Host range analysis of a chimeric simian virus 40 genome containing the BKV capsid genes.

Simian virus 40 (SV40) propagates poorly in cells from human embryonic kidney (HEK) and human fetal fibroblasts (HFF) while BK virus grows well in many human cell types. It has been suggested that sequences within the SV40 late region but not within the BKV late region may act to inhibit growth of virus in HEK and HFF cells. In order to test this and to identify a late region host range function, we have replaced the late region of wtSV40 DNA with the late region of RFV (a variant of BKV) to produce an intermolecular hybrid or chimera.

Host range determinant in the late region of SV40 and RF virus affecting growth in human cells.

WtSV40 and its variant EL-SV40 (contains two complementing defective genomes) fail to productively infect human embryonic kidney cells or human fibroblasts. However, early SV40 (E-SV40) genomes can propagate in human cells when complemented by a particular late RF virus (L-RFV) genome or the closely related wtBKV genome. The L-RFV genome (L-RFV clone H) contains a deleted early region, a complete set of BKV capsid genes, and a single SV40 regulatory region (acquired by recombination).

Transformation of human cells by a polyomavirus containing complementing JCV and RFV genomes.

Molecularly cloned viral DNA from late RFV (L-RFV) and early JCV (E-JCV) were transfected into human fetal brain (HFB) cells and complementation was demonstrated. A new infectious virus (E-JCV/L-RFV) was produced. Infection resulted in partial transformation of HFB and human embryonic kidney cells.

Late coding region sequences required for competition by SV40 defectives.

SV40 defectives containing the complete early coding region (E-SV40) or the complete late region (L-SV40) were separately transfected into green monkey cells. They were analyzed for their ability to compete with wtSV40 (introduced by infection) or to undergo replication in the presence of constitutively produced SV40 T-antigen. L-SV40 competed very strongly.

Colloidal silica coatings for KrF and Nd:glass laser applications.

In this paper we discuss the performance of colloidal silica antireflection coatings which have been developed for use in high-power KrF and Nd:glass lasers. These coatings have reproducibly given transmissions of more than 99.8% per surface and have exhibited laser damage thresholds as high as 20 J/cm(2)for l-ns pulses at 1.

Complementation between SV40 and RFV defectives and acquisition of SV40 origins by late RFV genomes.

EL SV40 and RFV are variants of SV40 and BKV which contain bipartite or dual genomes. One molecule contains all the early viral sequences (E-SV40, E-RFV) and the other all the late viral sequences (L-SV40, L-RFV). Early and late genomes complement one another during productive infection.

Isolation of a papovavirus with a bipartite genome containing unlinked SV40 and BKV sequences.

Wild-type (wt) BK virus was introduced into permissive BSC-1 cells along with either early or late defective SV40 genomes. The defectives contained all of the late (L-SV40) or all of the early (E-SV40) coding sequences. Persistently infected (PI) BSC-1 cultures were established and contained wt BKV DNA and E- or L-SV40 DNA in Hirt supernatants.

In vitro growth control phenotypes of transformed rodent cells prior to and following tumorigenesis.

A number of virus and chemical carcinogen-transformed cell lines were generated in tissue culture and analyzed for growth control phenotypes prior to and following tumorigenesis in appropriate hosts. The cell lines include those of mouse, rat, human, and Syrian hamster, transformed by papovaviruses and adenoviruses (DNA) or murine (RNA) tumor viruses. Cell lines were assayed for: (a) multinucleation or uncontrolled nuclear division (UND+) and uncontrolled DNA synthesis in cytochalasin B (CB) medium; and (b) the continuation of DNA synthesis in media containing reduced (0.

Role of defective simian virus 40 genomes in establishment and maintenance of persistently infected primate cell lines.

Studies are reported of persistent simian virus 40 (SV40) infections of fully permissive monkey (TC-7 and BSC-1) and human (A172) cell lines, with emphasis on the role of viral defectives in establishment and maintenance of persistence. The presence of defectives prevented complete cell killing and allowed the establishment of persistently infected cultures. Hirt supernate DNAs from these cultures showed the continuing presence of defective genomes.

Isolation and characterization of defective simian virus 40 genomes which complement for infectivity.

A new variant of simian virus 40 (EL SV40), containing the complete viral DNA separated into two molecules, was isolated. One DNA species contains nearly all of the early (E) SV40 sequences, and the other DNA contains nearly all of the late (L) viral sequences. Each genome was encircled by reiterated viral origins and termini and migrated in agarose gels as covalently closed supercoiled circles.

Temperature dependency for maintenance of transformation in mouse cells transformed by simian virus 40 tsA mutants.

Mouse embryo fibroblasts and 3T3 cells were transformed by wild-type, tsB4, tsA7, tsA58, and tsA209 simian virus 40. Clones of transformants were generated both in soft agar and in liquid medium by focus formation and at both high and relatively low multiplicities of infection. All transformants were assayed for three phenotypes of transformation: (i) the ability to form highly multinucleated cells in cytochalasin B-supplemented medium, i.

Effect of toal parenteral nutrition on gastric acid secretion.

While total parenteral nutrition is widely used, its effects on gastrointestinal function are not well understood. We measured acid secretion in 11 patients during total parenteral nutrition. Five of these patients were retested at least one month after resuming oral intake.

Prolongation of herpes simplex virus latency in cultured human cells by temperature elevation.

Treatment of herpes simplex virus type 2 (HSV-2)-infected human fibroblast cells with cytosine arabinoside (ara-C) at 25 microgram/ml resulted in complete inhibition of virus replication. Removal of ara-C after 7 days of treatment ultimately resulted in renewed virus replication, but after a delay of at least 5 days. If however, the temperature was elevated from 37 degrees C to 39.

Oncogenic transformation of human embryo lung cells by human cytomegalovirus.

Persistent infection of human embryo lung fibroblasts with a genital isolate of cytomegalovirus resulted in oncogenic transformation of these cells. Immunofluorescence techniques detected virus-specific antigens, while microcytotoxicity tests established that the transformed cells share a membrane antigen with hamster cells transformed by inactivated cytomegalovirus. The transformed human cells induced progressively growing tumors in weanling athymic nude mice.