Ten Japanese field isolates of beet necrotic yellow vein virus (BNYVV) were transmitted to Tetragonia expansa by inoculation with sap from rootlets of sugar-beet seedlings, to which the virus had been transmitted by the fungus Polymyxa betae. RNA extracted from BNYVV particles obtained from the T. expansa leaves was analysed by agarose gel electrophoresis. Some isolates contained RNA-1 (7.1 kb), RNA-2 (4.8 kb), RNA-3 (1.85 kb) and RNA-4 (1.5 kb) and the others contained, in addition, RNA-5 (1.4 kb). Further isolates, derived from single lesions produced by these isolates, had a variety of RNA compositions. Some contained only RNA-I and RNA-2. Others contained, in addition, RNA-3, RNA-4, RNA-5 or RNA-6 (1.0 kb), or combinations of two or three of these components. Such isolates generally maintained their RNA composition on further subculture, and their particles had length distributions corresponding to their RNA components. Isolates containing RNA-I + 2 + 3 caused yellow or strongly chlorotic local lesions in T. expansa, Beta vulgaris, B. macrocarpa and Chenopodium quinoa, and caused systemic stunting and yellow mosaic in B. macrocarpa and, occasionally, in B. vulgaris. In contrast, isolates containing RNA-1 + 2 + 4 or 1 + 2 + 5 induced chlorotic lesions, those containing RNA-1 + 2 + 6 or 1 + 2 induced faint chlorotic lesions, and none of these isolates easily infected B. macrocarpa systemically. Isolates containing different combinations of RNA-3,-4 and -5 induced more severe symptoms than those containing a single RNA. Such synergistic effects occurred between RNA-3 and RNA-4 or RNA-5, or between RNA-4 and RNA-5 or RNA-6, but not between RNA-3 and RNA-6, or between RNA-5 and RNA-6. These small RNA species therefore contain the genetic determinant(s) for lesion type and for ability to infect B. vulgaris and B. macrocarpa systemically. RNA-1 and RNA-2 are viral genome components. The other RNA components have some characteristics of viral satellite nucleic acids but they may not all be dispensable if the BNYVV isolates are to survive in nature.
Although numerous photosensitizers have been used experimentally to decontaminate viruses in cellular blood components, little is known about their mechanisms of photoinactivation. Using M13 bacteriophage and vesicular stomatitis virus (VSV) as model viruses, we have investigated alteration of the viral genome, protein and envelope after phototreatment. Methylene blue (MB) and aluminum phthalocyanine tetrasulfonate (AlPcS4) phototreatment inactivated bacteriophage M13 and decreased the fraction of single-stranded circular genomic DNA (sc-DNA) by converting it to linear form. This conversion was enhanced by treating the extracted DNA with piperidine at 55 degrees C. Piperidine-labile breaks were well correlated to phage survival (5.1% sc-DNA at 1.7% phage survival for MB) under conditions where only minor differences were seen in the relative abundance of M13 coat protein on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Neither aluminum phthalocyanine (AlPc) nor merocyanine 540 (MC540) inactivated M13 nor were there significant changes observed in DNA and coat protein. Methylene blue, AlPcS4 and AlPc inactivated VSV and inhibited fusion of the virus envelope to Vero cells at pH 5.7 (i.e. with plasma membrane). However, the degree of this inhibition was small compared to the extent of virus inactivation (43% inhibition vs. 4.7 log10 or 99.998% inactivation, for MB). In contrast, an antibody to VSV G-spike protein inhibited fusion at pH 5.7 by 52% with a concomitant decline in VSV infectivity of 0.15 log10 (30%). Few changes were observed in the relative abundance of G protein for MB and AlPcS4 phototreated samples and no additional protein bands were observed on SDS-PAGE.(ABSTRACT TRUNCATED AT 250 WORDS)
UVC radiation in the presence of catechins, especially epigallocatechin gallate, appears to be an effective method of increasing the viral safety of FVIII concentrates without the loss of coagulation activity.
Transfusion-associated graft-versus-host disease (TA-GVHD) is a complication of blood transfusion that results from the engraftment and clonal expansion of allogenic donor white cells.1) Although TA-GVHD is rare, patients respond poorly to treatment and the disorder is usually fatal. 2)Radiation treatment of blood components is currently used to prevent TA-GVHD. 3) This procedure is based on the large difference between the radiation sensitivities of T-lymphocytes and red blood cells (RBCs).3,4) Thus, one has to apply a dose high enough to destroy almost all the T-lymphocytes while causing as little damage as possible to RBCs. Recent studies indicate that the minimal dose required to fulfill this requirement is from 15 to 50 Gy. 5,6) Doses of this order of magnitude cause only minor changes in the essential constituents of RBCs, e.g. intracellular hemoglobin, ATP, membrane lipid and proteins. However, they promote the leakage of potassium from RBCs. 7,8) There have been concerns about possible side effects, such as hyperpotassemia and cardiac arrest, of the transfusion of blood components with an elevated potassium concentration. [9][10][11] The irradiation of aqueous solutions can lead to the generation of reactive oxygen species (ROS) such as the hydroxyl radical which is a powerful oxidant and can interact with lipids and proteins in the membranes of RBCs.12) It was reported that the increase in the extracellular potassium concentrations of RBC preparation on photosensitization resulted from the oxidative damage of RBC membranes by ROS produced by photosensitization, and furthermore, that the increase was sufficiently inhibited by the addition of an antioxidant such as dipyridamole (DPM) or Trolox before the photosensitization.13,14) Therefore, the leakage of potassium caused by the irradiation may also be due to the damage of RBC membranes by ROS. Although the use of an antioxidant could potentially minimize the leakage which may result from the irradiation, trials using antioxidants to prevent potassium leakage are rare. 15) Here we investigated the effect of antioxidants DPM, Trolox, human plasma or mannitol on the leakage of potassium ascribed to the irradiation of RBCs. MATERIALS AND METHODSPreparation of RBC Samples and Irradiation RBC in MAP solution (RC-MAP) were prepared according to the standard protocol of the Hokkaido Red Cross Blood Center. Briefly, after the centrifugation of donated human blood (400 ml) at 3000 g for 8 min, the supernatant was removed and 92 ml of MAP solution (1.34 g D-mannitol, 0.013 g adenin, 0.086 g sodium dihydrogenphosphate, 0.138 g sodium citrate dihydrate, 0.018g citric acid, 0.663 g D-glucose, and 0.457 g sodium chloride) was added (hematocrit: approximately 60%). RC-MAP stored for 7 d at 4°C was mixed with the same volume of MAP solution containing DPM, Trolox, human plasma or mannitol. RBC preparations (30 ml) in plastic tubes (50 ml centrifuge tube; IWAKI Inc., Tokyo, Japan) were agitated for 2 h at room temperature and subsequently exposed to 30 Gy of gamma ray i...
We investigated the photoinactivation of virus infectivity by hypocrellin A and its mechanism. The titers of vesicular stomatitis virus (VSV) and human immunodeficiency virus type 1 (HIV-1), both of which are enveloped viruses, were reduced upon illumination with hypocrellin A in a concentration-dependent manner, whereas canine parvovirus, a nonenveloped virus, was not killed. The removal of oxygen or addition of sodium azide or beta-carotene both inhibited VSV inactivation. Mannitol and superoxide dismutase had no effect on VSV inactivation. These results indicate that singlet oxygen was involved in the process of VSV inactivation. Of the three major VSV membrane proteins, peripheral membrane protein M was most damaged by the hypocrellin A phototreatment.
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