Factor V (pronounced factor five) is a protein of the coagulation system, rarely referred to as proaccelerin or labile factor. In contrast to most other coagulation factors, it is not enzymatically active but functions as a cofactor. Deficiency leads to predisposition for hemorrhage, while some mutations (most notably factor V Leiden) predispose for thrombosis. Genetics
The gene for factor V is located on the first chromosome (1q24). It is genomically related to the family of multicopper oxidases, and is homologous to coagulation factor VIII. The gene spans 70 kb, consists of 25 exons, and the resulting protein has a relative molecular mass of approximately 330kDa. Structure
Factor V protein consists of six domains: A1-A2-B-A3-C1-C2. The A domains are homologous to the A domains of the copper-binding protein ceruloplasmin, and form a triangular as in that protein. A copper ion is bound in the A1-A3 interface, and A3 interacts with the plasma.The C domains belong to the  phospholipid-binding discoidin domain family (unrelated to C2 domain), and the C2 domain mediates membrane binding. The B domain C-terminus acts as a cofactor for the anticoagulant protein C activation by protein S.Activation of factor V to factor Va is done by cleavage and release of the B domain, after which the protein no longer assists in activating protein C. The protein is now divided to a heavy chain, consisting of the A1-A2 domains, and a light chain, consisting of the A3-C1-C2 domains. Both form non-covalently a complex in a calcium-dependent manner.
Infection and mortality due to V. vulnificus causes over 95% of deaths in the United States that are known to have occurred due to ingested seafood. Surprisingly enough, while V. vulnificus claims 95% of seafood related deaths, if treatment with tetracycline or other cephalosporin antibiotics is initiated at the onset of symptoms and is managed appropriately, patients will experience no long term effects, provided they continue to take the full course of antibiotics—typically about two weeks.The worst prognosis is in those people arriving at hospital in a state of shock. Total mortality in treated people (ingestion and wound) is around 33%.People especially vulnerable are those with liver disease (especially cirrhosis and hepatitis) or immunocompromised states (some kinds of cancer, bone marrow suppression, HIV, diabetes, etc.). With these cases, V. vulnificus usually enters the bloodstream, where it may cause fever and chills, septic shock (with sharply decreased blood pressure), and blistering skin lesions. About half of those who contract blood infections die. Vibrio vulnificus infections also disproportionately affect males; 85% of those developing endotoxic shock from the bacteria are male. Females having had an oophorectomy experienced increased mortality rates, as  estrogen has been shown experimentally to have a protective effect against V. vulnificus. Epidemiology
Vibrio vulnificus is commonly found in the Gulf of Mexico, where more than a dozen people have died from the infection since 1990. Most deaths at that time were occurring due to fulminant sepsis, either in the area of oyster harvest and ingestion, or in tourists returning home.