What is pichinde virus

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what is pichinde virus

The NO synthase inhibition also has no effect on levels of activated caspases induced by PIC infection. Vascular leak can be caused by direct viral effects that alter barrier integrity, the induction of apoptosis of the endothelium, or indirectly through the effects of soluble mediators such as pro-inflammatory cytokines created by the host immune response [ 4 ].

Thomasomys fuscatus. Basal levels of NO are necessary for vasodilation, platelet aggregation, and the modulation of inflammatory cell adhesion to the endothelium [ 14 — 16 ].

what is pichinde virus

Cells were maintained in Clonetics Endothelial Growth Medium EGM-MV supplemented with hydrocortisone, human endothelial growth factor, fetal bovine serum, vascular endothelial growth factor, human fibroblast growth factor-B, insulin-like growth factor, ascorbic acid, gentamicin and amphotericin-B.

Cells were grown on 6 mm collagen-coated polycarbonate membrane inserts Corning with 0.

9 Replication of negative stranded RNA virus

Proinflammatory cytokines and elastase-alpha-1-antitrypsin in Argentine hemorrhagic fever. Figure 2 Time dependence of PIC-induced permeability.

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Each timepoint represents the mean of two experiments. After incubation for 1.

what is pichinde virus

Figure 6 Effect of PIC infection on caspase activation. Nitric oxide modulates microvascular permeability.

Status Not Arbovirus.

Centers for Disease Control and Prevention

J Invest Dermatol 1992, 99: Once cells had reached confluency, indicated by a constant resistance measurement, cells were infected with PIC at a multiplicity of infection MOI 0.

Nitric oxide NO is a free radical with diverse physiological functions in humans.

what is pichinde virus

To investigate the effect of viral infection on endothelial cell permeability, HMEC-1s were grown to confluence on porous membrane inserts and subsequently infected with PIC.

Supernatants of HMEC-1 cell cultures were collected at 24, 48, 72, and 96 hrs post infection.

what is pichinde virus

These studies will be critical as an in vitro model of VHF pathogenesis and to identify mechanisms of vascular leak and to identify potential inhibitors of VHF-induced leak in an effort to alleviate the severity of VHF. FEBS Lett 1998, 433: