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Biomedical subjects

Philip Rice

Publications and source records attributed to Philip Rice.

9 recordsLinked to original sources
PubMed2006

Performance of the automated Abbott RealTime HIV-1 assay on a genetically diverse panel of specimens from London: comparison to VERSANT HIV-1 RNA 3.0, AMPLICOR HIV-1 MONITOR v1.5, and LCx HIV RNA Quantitative assays.

Automated RNA extraction and quantitation of HIV-1 by real-time PCR offer potential advantages of efficient sample processing, improved sensitivity, expanded dynamic range and reduced contamination risk. In this study, plasma was collected from 100 HIV-1 infected patients visiting The Courtyard Clinic of St. George's Hospital in London, United Kingdom (UK). Viral loads measured using the automated Abbott RealTime HIV-1 assay (m2000sp sample preparation and m2000rt amplification and detection instruments) were compared to results obtained with Versant HIV-1 RNA 3.0 (bDNA), AMPLICOR HIV-1 MONITOR v1.5 (Monitor v1.5) and LCx HIV RNA Quantitative (LCx HIV) assays. Based on gag p24, pol integrase, and env gp41 sequences, the panel included 26 subtype A, 20 B, 27 C, 10 D, 1 CRF01_AE, 3 CRF02_AG and 13 recombinant viruses. RealTime HIV-1, bDNA, Monitor v1.5 and LCx HIV quantitated 82, 74, 82, and 83% of samples, respectively, with 82, 71, 69 and 80 of the 100 samples measured within the dynamic ranges. Viral loads were highly correlated with 99% of values within 1 log(10) copies/ml between tests. The automated m2000 system and RealTime HIV-1 assay can increase laboratory throughput, enhance overall efficiency and reduce operator-associated errors while providing reliable quantitation of genetically diverse strains of HIV-1.

Automation↗
PubMed2006

Enfurvitide prevents vertical transmission of multidrug-resistant HIV-1 in pregnancy but does not cross the placenta.

The use of previously successful antiretroviral regimens in mother-to-child transmission (MTCT) prevention will be increasingly challenged by the rising prevalence of multidrug-resistant (MDR) HIV. We used enfurvitide together with an optimized antiretroviral backbone to prevent the MTCT prevention of MDR HIV in two pregnant women. The measurement of maternal and foetal peripheral blood levels of enfurvitide showed no evidence of transplacental transfer.

Adult↗
PubMed2003

Dengue hemorrhagic fever with fulminant hepatic failure in an immigrant returning to Bangladesh.

An immigrant from Bangladesh living in the United Kingdom presented with a nonspecific febrile illness after visiting his homeland and subsequently developed fulminant hepatic failure accompanied by hypotension, ascites, a generalized coagulopathy, and thrombocytopenia. Serology and detection of dengue virus serotype 3 by PCR established a postmortem diagnosis of hepatic failure secondary to dengue hemorrhagic fever.

Ascites↗
PubMed2003

Buccal exposure to human papillomavirus type 16 is a common yet transitory event of childhood.

High-risk human papillomaviruses, such as type 16 (HPV-16), are established etiological agents for cervical carcinoma. In most cases, this virus is transmitted sexually, though can also be spread from mother to infant at delivery. We have demonstrated previously a high prevalence ( approximately 52%) of HPV-16 DNA in the mouths of prepubertal children, albeit with low levels of transcription [Rice et al., 2000]. We investigated whether childhood buccal infections with HPV-16 are persistent or transient and whether children became infected through contact with their immediate family members. Two groups of children were selected: one group were all initially HPV-16 E5 DNA-positive in sensitive polymerase chain reaction tests of swabs from their buccal mucosa (n = 20), and the other group consisted of children who were all HPV-16 E5-negative (n = 19). Thirty months later, a second oral swab was collected from each child and tested for HPV DNA. At this second visit, 40% of the HPV-16-positive group had no detectable HPV-16 DNA; conversely, 63% of children who were originally HPV-16-negative had now acquired the virus. Three months later, a third sample was collected from eight children and their immediate families (seven were HPV-16 E5 DNA-positive at the second visit). Amongst the family samples tested, in two families a single previously untested child was HPV-16 DNA-positive. It is concluded that HPV-16 DNA in the oral cavities of children is a transient event and is most probably acquired from their peers.

Case-Control Studies↗
PubMed2002

Antiretroviral drug resistance among HIV-1 infected children failing treatment.

High levels of HIV-1 replication occur following perinatal infection and antiretroviral drugs may not fully suppress viral load during the early years of childhood. Adherence to treatment may also be difficult among children. These two factors will contribute to development of drug resistance but limited paediatric data are available. This study has, therefore, evaluated the prevalence of drug resistance among children and assessed the contribution of adherence to failing therapy. Samples from 26 children who had experienced virological failure to antiretroviral therapy were tested for drug resistance using the Visible Genetics TRUGENE trade mark HIV-1 genotyping assay. HIV-1 subtype was determined using a peptide-based EIA and drug adherence determined by physician assessment. Twenty-four children were black African, 23 of whom were infected with a non-B subtype. HIV RNA sequence data was obtained for 21 of the 26 children; at treatment failure resistance mutations were detected in the protease gene of 7 (33%) and the reverse transcriptase gene of 19 (90%). A lower proportion of children had evidence of drug resistance at nadir and no resistance mutations were detected prior to treatment. Genotypic resistance was common in those treated with lamivudine (10/11, 91%), nevirapine (6/8, 75%), and zidovudine (7/11, 64%). The prevalence of mutations was lower among those receiving other nucleoside reverse transcriptase inhibitors and protease inhibitors. In 50% of children, drug adherence was >90%. Antiretroviral drug resistance was common among this group of children failing therapy, the majority of whom were infected with non-B subtypes of HIV-1. As adherence to treatment was low in 50%, this was likely to be an important contributory factor.

Adolescent↗