Bacteriophage T7 is a bacteriophage capable of infecting susceptible bacterial cells. It infects most strains of Escherichia coli (including E. coli O157:H7 - a strain of E. coli which can cause foodborne illness). Bacteriophage T7 is a DNA virus that has a lytic life cycle. The T7 bacteriophage has several properties that make it an ideal phage for experimentation.
Bacteriophage T7 was identified in 1945 as a member of the seven Type (“T”) phages that grow lytically on Escherichia coli B, although it is probably identical to phage δ, used earlier by Delbrück. A close relative of T7 was likely studied by d’Herelle in the 1920s.
T7 grows on rough strains of E. coli (i.e. those without full-length O-antigen polysaccharide on their surface) and some other enteric bacteria, but close relatives also infect smooth and even capsulated strains.
The virus has complex structural symmetry, with a capsid of the phage that is icosahedral with an inner diameter of 55 nm and a tail 19 nm in diameter and 28.5 nm long attached to the capsid.
Glycoprotein V (platelet) (GP5) also known as CD42d (Cluster of Differentiation 42d), is a human gene.
Human platelet glycoprotein V (GP5) is a part of the Ib-V-IX system of surface glycoproteins that constitute the receptor for von Willebrand factor (VWF; MIM 193400) and mediate the adhesion of platelets to injured vascular surfaces in the arterial circulation, a critical initiating event in hemostasis. The main portion of the receptor is a heterodimer composed of 2 polypeptide chains, an alpha chain (GP1BA; MIM 606672) and a beta chain (GP1BB; MIM 138720), that are linked by disulfide bonds. The complete receptor complex includes noncovalent association of the alpha and beta subunits with platelet glycoprotein IX (GP9; MIM 173515) and GP5. Mutations in GP1BA, GP1BB, and GP9 have been shown to cause Bernard-Soulier syndrome (MIM 231200), a bleeding disorder.[supplied by OMIM]