Lack of relationship between virus-specific surface and transplantation antigens in hamster cells transformed by simian papovavirus SV40.
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Biomedical subjects
Publications and source records attributed to F Rapp.
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A strain of human adenovirus type 7, adapted to replication in green-monkey kidney cells, requires the interaction of two particles to initiate plaque formation in the simian cells. One particle is a true adenovirion. The second, apparently defective, consists of a genome carrying amonkey-adapting component in an adenovirus capsid; this genome does not express known SV40 determinants. The addition of human adenovirus type 7 that is not adapted enhances the titer and changesconditions for plaque formation by the adapted virus to a one-particle requirement. Addition of nonadapted human adenovirus type 2 as helper virus results in the transfer of the monkey-adaptingcomponent from adenovirus type 7 to adenovirus type 2. The population containing the adenovirus 2 transcapsidant then has the ability to replicate in simian cells.
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Butel, Janet S. (Baylor University College of Medicine, Houston, Tex.), and Fred Rapp. Replication in simian cells of defective viruses in an SV40-adenovirus "hybrid" population. J. Bacteriol. 91:278-284. 1966.-An SV40-adenovirus type 7 "hybrid" virus population, previously shown to contain two viruses capable of complementation in green monkey kidney (GMK) cells, has a growth cycle in GMK cells similar to that of adenovirus type 7 in the presence of SV40. Extending previous preliminary results, the addition of adenovirus types 2, 7, or 12 to monolayers of GMK cells enhanced plaque formation by the SV40-adenovirus hybrid by as much as 200-fold. The terminal enhanced plaques, initiated by the hybrid in the presence of helper adenovirus, were found to contain progeny which could induce the synthesis of SV40 tumor antigen but which were coated with the protein of the helper adenovirus, type 2, 7, or 12, respectively. The particle carrying the SV40 tumor antigen determinant, named PARA, is defective in that it cannot direct the synthesis of capsid protein; information for the coat for PARA is supplied by the adenovirus. One-step growth curves of the hybrid virus population in monkey cells revealed that synthesis of both types of particles, adenovirus and PARA, proceeds at a similar rate, with a latent period of 16 to 20 hr being followed by an exponential increase in titer during the following 20 hr. Maximal titers for both particles were obtained 48 hr after inoculation of the cultures. Neither the PARA nor the adenovirus component replicated in GMK cells in the absence of the other.
Feldman, Lawrence A. (Baylor University College of Medicine, Houston, Tex.), Janet S. Butel, and Fred Rapp. Interaction of a simian papovavirus and adenoviruses. I. Induction of adenovirus tumor antigen during abortive infection of simian cells. J. Bacteriol. 91:813-818. 1966.-Adenovirus types 2, 7, and 12 undergo an abortive growth cycle in green monkey kidney cells; they induce the formation of adenovirus tumor antigen, but synthesis of adeno capsid antigen and infectious adenovirus was observed only when cultures were concomitantly infected with a simian papovavirus (SV40). Several other viruses, including herpes simplex and measles which replicate in monkey cells, and rabbit papilloma and human wart papovaviruses which do not, failed to stimulate adenovirus replication in the monkey cells. Adenovirus tumor antigen was detected 8 to 10 hr postinfection by immunofluorescent techniques. The antigen induced by adenovirus types 2 and 7 appeared as intranuclear masses; adenovirus type 12 tumor antigen also appeared as cytoplasmic and nuclear flecks. Sera from hamsters bearing tumors induced by adenovirus type 12 cross-reacted with tumor antigens induced by types 2 and 7 but not with antigens induced by SV40.
Wallis, Craig (Baylor University College of Medicine, Houston, Tex.), Joseph L. Melnick, and Fred Rapp. Effects of pancreatin on the growth of reovirus. J. Bacteriol. 92:155-160. 1966.-The influence of pancreatin and other proteolytic enzymes on the growth, plaque formation, and antigenicity of reovirus was studied. Single-cycle yields of virus in the presence of enzyme were not increased, but multiple-cycle yields of virus were greatly enhanced. Immunofluorescence studies demonstrated that the transmission of reovirus from cell to cell is more rapid in the presence of the enzyme. These findings led to the development of a rapid plaque assay system for reovirus, a virus which has previously been difficult to assay by the plaque method. In the recommended procedure, pancreatin is incorporated into the agar overlay. Monkeys immunized with enzyme-treated reovirus yielded higher antibody titers than animals receiving the same amount of untreated virus.
Butel, Janet S. (Baylor University College of Medicine, Houston, Tex.), Joseph L. Melnick, and Fred Rapp. Detection of biologically active adenovirions unable to plaque in human cells. J. Bacteriol. 92:433-438. 1966.-Plaque formation in green monkey kidney (GMK) cells by a defective simian virus 40-adenovirus 7 "hybrid" population (PARA-adenovirus 7) was enhanced by the addition of excess adenovirions. Adenovirus types 2, 7, and 12 were capable of providing enhancement, although none of these viruses gives rise to plaques in simian cells in the absence of PARA (particle aiding replication of adenovirus). Near maximal enhancement of the PARA plaque titer on simian cells was obtained with input multiplicities ranging from 0.02 to 0.14 plaque-forming units (PFU) of helper adenovirus per GMK cell. The PFU of helper adenoviruses tested (types 2, 7, and 12) were measured in the most sensitive assay system, human kidney cells. This input corresponded to three to nine helper virus particles per GMK cell. The majority of particles capable of enhancing plaque formation by PARA banded at a density of 1.34 in CsCl. Adenoviruses inactivated by heat or ultraviolet light were not capable of enhancing plaque formation by PARA. Highest titers were obtained when PARA and helper adenovirus were inoculated simultaneously. Inoculation of the helper adenovirus 24 hr prior to the inoculation of PARA resulted in the formation of only 50% as many plaques, and no enhanced plaques developed when the adenovirus preceded PARA by 48 hr. Conversely, the addition of adenovirus 48 hr after the inoculation of PARA initiated 56% as many plaques as simultaneous inoculation; 4% of the enhanced plaques still formed when helper virus was added as late as 5 days after inoculation of PARA. These results suggest that adenovirus particles unable to plaque on human or monkey kidney cells are nevertheless capable of interacting with PARA in simian cells, thereby facilitating replication of both particles.