Biomedical subjects

S J Vessey

Publications and source records attributed to S J Vessey.

6 recordsLinked to original sources

PubMed2001

Childhood vaccination against varicella: persistence of antibody, duration of protection, and vaccine efficacy.

OBJECTIVE: To document the duration of protection afforded by Oka/Merck varicella vaccine over a 7-year period. STUDY DESIGN: The subjects were healthy children 1 to 12 years of age originally enrolled in clinical studies to evaluate the primary immune response to varicella vaccine 6 weeks after vaccination. Each was monitored for antibody persistence, breakthrough infection, and household exposure to varicella to produce estimates of vaccine efficacy. RESULTS: The 6-year cumulative varicella antibody persistence rate was 99.5% (95% CI: 98.9%, 100.0%). The annual breakthrough rate through 7 years ranged from 0.2% to 2.3% per year; the estimated cumulative event rate was 6.5%. Comparison of the observed average annual breakthrough rate with the age-adjusted expected annual incidence rate of varicella in unvaccinated children corresponded to an estimated vaccine efficacy of 93.8% to 94.6%. Eighty vaccinated children were exposed to varicella in the household, resulting in 8 (10%) cases of infection. When compared with the historical attack rate of 86.8% in unvaccinated susceptible persons exposed to varicella in the household, this yields an estimated vaccine efficacy of 88.5% (95% CI: 80.9%, 96.1%). Varicella cases in vaccinated children generally were mild. CONCLUSION: The live attenuated varicella vaccine is highly effective in inducing persistent immunity and long-term protection against breakthrough varicella infection.

Age Distribution↗

PubMed1997

Engagement of a T cell receptor by major histocompatibility complex irrespective of peptide.

T cell receptors (TCR) identify target cells presenting a ligand consisting of a major histocompatibility complex molecule (MHC) and an antigenic peptide. A considerable amount of evidence indicates that the TCR contacts both the peptide and the MHC components of the ligand. In fully differentiated T cells the interaction between the peptide and the TCR makes the critical contribution to eliciting a cellular response. However, during the positive selection of thymocytes the contribution of peptide relative to MHC is less well established. Indeed it has been suggested that the critical interaction for positive selection is between the TCR and the MHC molecule and that peptides can be viewed as either allowing or obstructing this contact. This predicts that a given TCR is capable of engaging multiple MHC/peptide complexes. In this study a system is described which detects simply engagement of the TCR by MHC/peptide complexes rather than the functional outcome of such interactions. Using this approach the extent to which peptides can influence contacts between the TCR and the MHC molecule has been examined. The results show that the TCR does in fact engage a wide range of ligands in an MHC-restricted but largely peptide-independent manner, suggesting that only a few peptides are able to prevent the TCR from contacting the MHC molecule.

Animals↗

PubMed1996

A functionally significant allelic polymorphism in a T cell receptor V beta gene segment.

The effect of an allelic polymorphism in the BV1S1 gene segment on recognition of major histocompatibility complex (MHC)-peptide complexes by a specific T cell receptor (TCR) was studied using RBL 2H3 cells transfected with TCR-CD3 zeta chimeric receptors. An HLA-A2-restricted human immunodeficiency virus (HIV) pol-specific cytotoxic T lymphocyte (CTL) clone utilizing the BV1S1A2 gene in combination with AV2S1A2 was identified and the extracellular domains of the TCR were fused to CD3 zeta. In degranulation assays RBL 2H3 transfectants expressing this receptor maintained the specificity of the parental CTL clone. The allelic variant BV1S1A1N1 containing a glutamine for histidine substitution at position 48 in the loop of the second complementarity-determining region was generated by site-directed mutagenesis. Transfection of this molecule as a CD3 zeta chimera together with the original AV2S1A2 CD3 zeta molecule resulted in cell surface expression of both chains but a loss of recognition of HLA-A2 HIV pol peptide-pulsed targets. The effect of this polymorphism on MHC-peptide recognition supports current models of TCR MHC-peptide interaction and provides evidence for a functional role for polymorphism in the TCRV genes.

Alleles↗

PubMed1994

Absence of mutations in the Gs alpha and Gi2 alpha genes in sporadic parathyroid adenomas and insulinomas.

1. Activating mutations of the alpha-subunits of the Gs and Gi2 proteins give rise to the oncogenes gsp and gip2, respectively, which are found in a variety of endocrine tumours. 2. In this study the polymerase chain reaction and direct sequencing have been used to screen a small sample of parathyroid adenomas and insulinomas for these mutations. 3. No mutations were identified in nine insulinomas and 13 parathyroid adenomas screened for gsp, and 11 parathyroid adenomas and four insulinomas screened for gip2. In addition, two gastrinomas from patients with multiple endocrine neoplasia type 1 were found to be negative for both oncogenes. 4. This is the first report of screening for gip2 in parathyroid adenomas and gsp/gip2 in insulinomas, and it extends the range of tumours examined for these oncogenes.

Adenoma↗

PubMed1993

Laser photocoagulation for proliferative retinopathy in sickle haemoglobin C disease.

The effect of sectoral, scatter laser photocoagulation on proliferative sickle retinopathy (PSR) was investigated by reviewing fluorescein angiograms of 88 sickle cell-haemoglobin C patients enrolled in a controlled, randomised trial. Follow-up was for a median period of 2.9 years. Complete infarction of all PSR in an eye occurred in 7 of 74 treated eyes and 2 of 60 control eyes. Treatment resulted in significantly greater regression (decrease in number or size of PSR lesions) in eyes of patients aged < 25 years at enrollment but not in eyes of patients > or = 25 years at enrollment. Infarction of individual PSR lesions was significantly more common in treated eyes. Treated PSR was significantly more likely to infarct if small (< 15 degrees circumferential involvement) and if flat rather than elevated. New PSR was significantly less likely to develop in treated eyes.

Adult↗

PubMed1991

Influence of genotype on the natural history of untreated proliferative sickle retinopathy--an angiographic study.

The natural history of untreated proliferative sickle retinopathy (PSR) has been observed in 35 patients (40 eyes) with homozygous sickle cell (SS) disease and in 112 patients (114 eyes) with sickle cell-haemoglobin C (SC) disease over a mean follow-up period of 4.5 years (range 0.5-14.0 years). In both genotypes progression of PSR was most frequent between ages 20 and 39 years. Spontaneous regression was more common in SS disease (p = 0.01), and more likely to proceed to complete non-perfusion. In SC disease PSR tended to be stable in patients aged 40 and over, and non-perfused PSR lesions were significantly more likely to reperfuse (p = 0.01) than in SS disease. In both genotypes regression was not influenced by size or elevation of the PSR lesion. The tendency for PSR to regress in SS disease suggests that treatment is unnecessary in SS patients aged 40 and over.

Adolescent↗