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Biomedical subjects

N Burroughs

Publications and source records attributed to N Burroughs.

5 recordsLinked to original sources
PubMed2003

Interactions between Salmonella typhimurium and Acanthamoeba polyphaga, and observation of a new mode of intracellular growth within contractile vacuoles.

Acanthamoeba polyphaga feeding on Salmonella typhimurium in a simple model biofilm were observed by light microscopy and a detailed record of interactions kept by digital image capture and image analysis. A strain of S. typhimurium SL1344 carrying a fis: gfp reporter construct (pPDT105) was used to assess intracellular growth in A. polyphaga on non-nutrient agar (NNA) plates. Invasion of the contractile vacuole (CV) was observed at a frequency of 1:100-1000 acanthamoebae at 35 degrees C. The salmonellae contained in CVs illustrated significant up-regulation of fis relative to extracellular bacteria, indicating that they were in the early stages of logarithmic growth, and reached numbers of 100-200 cells per vacuole after 4 days. This is the first report of this mode of intracellular growth. Up-regulation of fis was also observed in a proportion of S. typhimurium cells contained within food vacuoles. Filamentation of S. typhimurium and E. coli cells was frequently observed in coculture with A. polyphaga on NNA plates, with bacterial cells reaching lengths of up to 500 microm after 10 days' incubation at 35 degrees C. A. polyphaga was also seen to mediate bacterial translocation over the agar surface; egested salmonellae subsequently formed microcolonies along amoebal tracks. This illustrated intracellular survival of a fraction of the S. typhimurium population. These phenomena suggest that protozoa such as A. polyhaga may play an important role in the ecology of S. typhimurium in soil and aquatic environments.

Acanthamoeba↗
PubMed2000

Defective deletion mutant amplification.

Defective deletion mutants can be replicated in superinfected cells by parasitism of the intact virus' replication machinery, and through replication with the host cell. We show by analysis of a mathematical model that dynamic stability of superinfected cell growth is crucial in determining the frequency of deletion mutant infected cells, i.e. there is a critical infectivity threshold rho(sc)below which the density of proliferative virus is significantly reduced by the presence of defective deletion mutants. Above rho(sc), proliferative virus principally occurs as superinfected cells (wild type with defective deletion mutant). The threshold rho(sc), and the interference effects of the deletion mutant, increase with deletion mutant parasitism of the wild-type replication machinery in superinfected cells. The interaction of virally infected cells with host homeostasis determines whether immune escape by deletion mutant infected cells is necessary for the interference window to exist. Only when the deletion mutant has a detrimental effect on infected host cell replication did we observe periodic behaviour.

Animals↗
PubMed1999

High pre-treatment serum hepatitis B virus titre predicts failure of lamivudine prophylaxis and graft re-infection after liver transplantation.

BACKGROUND/AIMS: Orthotopic liver transplantation has an established role for the treatment of patients with chronic liver failure secondary to hepatitis B virus (HBV) infection. Unfortunately, recurrent infection of the graft can be associated with aggressive disease, and with diminished graft and patient survival. Currently, the role of nucleoside analogues for prevention of graft re-infection is being evaluated. Preliminary results are encouraging, but treatment failure has been associated with emergence of drug-resistant virus. METHODS: We have studied ten consecutive patients who received lamivudine prophylaxis for prevention of HBV graft reinfection. Sequential sera, collected prelamivudine then during treatment before and after liver transplantation, were examined. Conventional serological markers were measured, as were serum viral DNA levels with a sensitive quantitative polymerase chain reaction assay. RESULTS: Lamivudine treatment effected a reduction in serum HBV levels, but six patients still had measurable viral DNA at the time of transplantation. Five patients developed graft re-infection with lamivudine-resistant virus. Resistant virus emerged 8 to 15 months post-transplant. The likelihood of emergence of resistant virus was related to the pre-treatment serum HBV titre. Persistent serum viral DNA positivity and evidence of graft re-infection during the early post-transplant period did not predict the subsequent emergence of resistant virus. CONCLUSIONS: Our observations suggest that the resistant species may be present in the viral quasispecies in the serum and liver of patients with high-level replication prior to lamivudine exposure. The resistant species can persist during lamivudine treatment prior to transplantation, and emerge following transplantation. These observations suggest strategies which might prevent the emergence of drug-resistant species, and imply that graft re-infection may be a preventable phenomenon.

Antiviral Agents↗
PubMed1978

Relationship of San Miguel sea lion virus to other members of the calicivirus group.

San Miguel sea lion virus (SMSV) is indistinguishable from vesicular exanthema virus (VEV) and feline calicivirus (FCV) in its morphology and in possessing a single capsid polypeptide with a molecular weight of approximately 65 X 10(3). Neutralization tests readily differentiate the three viruses, but immunodiffusion tests show that SMSV is closely related serologically to VEV but not to FCV. Although the RNAs of the three caliciviruses have similar base compositions, homology tests show that SMSV is closely related to VEV but is not related to FCV. Tryptic peptide maps of the single major polypeptide comprising the capsid of each virus also show that SMSV and VEV are more closely related to each other than to FCV.

Animals↗