678 research outputs found
Relative replication capacity of phenotypic SIV variants during primary infections differs with route of inoculation
BACKGROUND: Previous studies of human and simian immunodeficiency virus (HIV and SIV) have demonstrated that adaptive mutations selected during the course of infection alter viral replicative fitness, persistence, and pathogenicity. What is unclear from those studies is the impact of transmission on the replication and pathogenicity of the founding virus population. Using the SIV-macaque model, we examined whether the route of infection would affect the establishment and replication of two SIVmne variants of distinct in vitro and in vivo biological characteristics. For these studies, we performed dual-virus inoculations of pig-tailed macaques via intrarectal or intravenous routes with SIVmneCl8, a miminally pathogenic virus, and SIVmne027, a highly pathogenic variant that replicates more robustly in CD4(+ )T cells. RESULTS: The data demonstrate that SIVmne027 is the dominant virus regardless of the route of infection, indicating that the capacity to replicate efficiently in CD4(+ )T cells is important for fitness. Interestingly, in comparison to intravenous co-infection, intrarectal inoculation enabled greater relative replication of the less pathogenic virus, SIVmneCl8. Moreover, a higher level of SIVmneCl8 replication during primary infection of the intrarectally inoculated macaques was associated with lower overall plasma viral load and slower decline in CD4(+ )T cells, even though SIVmne027 eventually became the dominant virus. CONCLUSIONS: These results suggest that the capacity to replicate in CD4(+ )T cells is a significant determinant of SIV fitness and pathogenicity. Furthermore, the data also suggest that mucosal transmission may support early replication of phenotypically diverse variants, while slowing the rate of CD4(+ )T cell decline during the initial stages of infection
Phase Diagram of Pressure-Induced Superconductivity in EuFe2As2 Probed by High-Pressure Resistivity up to 3.2 GPa
We have constructed a pressuretemperature () phase diagram of
-induced superconductivity in EuFeAs single crystals, via
resistivity () measurements up to 3.2 GPa. As hydrostatic pressure is
applied, an antiferromagnetic (AF) transition attributed to the FeAs layers at
shifts to lower temperatures, and the corresponding resistive
anomaly becomes undetectable for 2.5 GPa. This suggests that the
critical pressure where becomes zero is about 2.5
GPa. We have found that the AF order of the Eu moments survives up to
3.2 GPa without significant changes in the AF ordering temperature
. The superconducting (SC) ground state with a sharp transition
to zero resistivity at 30 K, indicative of bulk
superconductivity, emerges in a pressure range from 2.5
GPa to 3.0 GPa. At pressures close to but outside the SC phase, the
curve shows a partial SC transition (i.e., zero resistivity is not
attained) followed by a reentrant-like hump at approximately
with decreasing temperature. When nonhydrostatic pressure with a uniaxial-like
strain component is applied using a solid pressure medium, the partial
superconductivity is continuously observed in a wide pressure range from 1.1
GPa to 3.2 GPa.Comment: 7 pages, 6 figures, accepted for publication in Physical Review B,
selected as "Editors' Suggestion
High-Pressure Electrical Resistivity Measurements of EuFe2As2 Single Crystals
High-pressure electrical resistivity measurements up to 3.0GPa have been
performed on EuFe2As2 single crystals with residual resistivity ratios RRR=7
and 15. At ambient pressure, a magnetic / structural transition related to
FeAs-layers is observed at T0 =190K and 194K for samples with RRR=7 and 15,
respectively. Application of hydrostatic pressure suppresses T0, and then
induces similar superconducting behavior in the samples with different RRR
values. However, the critical pressure 2.7GPa, where T0=0, for the samples with
RRR=15 is slightly but distinctly larger than 2.5GPa for the samples with
RRR=7.Comment: To be published in J. Phys.: Conf. Se
Mouse aggrecan, a large cartilage proteoglycan: protein sequence, gene structure and promoter sequence
Altered proteoglycan synthesis by micromelial limbs induced by 6-aminonicotinamide. Appearance of abnormal forms of cartilage-characteristic proteoglycan (PG-H)
Aortic endothelial cells synthesize a large chondroitin sulphate proteoglycan capable of binding to hyaluronate
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