Shear turbulence in the high-wind Southern Ocean using direct measurements

The ocean surface boundary layer is a gateway of energy transfer into the ocean. Wind-driven shear and meteorologically forced convection inject turbulent kinetic energy into the surface boundary layer, mixing the upper ocean and transforming its density structure. In the absence of direct observations or the capability to resolve sub-grid scale 3D turbulence in operational ocean models, the oceanography community relies on surface boundary layer similarity scalings (BLS) of shear and convective turbulence to represent this mixing. Despite their importance, near-surface mixing processes (and ubiquitous BLS representations of these processes) have been under-sampled in high energy forcing regimes such as the Southern Ocean. With the maturing of autonomous sampling platforms, there is now an opportunity to collect high-resolution spatial and temporal measurements in the full range of forcing conditions. Here, we characterize near-surface turbulence under strong wind forcing using the first long-duration glider microstructure survey of the Southern Ocean. We leverage these data to show that the measured turbulence is significantly higher than standard shear-convective BLS in the shallower parts of the surface boundary layer and lower than standard shear-convective BLS in the deeper parts of the surface boundary layer; the latter of which is not easily explained by present wave-effect literature. Consistent with the CBLAST (Coupled Boundary Layers and Air Sea Transfer) low winds experiment, this bias has the largest magnitude and spread in shallowest 10% of the actively mixing layer under low-wind and breaking wave conditions, when relatively low levels of turbulent kinetic energy (TKE) in surface regim

Dynamics of HEV viremia, fecal shedding and its relationship with transaminases and antibody response in patients with sporadic acute hepatitis E

<p>Abstract</p> <p>Background</p> <p>There is paucity of data regarding duration of fecal excretion and viremia on sequential samples from individual patients and its correlation with serum transaminases and antibody responses in patients with acute hepatitis E. This prospective study was undertaken at a tertiary care center in Northern India over 15 months. Only those patients of sporadic acute hepatitis E who were in their first week of illness and followed up weekly for liver function tests, IgM anti HEV antibody and HEV RNA in sera and stool were included. HEV RNA was done by RT - nPCR using two pairs of primers from RdRp region of ORF 1 of the HEV genome.</p> <p>Results</p> <p>Over a period of 15 months 60 patients met the inclusion criterion and were enrolled for the final analysis. The mean age of the patients was 29.2 ± 8.92 years, there were 39 males. The positivity of IgM anti HEV was 80% at diagnosis and 18.3% at 7th week, HEV RNA 85% at diagnosis and 6.6% at 7th week and fecal RNA 70% at the time of diagnosis and 20% at 4th week. The maximum duration of viremia detected was 42 days and fecal viral shedding was 28 days after the onset of illness.</p> <p>Conclusion</p> <p>Present study reported HEV RNA positivity in sera after normalization of transaminases. Fecal shedding was not seen beyond normalization of transaminases. However, viremia lasted beyond normalization of transaminases suggesting that liver injury is independent of viral replication.</p

Replication, Gene Expression and Particle Production by a Consensus Merkel Cell Polyomavirus (MCPyV) Genome

Merkel Cell Polyomavirus (MCPyV) genomes are clonally integrated in tumor tissues of approximately 85% of all Merkel cell carcinoma (MCC) cases, a highly aggressive tumor of the skin which predominantly afflicts elderly and immunosuppressed patients. All integrated viral genomes recovered from MCC tissue or MCC cell lines harbor signature mutations in the early gene transcript encoding for the large T-Antigen (LT-Ag). These mutations selectively abrogate the ability of LT-Ag to support viral replication while still maintaining its Rb-binding activity, suggesting a continuous requirement for LT-Ag mediated cell cycle deregulation during MCC pathogenesis. To gain a better understanding of MCPyV biology, in vitro MCPyV replication systems are required. We have generated a synthetic MCPyV genomic clone (MCVSyn) based on the consensus sequence of MCC-derived sequences deposited in the NCBI database. Here, we demonstrate that transfection of recircularized MCVSyn DNA into some human cell lines recapitulates efficient replication of the viral genome, early and late gene expression together with virus particle formation. However, serial transmission of infectious virus was not observed. This in vitro culturing system allows the study of viral replication and will facilitate the molecular dissection of important aspects of the MCPyV lifecycle