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At least 865 records · Page 48Linked to original sources
PubMed1979

Subfractionation of CsCl-purified H-1 parvovirus on metrizamide gradients.

The different density classes of H-l parvovirus, collected within 30 hr of infection of par-asynchronous cultures, following the standard CsCl purification step, have been shown to be heterogeneous. Rebanding of the denser form (HF, p = 1.46 g/cm3) and the less dense form (LF, p = 1.42 g/cm3) of infectious virus in the nonionic density generating solute, metrizamide, showed that both HF and LF virus bands were heterogeneous in density. The infectivity banded with isotopically labeled virus protein and DNA at 1.32 g/cm3 for both HF and LF virus. Amounts of protein and DNA which varied from preparation to preparation, but which were greater from the HF virus band, were distributed throughout the rest of the gradient, but predominated in a peak at a density of 1.2 g/cm3. The protein in this peak was without hemagglutinating activity but had the molecular weights and proportions of the H-l virion proteins (VPl, VP2', and VPZ). The DNA was of the same size as H-l DNA monomers and its proportion to the protein was similar to that of the infectious peak. The DNA was susceptible to micrococcal nuclease digestion. The nature of this noninfectious viral material thus seemed to be incompletely assembled virus. Radiolabeled H-l virus collected after 72 hr of infection formed a discrete single peak in both CsCl (p = 1.42 g/cm3), and metrizamide gradients (p = 1.32 g/cm3). There was no significant amount of the 1.20 g/cm3 viral protein-DNA complex in these mature preparations.

Centrifugation, Density Gradient↗
PubMed1980

Heavy and light particles of adeno-associated virus.

KB cells coinfected with adenovirus and adeno-associated virus (AAV) yielded two kinds of infectious AAV particles that banded in CsCl at densities of 1.45 and 1.41 g/cm(2), respectively. The 1.45 band was found to be composed of a heterogeneous group of viral particles that could be subfractionated by velocity sedimentation. The main component from this band had a smaller S value (109) than the main component from the 1.41 band (111S), although both had the same DNA/protein ratio and the same density in metrizamide gradients. Continuous-label experiments showed that early after infection, both components (1.45 and 1.41) were generated in the same amounts, but this was followed by a relative increase in the proportion of the 1.41 component over the 1.45 particles. Pulse-chase analysis failed to demonstrate a precursor-product relationship between these two bands. The slower-sedimenting components from the 1.45 band were unstable in CsCl and were present in a greater proportion early after infection. These particles contained DNA that was enriched for the terminal sequences of the AAV genomes and was accessible to digestion with micrococcal nuclease.

Base Sequence↗
PubMed2002

Rapid detection of methicillin-resistant staphylococci from blood culture bottles by using a multiplex PCR assay.

Rapid detection and accurate identification of methicillin-resistant staphylococci are critical for the effective management of infections caused by these organisms. We describe a multiplex PCR-based assay for the direct detection of methicillin-resistant staphylococci from blood culture bottles (BacT/Alert; Organon-Teknika, Durham, N.C.). A simple lysis method followed by a multiplex PCR assay designed to detect the nuc, mecA, and bacterial 16S rRNA genes was performed. A total of 306 blood culture specimens were collected over a period of 10 months from June 1998 to April 1999, consisting of 236 blood cultures growing staphylococci (including 124 methicillin-resistant Staphylococcus spp.), 50 positive blood cultures which grew organisms other than staphylococci, and 20 blood cultures that were negative for bacterial and fungal pathogens after 5 days of incubation and terminal subculture. DNA extraction, PCR, and detection could be completed in 2.5 h. Of the positive blood cultures with staphylococci, the multiplex PCR assay had a sensitivity and specificity of 99.2% and 100%, respectively. Our results show that rapid, direct detection of methicillin-resistant staphylococci is possible, allowing clinicians to make prompt and effective decisions for the management of patients with staphylococcal bacteremia.

Bacteremia↗
PubMed1988

Induction of the heat shock regulon of Escherichia coli markedly increases production of bacterial viruses at high temperatures.

Production of bacteriophages T2, T4, and T6 at 42.8 to 44 degrees C was increased from 8- to 260-fold by adapting the Escherichia coli host (grown at 30 degrees C) to growth at the high temperature for 8 min before infection; this increase was abolished if the host htpR (rpoH) gene was inactive. Others have shown that the htpR protein increases or activates the synthesis of at least 17 E. coli heat shock proteins upon raising the growth temperature above a certain level. At 43.8 to 44 degrees C in T4-infected, unadapted cells, the rates of RNA, DNA, and protein synthesis were about 100, 70, and 70%, respectively, of those in T4-infected, adapted cells. Production of the major processed capsid protein, gp23, was reduced significantly more than that of most other T4 proteins in unadapted cells relative to adapted cells. Only 4.6% of the T4 DNA made in unadapted cells was resistant to micrococcal nuclease, versus 50% in adapted cells. Thus, defective maturation of T4 heads appears to explain the failure of phage production in unadapted cells. Overproduction of the heat shock protein GroEL from plasmids restored T4 production in unadapted cells to about 50% of that seen in adapted cells. T4-infected, adapted E. coli B at around 44 degrees C exhibited a partial tryptophan deficiency; this correlated with reduced uptake of uracil that is probably caused by partial induction of stringency. Production of bacteriophage T7 at 44 degrees C was increased two- to fourfold by adapting the host to 44 degrees C before infection; evidence against involvement of the htpR (rpoH) gene is presented. This work and recent work with bacteriophage lambda (C. Waghorne and C.R. Fuerst, Virology 141:51-64, 1985) appear to represent the first demonstrations for any virus that expression of the heat shock regulon of a host is necessary for virus production at high temperature.

Adaptation, Physiological↗
PubMed1980

the influence of the host cell on the inhibition of virus protein synthesis in cells double infected with vesicular stomatitis virus and mengovirus.

The ability of mengovirus to inhibit the synthesis of vesicular stomatitis virus (VSV) proteins and of VSV to inhibit the synthesis of mengovirus proteins during double infection in three different cell lines was investigated. Although cellular protein synthesis was inhibited after infection of cells by each virus, the ability of one virus to decrease translation of the mRNA species of the co-infecting virus varied with the cell type. Superinfection of mengovirus-infected L-929 cells by VSV resulted in essentially no inhibition in the synthesis of either mengovirus or VSV proteins. In HeLa cells and CHO cells the synthesis of both VSV and mengovirus proteins was inhibited under conditions of simultaneous or sequential infection. The inhibition of VSV protein synthesis after infection of HeLa cells by mengovirus was not a result of a modification or inactivation of virus mRNAs. When extracted from double infected cells, the VSV mRNAs manifested normal biological activity, as determined by their ability to stimulate the synthesis of VSV proteins in a micrococcal nuclease-treated cell-free system from L cells. The interference of non-interference of one virus by another in different cell lines was also measured by quantifying the number of infectious particles produced in each cell line. The results were similar to those reported above for protein synthesis inhibition. These experiments suggest that the interference of mengovirus with VSV mRNA translation in HeLa cells is not necessarily reflective of the mechanism by which mengovirus inhibits cellular protein synthesis. Also, the host cell appears to influence the extent or nature of the interference of one virus by the other.

Animals↗