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D G SHARP

Publications and source records attributed to D G SHARP.

At least 19 recordsLinked to original sources

EFFECTS OF HEAT ON THE INFECTING, ANTIBODY-ABSORBING, AND INTERFERING POWERS OF VACCINIA VIRUS.

Galasso, G. J. (University of North Carolina School of Medicine, Chapel Hill), and D. G. Sharp. Effects of heat on the infecting, antibody-absorbing, and interfering powers of vaccinia virus. J. Bacteriol. 89:611-616. 1965.-At 56 C the infectivity of vaccinia virus particles is destroyed rapidly, but even when it is reduced by a factor of 10(6) the particles are capable of producing strong interference in L cells. The rate constant K for thermal inactivation of plaque-forming power is greater than that for interfering power by the factor e(3.8) or about 45 times. At 37 C both properties of the virus decline more slowly and at equal rates. The temperature coefficient of K is discontinuous in the region of 40 C, indicating quite different activation energies for the reactions above and below this critical point. The degradation of interfering power exhibits a similar discontinuity, although less in magnitude, but none has been found in the antibody-reactive power of the virus, which is much more heat resistant.

Antibodies↗

QUALITY CHANGES IN VACCINIA VIRUS DURING ADAPTATION TO GROWTH IN CULTURES OF EARLE'S L CELLS.

Sharp, D. G. (University of North Carolina School of Medicine, Chapel Hill), P. Sadhukhan, and G. J. Galasso. Quality changes in vaccinia virus during adaptation to growth in cultures of Earle's L cells. J. Bacteriol. 88:309-312. 1964.-Although particle production improves rapidly with passage of vaccinia (mouse neurotropic strain) virus in L cells, plaque production improves much more slowly. Beyond the passage when maximal particle yield was reached (18th), further improvement in plaquing quality of 1,000-fold was observed. Particle count and plaque titrations showed that plaquing efficiency improves at comparable rates in either plaque-to-plaque passage on plates or in tube cultures inoculated at high multiplicity. The host cell is probably exerting some influence in addition to that of the selection of mutants from the initial population.

Animals↗

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.

Hot Temperature↗

HOMOLOGOUS INHIBITION, TOXICITY, AND MULTIPLICITY REACTIVATION WITH ULTRAVIOLET-IRRADIATED VACCINIA VIRUS.

Galasso, G. J. (University of North Carolina, Chapel Hill) and D. G. Sharp. Homologous inhibition, toxicity, and multiplicity reactivation with ultraviolet-irradiated vaccinia virus. J. Bacteriol. 85:1309-1314. 1963.-Vaccinia virus whose plaque-forming capacity had been destroyed by ultraviolet rays (2,537 A) was shown to retard the growth of L cells in tube cultures. At input multiplicities (M) of 0 < M < 10, no interference was detected, but at M >== 100 the irradiated virus particles exerted a strong toxic effect on the L cells in monolayer cultures, affecting the plaque formation by active virus which was added. Multiplicity reactivation occurs in sublethally irradiated vaccinia, as shown by virus particle counts via electron microscopy and plaque counts. It is clearly demonstrated in this system because there is no complicating interference. It sets in at a total virus particle multiplicity of about one, even though the multiplicity of the original plaque-forming particles is much below one.

Animals↗

Ratios of vaccinia virus particles to virus infectious units; studies of ratio changes during growth and adaptation in eggs, guinea pigs, and rabbits.

Total virus particle counts, infectivity titrations and the ratios between particles and infective units have been determined for vaccinia virus infected tissues. Growth curves of vaccinia in the chorioallantoic membrane are characterized by relatively low ratios from 1 to 4 days after inoculation and a marked rise in the ratio at more prolonged intervals. Ratio determinations of vaccinia virus passages in the egg, rabbit skin, and guinea pig skin have been made to study the phenomenon of adaptation in different hosts. The embryonated egg chorioallantoic membrane shows no variation in the ratio of particles to infectious units during passage and it is concluded that this host is completely susceptible to vaccinia. During adaptive passages on the skin of rabbits and guinea pigs relatively large amounts of non-infective virus appear as indicated by a rise in the particle-infectivity ratios. The extent of ratio increase appears related to the general resistance of the host to the virus. Finally, treatment of crude tissue extracts with sonic vibration is described as an aid in dispersing the virus particles for quantitative particle counts.

Animals↗