In conclusion, in a population of healthy young adults, elevated CRP with normal ESR and WBC levels combined with GGOs and nodules on thin-section CT scans may indicate early signs of infection by the pandemic H1N1 2009 influenza virus. A Clathrin Independent Macropinocytosis-Like Entry Mechanism Used by Bluetongue Virus-1 during Infection of BHK Cells Acid dependent infection of Hela and Vero cells by BTV-10 occurs from within early-endosomes following virus uptake by clathrin-mediated endocytosis (Forzan et al., 2007: J Virol 81: 4819–4827). Here we report that BTV-1 infection of BHK cells is also dependent on a low endosomal pH; however, virus entry and infection were not inhibited by dominant-negative mutants of Eps15, AP180 or the ‘aa’ splice variant of dynamin-2, which were shown to inhibit clathrin-mediated endocytosis. In addition, infection was not inhibited by depletion of cellular cholesterol, which suggests that virus entry is not mediated by a lipid-raft dependent process such as caveolae-mediated endocytosis. Although virus entry and infection were not inhibited by the dominant-negative dynamin-2 mutant, entry was inhibited by the general dynamin inhibitor, dynasore, indicating that virus entry is dynamin dependent. During entry, BTV-1 co-localised with LAMP-1 but not with transferrin, suggesting that virus is delivered to late-endosomal compartments without first passing through early-endosomes. BTV-1 entry and infection were inhibited by EIPA and cytochalasin-D, known macropinocytosis inhibitors, and during entry virus co-localised with dextran, a known marker for macropinocytosis/fluid-phase uptake. Our results extend earlier observations with BTV-10, and show that BTV-1 can infect BHK cells via an entry mechanism that is clathrin and cholesterol-independent, but requires dynamin, and shares certain characteristics in common with macropinocytosis. Virus internalisation is initiated by binding to specific receptors at the cell-surface and culminates in host-cell membrane penetration and delivery of the viral genome to the site of replication. For many viruses, membrane penetration follows virus endocytosis. Several different endocytosis pathways operate in mammalian cells which deliver cargoes to distinct intracellular locations [1, 2] . Clathrin-mediated endocytosis (CME) is the major pathway for receptor-dependent endocytosis in many cell types and is dependent on adaptor proteins, such as the AP-2 complex, the GTPase dynamin [2, 3] , and several other important accessory molecules including AP180 and Eps-15 [4, 5, 6] . CME delivers cargoes to acidic endosomes; initially to early-endosomes where they are sorted for transport to either late-endosomes/lysosomes for degradation or to recycling-endosomes for recycling back to the cell surface. Several acid-activated viruses are known to exploit the low pH within vesicles derived from the clathrin pathway, to trigger capsid un-coating and/or membrane penetration [7] .