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R J Cooper

Publications and source records attributed to R J Cooper.

67 records · Page 4Linked to original sources
PubMed1976

Molluscum contagiosum -- a defective poxvirus?

Purified preparations of molluscum contagiosum virus contain a DNA-dependent RNA polymerase (EC 2.7.7.6) with similar but not identical properties to those of the enzyme found in vaccinia virions. The ultraviolet inactivation kinetics of the RNA polymerase from both viruses were similar, displaying fast and slow components. Ultraviolet irradiation destroyed the interfering capacities of molluscum and inactivated vaccinia virions, and the interferon-inducing capacity of molluscum virus slowly and with first-order kinetics. Inactivation studies of the interferon-inducing capacity of vaccinia virus were complicated by cytotoxic effects. Electron microscopical studies showed all stages of virus growth in vaccinia-infected mouse embryo cells; molluscum virus appeared to be degraded in lysosome-like bodies. In preliminary studies, marked changes in cytoplasmic RNA synthesis and in patterns of polypeptide synthesis were found in vaccinia-infected but not in molluscum-infected mouse embryo cells.

Adsorption↗
PubMed1975

Deoxyribonucleic acid-dependent ribonucleic acid polymerases from normal and polyoma-transformed BHK-21/C13 cells.

DNA-dependent RNA polymerase (EC 2.7.7.6) ACTIVITIES FROM NORMAL BHK-21/C13 cells and from BHK-21/C13 cells transformed by polyoma virus (PYY cells) were solubilized and fractionated on columns of DEAE-Sephadex. Various properties of the A and B enzymes from the two types of cell were compared. 1. The yields of polymerase relative to the DNA content of the nuclear preparations are similar for both cell types. 2. The ionic-strength optima of polymerases A and B are 12.5 mM and 100mM with respect to (NH4)2SO4 for both cell types. 3. The Mn2+/Mg2+ activity ratio (measured at the respective optimum for each cation) for polymerase A from BHK-21/C13 cells was 1.48 and for the polymerase A from PYY cells was 0.55. The corresponding ratios for polymerase B were 10.11 for BHK-21/C13 cells and 22.75 for PYY cells. 4. Minor differences in the ability of the A polymerases to transcribe native and denatured DNA templates were observed; such differences were not apparent when the B polymerases were compared. 5. All the polymerases were inhibited completely by actinomycin D and by rifampicin AF/013, but not markedly so by rifampicin. Alpha-amanitin inhibited polymerase B but not polymerase A.

Amanitins↗
PubMedDate not supplied

Investigation of cytomegalovirus and human herpes viruses 6 and 7 as possible causative antigens in psoriasis.

Psoriasis is probably a T-cell-mediated autoimmune disease. Infectious models of autoimmune diseases have been proposed and in psoriasis, it has been suggested that there may be molecular mimicry between streptococcal antigens and epidermal keratins. The immunological profile of stable psoriasis plaques suggests, however, that viral antigens may be important. We investigated, using polymerase chain reaction techniques, whether DNA from either cytomegalovirus (CMV) or human herpes viruses (HHV) 6 and 7 is present in the skin of patients (n = 10) with chronic plaque psoriasis. We also investigated 29 patients for the presence of serum IgG to CMV. We found no evidence of CMV or HHV 7 DNA in psoriasis plaques although DNA for HHV 6 was detected in both involved and uninvolved skin in 1 out of 10 patients. There was no statistically significant increase in prior CMV infection, as assessed by the presence or absence of serum IgG to CMV, in psoriasis, compared to our local population. Although there is circumstantial evidence that viral antigens may be important in the pathogenesis of psoriasis we found no evidence to link infection with CMV or HHV 6 and 7 with subsequent development of chronic plaque psoriasis.

Adult↗