A number of agents in other classes are in human trials as well. Polymerase inhibitors have somewhat lower efficacy than protease inhibitors,

but appear to have a higher intrinsic barrier to emergence of drug resistance [28]. Cyclophilin inhibitors target host proteins that the virus utilizes and appear quite potent as well with a good resistance profile, but need better characterization in terms of side-effect profiles [29]. NS5a inhibitors Metformin datasheet have also shown promising results in early trials. The opportunity to cure more patients with chronic HCV infection is now a reality, as multiple new agents become available. The next decade will see a rapid evolution of treatment modalities that will provide greater efficacy, less toxicity and shorter treatment duration. This will usher in the beginning of the end for chronic HCV infection. Human parvovirus B19 (B19) circulates worldwide. In temperate climates, epidemic manifestations occur more commonly in late winter, spring or early summer. B19 infection is commonly associated with rash-like illness in children [30]. B19 seroprevalence increases with age so that by the time one reaches adulthood, 50% of individuals have circulating B19-specific IgG. B19 infects, selleckchem replicates in and destroys the precursor cells that are responsible for

producing mature red blood cells. In an infected individual, destroying the source of mature red blood Ergoloid cells will result in dramatically lower haematocrit levels and a temporary anaemic state [31,32]. For those individuals who have disorders that shorten their red cell half-life, B19 infection worsens the presentation producing a more severe transient aplastic crisis. Symptoms in a B19 infected individual will vary considerably from one person to the next. An individual

can be infected and yet be completely asymptomatic, or have a mild flu-like illness, or a life-threatening illness. Despite the infected individual’s presentation, the viral load present within their bloodstream can be extremely high, at ∼1012 genome equivalents mL−1 (geq mL−1). This poses the risk that virus can be transmitted by transfusion of blood components obtained from asymptomatic viremic donors [33,34]. The incidence of B19 in the blood of healthy donors ranges from 1 in 20 000 to 1 in 50 000 donors [34,35]. The risk of transmission is greater when the blood components are made from pooled units compared with those made from single units. This fact places those individuals requiring repeated doses of any of these blood products at risk of becoming infected with B19 over time, including individuals living with haemophilia, who require life-long administration of clotting factor concentrate [34,36]. B19 DNA has also been detected in numerous batches of albumin, factor VIII, factor IX, clotting factor concentrates and immunoglobulin [37,38].