Currently there is no FDA-approved treatment to stop the spread of MACV once humans are infected. Defining interactions between the viral glycoprotein and a cellular receptor may allow for drug development that could limit viral spread in the infected individual and reduce infection during an outbreak. Our mutagenesis analysis of MACV GP1 experimentally elucidates the structure and functional interaction motifs of MACV GP1 and its receptor hTfR1. These studies therefore provide a solid platform for the future design and development of small molecule inhibitors and antivirals specifically targeting viral entry. The advent of ECMO and pumpless extracorporeal lung assist in ARDS Despite advances in critical care facilities and ventilation therapies acute respiratory distress syndrome (ARDS) is associated with high mortality rates. The condition can stem from a multitude of causes including pneumonia, septicemia and trauma ultimately resulting in ARDS. ARDS is characterized by respiratory insufficiency with severe hypoxemia or hypercapnia. The treatment strategy depends on the knowledge of the underlying disease. But lung-protective ventilation with adjusted positive end-expiratory pressure remains the most effective therapeutic tool despite advances in prone positioning, inhalation of nitric oxide and the use of steroids. Newer modalities including extracorporeal membrane oxygenation (ECMO) and pumpless extracorporeal lung assist (PECLA) are being increasingly introduced in critical care settings as rescue therapies in patients who fail to respond to conservative measures. We describe here the introduction and advances of both ECMO and PECLA in the management of ARDS.  GI-type T4SS-mediated horizontal transfer of the 89K pathogenicity island in epidemic Streptococcus suis serotype 2 Pathogenicity islands (PAIs), a distinct type of genomic island (GI), play important roles in the rapid adaptation and increased virulence of pathogens. 89K is a newly identified PAI in epidemic Streptococcus suis isolates that are related to the two recent large-scale outbreaks of human infection in China. However, its mechanism of evolution and contribution to the epidemic spread of S. suis 2 remain unknown. In this study, the potential for mobilization of 89K was evaluated, and its putative transfer mechanism was investigated. We report that 89K can spontaneously excise to form an extrachromosomal circular product. The precise excision is mediated by an 89K-borne integrase through site-specific recombination, with help from an excisionase. The 89K excision intermediate acts as a substrate for lateral transfer to non-89K S. suis 2 recipients, where it reintegrates site-specifically into the target site. The conjugal transfer of 89K occurred via a GI type IV secretion system (T4SS) encoded in 89K, at a frequency of 10(−6) transconjugants per donor. This is the first demonstration of horizontal transfer of a Gram-positive PAI mediated by a GI-type T4SS. We propose that these genetic events are important in the emergence, pathogenesis and persistence of epidemic S. suis 2 strains. Streptococcus suis serotype 2 (S. suis 2) is a Grampositive, economically important, zoonotic pathogen that is a leading cause of contagious porcine diseases, including meningitis, arthritis, pneumonia, endocarditis and septicaemia Feng et al., 2010) . Further, S. suis 2 can also be transmitted to humans by direct contact with infected swine, causing meningitis, permanent hearing loss, septic shock and even death (Gottschalk et al., 2007) . Due to its high incidence, transmissibility, persistence in the environment and its ability to occur in explosive epidemic form, S. suis 2 continues to be a global public health concern. After two extensive human outbreaks of streptococcal toxic shock syndrome (STSS) caused by S. suis 2 in China in 1998 (Tang et al., 2006 , S. suis 2 has been recognized as a re-emerging zoonotic pathogen and was found to characteristically harbour a candidate pathogenicity island (PAI) designated 89K (Chen et al., 2007) . Recent genetic evidence showing that a two-component system (SalK/R) encoded within this island mediates a piglet-lethal phenotype has strengthened the case that 89K is a PAI (Li et al., 2008) .