Flipping the wound that doesn't heal: the upside of coagulation in cancer.

modified to alter levels of Pk expression.5 The results were significant. P1k cells were protected from R5 and X4 HIV-1 infection and had increased CD4, coreceptor, and Pk expression, while PBMCs with the p phenotype had heightened susceptibility to R5 and X4 HIV-1 infection. Further supporting a role for Pk was that Pk -liposome fusion in Jurkat cells decreased susceptibility to HIV and cells transduced with Pk -synthase (augmenting Pk expression) showed decreased HIV-1 infectability, while Pk depletion or Pk-synthase gene silencing promoted HIV infection. Mechanistically, it may prove to be that the Pk effect is due to altered lipid raft formation and/or HIV receptor or coreceptor localization, function, or accessibility. Alternatively or perhaps additionally, Pk may be critical to viral internalization. That Pk and indeed other blood groups have a more defined role in host-microbial infection is an important new finding. Other examples include Fya as the binding epitope for plasmodium6 and the P antigen as a receptor for the B19 parvovirus.7 With this discovery, Pk adds to our list of genetic polymorphisms that individually and/or in concert contribute to HIV resistance/susceptibility and potentially generates a site for possible future therapeutic use.8 Conflict-of-interest disclosure: The author declares no competing financial interests. ■