Hepatitis: Taylor G

Hawkins D, Blott M, Clayden P, de Ruiter A, Foster G, Gilling-Smith C, Gosrani B, Lyall H, Mercey D, Newell ML, O'Shea S, Smith R, Sunderland J, Wood C, Taylor G, Anonymous00122. · Chelsea and Westimnster Hospital, London, UK. · HIV Med. · Pubmed #16033339 No free full text.

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Barton M, Finkelstein Y, Opavsky MA, Ito S, Ho T, Ford-Jones LE, Taylor G, Benson L, Gold R. · Division of Infectious Diseases, the Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada. · Pediatr Infect Dis J. · Pubmed #18664932 No free full text.

Abstract: We report the first cases of tissue-proven eosinophilic myocarditis after single vaccine administration of conjugate meningococcal C and hepatitis B vaccine, respectively. The nature of histopathologic findings strongly supports hypersensitivity reaction and negates viral etiology, which is typically characterized by a lymphocytic infiltrate. Both episodes resolved with corticosteroid therapy.To enhance discussion of our cases, we performed a systematic review of the literature on postimmunization myocarditis or pericarditis, and identified 37 publications, reporting 269 cases during the search period (1966-2007). Time of onset of cardiac symptoms in all patients ranged from 1 to 30 days postimmunization.

Sathia L, Obiorah I, Taylor G, Kon O, O'Donoghue M, Gibbins S, Walsh J, Winston A. · Imperial College Healthcare NHS Trust, London W21NY, UK. · AIDS Res Hum Retroviruses. · Pubmed #18671475 No free full text.

Abstract: Pharmacokinetic interactions between rifampicin and nonnucleoside analogue reverse transcriptase inhibitors (NNRTIs) pose challenges in the treatment of TB/HIV coinfection. We describe NNRTI plasma concentrations (PC) and treatment outcomes in TB/HIV coinfected patients receiving rifampicin and NNRTIs concomitantly. Single center prospective data were collected on all TB/HIV-coinfected patients who received concomitant NNRTI and rifampicin between 2001 and 2005. Of 103 TB/HIV coinfected patients, 26 received concomitant rifampicin with efavirenz (EFV) and 17 with nevirapine (NVP). NNRTIs were commenced after rifampicin in 18/26 (69%) and 7/17 (41%) subjects treated with EFV and NVP, respectively. Of these 88% completed antituberculosis therapy. There were two (5%) deaths, both due to lymphoproliferative malignancy. Three (7%) patients transferred care or discontinued therapy. Of subjects 83% had normal liver function tests (LFTs) and 11% had Grade 1-2 and 6% Grade 3-4 LFT abnormalities during concomitant therapy. PCs were measured in 31 patients. The first PCs were within the therapeutic range in 5/7 on NVP 200 mg bd, 2/4 on NVP 300 mg bd, 3/7 EFV 600 mg od, and 7/13 on EFV 800 mg od. PCs were subtherapeutic in 4/11 (36%) and 3/20 (20%) subjects on NVP and EFV, respectively. No virological rebounds were observed. Of subjects receiving concomitant NVP or EFV with rifampicin, 64% and 80%, respectively, had therapeutic NNRTI PCs. Subtherapeutic PCs were not associated with virological failure. Good clinical outcomes and a low incidence of hepatotoxicity were observed.

Miedzinski L, Taylor G. · University of Alberta, Edmonton, Alberta. · Can J Infect Dis Med Microbiol. · Pubmed #19436516 links to  free full text

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Netherton CL, Simpson J, Haller O, Wileman TE, Takamatsu HH, Monaghan P, Taylor G. · Vaccinology Group, Division of Immunology, Pirbright Laboratory, Institute for Animal Health, Ash Road, Pirbright, Woking, Surrey GU24 0NF, United Kingdom. · J Virol. · Pubmed #19109387 No free full text.

Abstract: Increasing evidence points to the importance of the interferon (IFN) response in determining the host range and virulence of African swine fever virus (ASFV). Infection with attenuated strains of ASFV leads to the upregulation of genes controlled by IFN pathways, including myxovirus resistance (Mx) genes that are potent effectors of the antiviral state. Mx gene products are known to inhibit the replication of many negative-sense single-stranded RNA viruses, as well as double-stranded RNA viruses, positive-sense single-stranded RNA viruses, and the reverse-transcribing DNA virus hepatitis B virus. Here, we provide data that extend the known range of viruses inhibited by Mx to include the large double-stranded DNA viruses. Stably transfected Vero cells expressing human MxA protein did not support ASFV plaque formation, and virus replication in these cells was reduced 100-fold compared with that in control cells. In contrast, ASFV replication in cells expressing MxB protein or a mutant MxA protein was similar to that in control Vero cells. There was a drastic reduction in ASFV late protein synthesis in MxA-expressing cells, correlating with the results of previous work on the effect of IFN on viral replication. Strikingly, the inhibition of ASFV replication was linked to the recruitment of MxA protein to perinuclear viral assembly sites, where the protein surrounded the virus factories. Interactions between ASFV and MxA were similar to those seen between MxA and different RNA viruses, suggesting a common inhibitory mechanism.

Taylor G. · Hemophilia Program, Vancouver General Hospital, Mary Pack Arthritis Centre Site, 895 West 10th Avenue, Vancouver, British Columbia V5Z 1LZ. · Health Soc Work. · Pubmed #15156848 No free full text.

This publication has no abstract.