Factor VIII

of a blood protein essential for clotting causes both. Patients with hemophilia A lack the blood clotting protein, factor VIII, and those with hemophilia B lack factor IX. A person with severe hemophilia has less than 1% of the normal amount of a clotting factor - either Factor VIII (8) or Factor IX (9). People without hemophilia have between 50-150% of the normal level of factor VIII or IX. There are about 20,000 hemophilia patients in the United States. Each year, about 400 babies are born with

protein, known as factor VIII (NCBI, 2011). The specific gene that codes for factor VIII is known as the HEMA gene (NCBI, 2011). Factor VIII is mainly synthesized in the liver (NCBI, 2011). Any lack of factor VIII

portal hypertension1.After prothrombin, factor V, next most common cause of thrombophilia is high plasma levels of coagulation factor VIII, which are present in approximately 20% of patients with deep vein thrombosis (DVT) of the lower limbs and increase the risk of the disease in a dose-dependent manner 2. Like fibrinogen, factor VIII is an acute phase reactant whose concentration rises in plasma in the presence of inflammation. However, high factor VIII levels are associated with an increased risk

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one inversion of the Factor VIII gene. This mutation occurs in 40-50 percent of people with Hemophilia A. It is caused by the homologous recombination between copies of a DNA sequence. One copy is located on the intron 22 region of factor VIII and the other copies are distal to the factor VIII. Intron one of the factor VIII gene occurs when the factor VIII gene is split which results in the production of two chimeric mRNAs. One of the mRNA has have the exon of the factor VIII and the exons 2-6 on

well (HoG Handbook). This is possible if all of the family members who have hemophilia or who carry the hemophilia gene give birth to children who by chance do not inherit the gene (HoG Handbook). As far as the level of severity goes, the clotting factor level will be about the same from one generation to the next. For example, a son who inherited the recessive allele from his mother will typically have the same severity level as his mother, if she also has the disease or is a carrier of the disease

absence of a coagulation factor, which arise from mutations in the VIII (FVIII) and IX (FIX) factor genes1. Recent advances in the field of gene therapy have unveiled the use of adeno-associated vectors (AAV) and adenovirus vectors (Ad) to increase the levels of expression of the VIII and IX factors, counteracting the effects of the mutation 1. Gene transfer methods of the coagulation factor IX using AAV has resulted in dogs that had either sustained expression of the factor or that were completely

disorder. This condition or bleeding disorder is characterized by a deficiency in the activity of a coagulation factor, which in this case is F8 or coagulation factor VIII. This condition is clinically known to be heterogeneous and its severity depends on the plasma level of the coagulation factor VIII. Varying levels of hemophilia exist which are categorized based on percentage of coagulation factor within blood plasma compared to normal levels. According to the CDC website, Hemophilia, is a hereditary