This acquired immunity reduces the risk of severe, non-cerebral malaria to negligible levels. Their findings contradict other epidemiological studies showing that immunity to the disease is acquired slowly and may never be complete. The data are good news for vaccine development, writes Druilhe. Vaccination could be an easier task to achieve than previously thought because immunity may depend on well conserved rather than polymorphic antigens. Heart function is impaired progressively and sudden death can occur.
Heart transplantation is at presently the only therapy for the disease.
However, new data show that an understanding of the molecular cardiology associated with the disease may offer new therapeutic perspectives for its treatment. David Kass and colleagues from Johns Hopkins assessed the effects of this mutation in a mouse model of the disease. Using new methods of measuring ventricular function in vivo, the researchers show that the initial effect of the genetic mutation is altered contraction dynamics. And for the first time, they report age-related changes in the heart associated with FHC, such as increased heart chamber stiffness and a decline in cardiac output in older mice with the disease. Thus, while the mutation that causes FHC has primary effects on contractile proteins, long-term responses to the mutation are equally important in the evolution of cardiomyopathy.