For RNA analyses, cells were lysed at 14 h post-transfection. Intracellular RNA isolation was performed using the acidic phenol method as described by Pasternak et al. (2000) . Total intracellular RNA was resolved in denaturing agarose±formaldehyde gels. Hybridization of dried gels with the radioactively labelled oligonucleotide probe E154, which is complementary to the 3¢ end of the EAV genome and recognizes all viral mRNA molecules (genomic and subgenomic), and phosphoimager quantitation of individual bands were performed as described by Pasternak et al. (2000) . To determine the leader±body junction sequence of sg mRNA7, mRNA7-speci®c RT±PCRs were carried out as described by van Marle et al. (1999b) using an antisense (RT and PCR) primer from the RNA7 body region and a sense PCR primer matching a part of the leader sequence. RT±PCR products were sequenced directly as described by Pasternak et al. (2000) using the leader-derived primer, an ABI PRISMÔ sequencing kit (Perkin Elmer) and an ABI PRISMÔ 310 Genetic Analyser (Perkin Elmer). Debate: Transfusing to normal haemoglobin levels will not improve outcome Recent evidence suggests that critically ill patients are able to tolerate lower levels of haemoglobin than was previously believed. It is our goal to show that transfusing to a level of 100 g/l does not improve mortality and other clinically important outcomes in a critical care setting. Although many questions remain, many laboratory and clinical studies, including a recent randomized controlled trial (RCT), have established that transfusing to normal haemoglobin concentrations does not improve organ failure and mortality in the critically ill patient. In addition, a restrictive transfusion strategy will reduce exposure to allogeneic transfusions, result in more efficient use of red blood cells (RBCs), save blood overall, and decrease health care costs. Anaemia is a common condition in critically ill patients, and RBC transfusions are often used in the treatment and management of this patient population. In fact, one study [1] reported that 25% of all critically ill patients received RBC transfusions. Many laboratory studies [2] [3] [4] [5] [6] [7] [8] have examined the physiological responses (ie compensatory mechanisms) of the body to anaemia, which include the following [9] : increased cardiac output, decreased blood viscosity, capillary changes, increased oxygen extraction, and other tissue adaptations to meet oxygen requirements. Although critically ill patients are affected by a number of factors that predispose them to the adverse consequences of anaemia, persistence of this condition is of particular concern because it may cause the compensatory mechanisms in these patients to become impaired, risking oxygen deprivation in vital organs [9] . However, critically ill patients may also be at increased risk from the adverse effects of RBC transfusions, such as pulmonary oedema from volume overload, immune suppression resulting in increased risk of infection, and microcirculatory injury from poorly deformable RBCs.