development of the vaccine for Mareks disease, Mareks disease caused substantial revenue loss in the poultry industries of the United States and the United Kingdom. The vaccine can be administered to one-day-old chicks through subcutaneous inoculation or by in ovo vaccination when the eggs are transferred from the incubator to the hatcher. In ovo vaccination is the preferred method, as it does not require handling of the chicks and can be done rapidly by automated methods. Immunity develops within two weeks.Because vaccination does not prevent infection with the virus, Mareks is still transmissible from vaccinated flocks to other birds, including the wild bird population. The first Mareks disease vaccine was introduced in 1970. The disease would cause mild paralysis, with the only identifiable lesions being in neural tissue. Mortality of chickens infected with Mareks disease was quite low. Current strains of Marek virus, decades after the first vaccine was introduced, cause lymphoma formation throughout the chickens body and mortality rates have reached 100% in unvaccinated chickens. The Mareks disease vaccine is a "leaky vaccine", which means that only the symptoms of the disease are prevented.
XP repair proteins
The XPA protein acts during NER as a scaffold for assembly of other DNA repair proteins at sites of DNA damage to ensure appropriate excision of the damage.The XPB (ERCC3) protein is employed in unwinding the DNA double helix after DNA damage is initially recognized. Mutations in the XPB(ERCC3) gene can lead to XP or XP combined with Cockayne syndrome.The XPC protein forms a complex with RAD23B protein to form the initial damage recognition factor in global genomic nucleotide excision repair (GG-NER). This complex recognizes a wide variety of damages that thermodynamically destabilize DNA duplexes.The XPD (ERCC2) protein, in combination with the XPB helicase-containing transcription/repair complex TFIIH, is employed in unwinding the DNA duplex after damage is initially recognized. Mutations in the XPD(ERCC2) gene cause a variety of syndromes; XP, trichothiodystrophy (TTD), or a combination of XP and Cockayne syndrome (XPCS). Both trichothiodystrophy and Cockayne syndrome display features of premature aging, suggesting an association between deficient DNA repair and premature aging (see DNA damage theory of aging). XPE is a heterodimeric protein composed of two subunits. The larger subunit DDB1 primarily functions as a core component of CUL4A- and CUL4B-based E3 ubiquitin ligase complexes. Substrates that are ubiquitinnated by these complexes include proteins employed in DNA repair.The XPF (ERCC4) protein together with the ERCC1 protein forms a complex usually designated ERCC1-XPF. This complex separates the DNA helix for a short distance on either side of the site of damage.