Number Of Plaque-forming Units Research Articles

Distribution of coliphages in Hong Kong sewage.

Coliphage content of sewage collected from 11 different localities in Hong Kong was determined. The number of plaque-forming units (PFU) ranged from 0.036 x 10(3) to 15.9 x 10(3) per ml. In general, urban sewage tended to be richer than rural sewage both in PFU count as well as plaque morphological variation. Seventy-seven isolates were subjected to a host range study. Fifty per cent of these were able to grow on Escherichia coli K-12 as well as E. coli B. Approximately 32% were found to be male specific, and the remaining 18% were K-12 specific although sex-indifferent.

Distribution of Coliphages in Hong Kong Sewage

Coliphage content of sewage collected from 11 different localities in Hong Kong was determined. The number of plaque-forming units (PFU) ranged from 0.036 x 10(3) to 15.9 x 10(3) per ml. In general, urban sewage tended to be richer than rural sewage both in PFU count as well as plaque morphological variation. Seventy-seven isolates were subjected to a host range study. Fifty per cent of these were able to grow on Escherichia coli K-12 as well as E. coli B. Approximately 32% were found to be male specific, and the remaining 18% were K-12 specific although sex-indifferent.

Kinetics of viral deoxyribonucleic acid, protein, and infectious particle production and alterations in host macromolecular syntheses in equine abortion (herpes) virus-infected cells.

Infection of exponential-phase suspension cultures of mouse fibroblast cells (L-M) with equine abortion virus (EAV) resulted in inhibition of cell growth and marked alterations in host metabolic processes. The synthesis of deoxyribonucleic acid (DNA) and ribonucleic acid was inhibited within 4 hr after infection and was suppressed by more than 90% by the time of maximal virus replication (14 to 18 hr). The overall rate of protein synthesis, however, was similar in uninfected and virus-producing cells as determined by measurements of net protein and isotope incorporation. The time course of viral DNA and protein synthesis and assembly into mature virus was determined with the inhibitors 5-fluorodeoxyuridine (FUdR) and cycloheximide, respectively. Thus, viral DNA synthesis was essentially completed at 14 hr, and viral protein and infectious virus synthesis was completed at 18 hr. Although the number of plaque-forming units (PFU) produced by FUdR-treated cells (10(3) to 10(4) PFU/ml) was at least 3 logs less than that produced by untreated cells, the yield of physical particles (as determined by electron microscopy) was approximately the same at 30 hr after infection. Besides being relatively non-infective, the particles produced in FUdR-treated cells appeared morphologically incomplete as they contained little or no nucleoid material.

Immunosuppressive Effects of Selected Metabolic Inhibitors in Vivo and in Vitro

SummaryActinomycin D, puromycin, 6-mercaptopurine, and cytosine arabinoside were shown to decrease the number of plaque-forming units upon in vitro incubation with suspensions of spleen cells taken from sheep-cell immunized mice. Under similar conditions, 5-iodo-2′-deoxyuridine, 5-bromo-2′-deoxyuridine, azauridine, and chloramphenicol had no effect. Administered in vivo, 6-mercaptopurine, cytosine arabinoside, and chloramphenicol all suppressed plaque production. In the case of the latter two antimetabolites, serum antibody titers remained unaffected by the dosages given.

SEROLOGICAL RELATIONSHIPS OF SOIL ACTINOPHAGES.

Actinophages first appeared in soil perfusates 4 hours after perfusion began, and, with certain species of Streptomyces, titers as high as 106 plaque-forming units (PFU) per ml of perfusate were reached in from 18 to 24 hours. Samples of soils collected in late summer and fall yielded larger numbers of PFU than did samples collected in the spring. Antisera against two isolated S. scabies phages were used to characterize the "wild" phage populations appearing in soil perfusates. With S. scabies as the plating indicator most phages (92–98%) were found to be related serologically to phage L, and from 2.5% to 7.5% of the total PFU were related to phage S. Further experiments showed that phages related to L appearing in perfused soil were the dominant group acting on S. lavendulae and S. olivaceus.The use of combined antisera for inactivation of perfusate permitted the isolation of new phages normally obscured by the dominant serological groups L and S.

EFFECT OF 6-AMINONICOTINAMIDE ON CHICK-EMBRYO TISSUE CULTURES INFECTED WITH VACCINIA VIRUS.

Lee, Spencer H. S. (Dalhousie University, Halifax, Nova Scotia). Effect of 6-aminonicotinamide on chick-embryo tissue cultures infected with vaccinia virus. J. Bacteriol. 88:885-892. 1964.-6-Aminonicotinamide (6-AN) was shown to render chick-embryo fibroblast (CEF) tissue cultures refractory to infection with vaccinia virus. Pretreatment of CEF cultures for 8 hr at 36 C with 5 mug/ml of 6-AN prior to addition of vaccinia virus reduced the titer of active virus to about 0.4% of the levels obtained in the untreated controls, when measured by the number of plaque-forming units per milliliter. The addition of 5 mug of 6-AN to CEF cultures before virus infection retarded the progress of vaccinial infection by 8 to 10 hr at 36 C. The inhibitory effect caused by 5 mug/ml of 6-AN could be reversed by the simultaneous addition of 5 to 50 mug/ml of nicotinamide, but not if added at a later time. 6-AN appears to act on the host cell and not on vaccinia virus. For these tests, a simple plaque assay method was devised, by use of a fluid overlay technique with screw-capped tubes (16 by 125 mm) containing CEF cultures.

RELATIVE PLAQUE-FORMING, CELL-INFECTING, AND INTERFERING QUALITIES OF VACCINIA VIRUS.

Galasso, G. J. (University of North Carolina School of Medicine, Chapel Hill), and D. G. Sharp. Relative plaque-forming, cell-infecting, and interfering qualities of vaccinia virus. J. Bacteriol. 88:433-439. 1964.-The growth of vaccinia virus in slant cultures of L cells inoculated with different multiplicities of counted particles suggests a higher incidence of cell infection than can be accounted for by the number of plaque-forming units. From cultures containing antiserum or heated virus to limit the passage of progeny to uninfected cells, the data clearly indicate the ability of all the particles to infect cells even though the plaque titer is only one-tenth of this number. Analogous experiments show that an average of two heat-inactivated (56 C, 45 min) particles induce interference in L cells. There is nothing yet to show whether the few plaque-forming particles are different from the majority or whether they are just statistically fortunate in the complex process of plaque formation.