Financial Incentives for Preventing Postpartum return to Smoking (FIPPS): study protocol for a three-arm randomised controlled trial.

BACKGROUND: Financial incentives are an effective way of helping women to stop smoking during pregnancy. Unfortunately, most women who stop smoking at this time return to smoking within 12 months of the infant's birth. There is no evidence for interventions that are effective at preventing postpartum smoking relapse. Financial incentives provided after the birth may help women to sustain cessation. This randomised controlled trial will assess the effectiveness and cost-effectiveness of financial incentives to help women who are abstinent from smoking at end-of-pregnancy to avoid return to smoking up to 12 months postpartum. METHODS: This is a UK-based, multi-centre, three-arm, superiority, parallel group, individually randomised controlled trial, with 1:1:1 allocation. It will compare the effectiveness of two financial incentive interventions with each other (one intervention for up to 3 months postpartum offering up to £120 of incentives (£60 for the participant and £60 for a significant other support); the other for up to 12 months postpartum with up to £300 of incentives (£240 for the participant and £60 for a significant other support) and with a no incentives/usual care control group. Eligible women will be between 34 weeks gestation and 2 weeks postpartum, abstinent from smoking for at least 4 weeks, have an expired carbon monoxide (CO) reading < 4 parts per million (ppm), aged at least 16 years, intend remaining abstinent from smoking after the birth and able to speak and read English. The primary outcome is self-reported, lapse-free, smoking abstinence from the last quit attempt in pregnancy until 12 months postpartum, biochemically validated by expired CO and/or salivary cotinine or anabasine. Outcomes will be analysed by intention-to-treat and regression models used to compare the proportion of abstinent women between the two intervention groups and between each intervention group and the control group. An economic evaluation will assess the cost-effectiveness of offering incentives and a qualitative process evaluation will examine barriers and facilitators to trial retention, effectiveness and implementation. DISCUSSION: This pragmatic randomised controlled trial will test whether offering financial incentives is effective and cost-effective for helping women to avoid smoking relapse during the 12 months after the birth of their baby. TRIAL REGISTRATION: International Standard Randomised Controlled Trial Number 55218215 . Registered retrospectively on 5th June 2019.

Pregnant women's use of e-cigarettes in the UK: a cross-sectional survey.

OBJECTIVE: To estimate prevalence of vaping in pregnancy. Compare characteristics and attitudes between exclusive smokers and vapers, and between exclusive vapers and dual users (smoke and vape). DESIGN: Cross-sectional survey. SETTING: Hospitals across England and Scotland. POPULATION: Pregnant women attending antenatal clinics in 2017. METHODS: Women at 8-24 weeks' gestation completed screening questions about their smoking and vaping. Current or recent ex-smokers and/or vapers completed a full detailed survey about vaping and smoking. MAIN OUTCOME MEASURES: The prevalence of vaping, characteristics and attitudes of women who vape and/or smoke. RESULTS: Of 3360 pregnant women who completed screening questions, 515 (15.3%, 95% CI 14.1-16.6) were exclusive smokers, 44 (1.3%, 95% CI 1.0-1.8) exclusive vapers and 118 (3.5%, 95% CI 2.9-4.2) dual users. In total, 867 (25.8%) women completed the full survey; compared with smokers (n = 434), vapers (n = 140) were more likely to hold higher educational qualifications (odds ratio [OR) 1.51, 95% CI 1.01-2.25). Compared with exclusive vapers (n = 33), dual users (n = 107) were younger (OR 0.91 95% CI 0.85-0.98) and less likely to hold high qualifications (OR 0.43, 95% CI 0.20-0.96). Compared with smokers, dual users were more likely to be planning to quit smoking (OR 2.27, 95% CI 1.24-4.18). Compared with smokers, vapers were more likely to think vaping was safer than smoking (78.6% versus 36.4%). CONCLUSIONS: One in 20 pregnant women report vaping, and most also smoke. Dual users are more motivated towards stopping smoking than smokers. Where women have tried but cannot stop smoking, clinicians could encourage them to consider vaping for smoking cessation. TWEETABLE EXTRACT: One in 20 women report vaping during pregnancy but of those that do vape, most also smoke, despite having intentions to quit.

Association of UV radiation with multiple sclerosis prevalence and sex ratio in France.

BACKGROUND: French farmers and their families constitute an informative population to study multiple sclerosis (MS) prevalence and related epidemiology. We carried out an ecological study to evaluate the association of MS prevalence and ultraviolet (UV) radiation, a candidate climatologic risk factor. METHODS: Mean annual and winter (December-March) UVB irradiation values were systematically compared to MS prevalence rates in corresponding regions of France. UVB data were obtained from the solar radiation database (SoDa) service and prevalence rates from previously published data on 2,667 MS cases registered with the national farmer health insurance system, Mutualité Sociale Agricole (MSA). Pearson correlation was used to examine the relationship of annual and winter UVB values with MS prevalence. Male and female prevalence were also analyzed separately. Linear regression was used to test for interaction of annual and winter UVB with sex in predicting MS prevalence. RESULTS: There was a strong association between MS prevalence and annual mean UVB irradiation (r = -0.80, p < 0.001) and average winter UVB (r = -0.87, p < 0.001). Both female (r = -0.76, p < 0.001) and male (r = -0.46, p = 0.032) prevalence rates were correlated with annual UVB. Regression modeling showed that the effect of UVB on prevalence rates differed by sex; the interaction effect was significant for both annual UVB (p = 0.003) and winter UVB (p = 0.002). CONCLUSIONS: The findings suggest that regional UVB radiation is predictive of corresponding MS prevalence rates and supports the hypothesis that sunlight exposure influences MS risk. The evidence also supports a potential role for gender-specific effects of UVB exposure.

Revisiting the T-cell receptor alpha/delta locus and possible associations with multiple sclerosis.

A role for T cells in the pathogenesis of multiple sclerosis (MS) is well supported, evidenced by myriad immunological studies, as well as the unequivocal genetic influence of the major histocompatibility complex (MHC). Despite many attempts, no convincing genetic associations have been made between T-cell receptor (TCR) gene loci and MS. However, these studies may not be definitive because of small sample sizes and under-representative marker coverage of the chromosomal regions being investigated. To explore potential roles between the TCR alpha locus and MS, we have genotyped a large family-based cohort, including 1360 affected individuals and 1659 of their unaffected first-degree relatives, at 40 single-nucleotide polymorphism (SNP) markers within the TCR alpha/delta locus. This represents the largest TCR alpha-MS study to date. From this screen, we identified three potential loci of interest in TCR alpha variable and constant gene regions using the transmission disequilibrium test. Although SNPs implicating each of these regions of interest will require genotyping in independent replication cohorts, these findings suggest a role for TCR gene polymorphisms in MS susceptibility. In the context of these findings we review the evidence.

MHC transmission: insights into gender bias in MS susceptibility.

OBJECTIVE: Major histocompatibility complex (MHC) genes dominate genetic susceptibility factors in multiple sclerosis (MS). Given the general consensus that incidence and prevalence of MS has been rising and specifically in women, we evaluated MHC-gender interactions. METHODS: In a large family-based cohort consisting of 7,093 individuals (2,127 affected individuals) from 1,055 MS families, we examined MHC transmission by family structure and gender stratified by genetic distance of affected relatives from the MS proband. RESULTS: We found that affected individuals with HLA-DRB1*15-positive genotypes have higher female-to-male ratios as compared with affected individuals with HLA-DRB1*15-negative genotypes (χ(2) = 9.97, p = 0.0015) with the exception of multiplex families with 3 or more affected across 2 generations. Transmission disequilibrium test results show that HLA-DRB1*15 transmission was more distorted in collateral families vs nuclear families (χ(2) = 8.030, p = 0.0046), exclusively in affected female-female pairs (χ(2) = 7.81, p = 0.0051), but not in mixed gender pairs (χ(2) = 1.58, p = 0.21) or matched male pairs (Fisher p = 0.21). CONCLUSIONS: These observations implicate the MHC as the site of interactions and modifications mediating the female-to-male gender ratio in MS and its progressive increase. They further suggest this occurs via gene-environment interactions and epigenetic modifications in this region. The difference between collateral and nuclear families provides some insight into the inheritance, decay, and gender specificity of putative epigenetic marks.

Sex ratio of multiple sclerosis and clinical phenotype.

BACKGROUND AND PURPOSE: In a longitudinal population-based dataset of patients with multiple sclerosis (MS), we have previously observed a substantial increase in the female to male sex ratio in Canada over the last 50 years. Here, we aimed to determine whether this change in sex ratio is related to the clinical course of MS. METHODS: We calculated sex ratios by birth year in 11 868 patients with relapsing-remitting (RR) MS and 2825 patients with primary progressive (PP) MS identified as part of the Canadian Collaborative Project on the Genetic Susceptibility to MS. RESULTS: Year of birth was a significant predictor for sex ratio in RR MS (P < 0.0001, chi(2) = 21.2; Spearman's rank correlation r = 0.67), but not for PP MS (P = 0.44, chi(2) = 0.6; Spearman's rank correlation r = 0.11). CONCLUSIONS: An increase in the number of female RR MS patients over time accounts for the increasing sex ratio of MS. This has implications for pathogenesis, for assessment of clinical trial results and for disease prevention. The factors underlying the selective increase in MS in females need to be uncovered.

Effect of immigration on multiple sclerosis sex ratio in Canada: the Canadian Collaborative Study.

BACKGROUND: The ratio of female to male (F:M) multiple sclerosis (MS) cases varies geographically, generally being greater in areas of high prevalence. In many regions, including Canada, rising MS incidence in women has been implied by the marked increase in F:M ratio. METHODS: We examined the F:M ratio over time in MS patients in the Canadian Collaborative Study born outside Canada, with onset postmigration (n = 2531). We compared the trends to native-born Canadians, by region of origin and age at migration. RESULTS: Regression analysis showed that year of birth (YOB) was a significant predictor of sex ratio in immigrants (chi(2) = 21.4, p<0.001 correlation r = 0.61). The rate of change in sex ratio was increasing in all migrant subgroups (by a factor of 1.16 per 10-year period, p<0.001), with the steepest increase observed in those from Southern Europe (1.27/10 years, p<0.001). The overall immigrant F:M ratio was 2.17, but varied by country of origin. It was significantly lower in migrants from Southern Europe compared with Northern Europe or USA (1.89 vs 2.14 and 2.86, p = 0.023 and p = 0.0003, respectively). Increasing age at immigration was associated with decreasing sex ratio (p = 0.041). The sex ratio of individuals migrating <21 was significantly higher than those migrating > or =21 (2.79 vs 1.96, p = 0.004). CONCLUSIONS: MS sex ratio in immigrants to Canada is increasing but variable by region of origin and influenced by age at migration. The findings highlight the importance of environmental effect(s) in MS risk, which are likely gender-specific.

Parent-of-origin effect in multiple sclerosis: observations from interracial matings.

BACKGROUND: Multiple sclerosis (MS) is a complex neurologic disease with a striking geographical distribution. In Canada, prevalence is high in Caucasians of Northern European ancestry and uncommon in North American Aboriginals, many of whom now have Caucasian admixture. METHODS: The population-based Canadian Collaborative Project on the Genetic Susceptibility to MS provided the characteristics of 58 individuals with 1 Caucasian and 1 North American Aboriginal parent from a database of 30,000 MS index cases. RESULTS: We found that MS index cases with a Caucasian mother and a North American Aboriginal father had a higher sib recurrence risk and greater F:M sex ratio (p = 0.043) than patients with a North American Aboriginal mother and Caucasian father. CONCLUSIONS: Maternal parent-of-origin effects in multiple sclerosis disease etiology previously seen in studies of half-siblings and avuncular pairs are also seen in Caucasian-North American Aboriginal admixture matings and warrant further investigation. A differential influence of maternal risk transmission on the sex ratio of affected offspring is implied. The method of analysis used may have broader implications for detection of parent-of-origin effects in admixture cohorts.

Age of puberty and the risk of multiple sclerosis: a population based study.

BACKGROUND AND PURPOSE: Genetic and environmental factors have important roles in multiple sclerosis (MS) susceptibility. Given a potential role for sex hormones in MS, we have investigated whether or not the age of puberty influences the risk of developing MS in a population-based cohort. METHODS: We identified 5493 MS index cases and 1759 spousal controls with age of puberty information from the Canadian Collaborative Project on Genetic Susceptibility to MS. Age of puberty was compared between index cases and controls, and any effect of age of puberty on the age of onset of MS was also investigated. RESULTS: There were no significant differences between male index cases and controls with respect to age of puberty, P = 0.70. However, a significant difference was observed between female index cases and female controls, with average age of puberty being 12.4 and 12.6 years respectively, P = 0.00017, providing a relative risk decrease of 0.9 per year increase of age of puberty. There was no effect of the age of puberty on the age of MS onset in either sex. CONCLUSIONS: Earlier age at menarche increases the risk of MS in women. Whether this association is a surrogate for a disease causative factor or directly involved in MS disease aetiology needs to be uncovered.

Parent-of-origin effects in MS: observations from avuncular pairs.

BACKGROUND: Multiple sclerosis (MS) is a complex neurologic disease of unknown etiology and inheritance pattern, but with increasing incidence among females. The study of aunt/uncle-niece/nephew (AUNN) pairs has potential to shed light on the on complex trait inheritance as this group can be divided into eight different pair types by gender, MS status, and parent of origin. METHODS: Using a cohort of 807 avuncular MS families with 938 affected AUNN pairs ascertained from a longitudinal, population-based Canadian database, we examined differential MS transmission by separating affected pairs into likely maternal and paternal trait origin. RESULTS: We observed an increased number of avuncular pairs connected through unaffected mothers compared to unaffected fathers (p = 0.008). To restrict confounders introduced by families with multiple pairs the overall number of maternal and paternal families were compared, to reveal a significantly higher number of maternal families (p = 0.038). Female-to-male sex ratios were higher among affected nieces/nephews when compared to the sex ratio for aunts/uncles (0.00042). CONCLUSIONS: This observation independently confirms previous findings of a "maternal parent-of-origin" effect in multiple sclerosis (MS) susceptibility. These findings highlight the special contribution that can be derived from avuncular pairs. These underutilized pairings can compare transmission by the gender of affected aunt-uncle, the unaffected transmitting parent, and by that of the affected offspring. This strategy may be especially profitable in diseases where parent-of-origin effects are being sought. These findings also independently confirm the increasing rate of MS in females, demonstrating that familial cases are influenced by the same environmental factors as the general MS population.

A genome scan in a single pedigree with a high prevalence of multiple sclerosis.

BACKGROUND: Multiple sclerosis (MS) is a disease that is widely believed to be autoimmune in nature. Genetic-epidemiological studies implicate susceptibility genes in the pathogenesis of MS, although non-MHC susceptibility linkages have been difficult to confirm. Insight into pathways that are intrinsic to other complex diseases has come from the genetic analysis of large, autosomal-dominant kindreds. Here, we present a genetic study of a large and unique kindred in which MS appears to follow an autosomal-dominant pattern of inheritance, with consistent penetrance in four generations. METHODS: Eighty-two individuals of this 370-member family were genotyped with 681 microsatellite markers spanning the genome, with an average spacing of 5.3 cM. RESULTS: Parametric linkage analysis was performed and no significant LOD score (LOD >3.3) was observed. For a rare dominant disease model with reduced penetrance, 99.6% of the genome was excluded at a LOD score <-1 and 96% at a LOD score <-2. The HLA-DRB1 candidate gene was also genotyped by allele-specific methods. In each instance where at least one parent was positive for HLA-DRB1*15, one or more HLA-DRB1*15 alleles were transmitted to the affected offspring (11/11). HLA-DRB1*15 was transmitted equally from both the familial and the married-in parents and therefore this locus does not appear to be an autosomal-dominant acting gene in this family but an important modifier of risk. CONCLUSIONS: These results further stress the importance of the HLA-DRB1*15-bearing haplotype in determining MS susceptibility. Furthermore, this study highlights the complexity of MS genetics, even in the presence of a single family, seemingly segregating MS as an autosomal-dominant trait.

Multiple sclerosis susceptibility and the X chromosome.

Multiple sclerosis (MS) is a chronic autoimmune complex trait with strong evidence for a genetic component. A female gender bias is clear but unexplained and a maternal parent-of-origin effect has been described. X-linked transmission of susceptibility has been previously proposed, based on pedigree, association and linkage studies. We genotyped 726 relative pairs including 552 affected sib-pairs for 22 X-chromosome microsatellite markers and a novel dataset of 195 aunt-uncle/niece-nephew (AUNN) affected pairs for 18 markers. Parent-of-origin effects were explored by dividing AUNN families into likely maternal and paternal trait transmission. For the sib-pair dataset we were able to establish exclusion at a lambda s = 1.9 for all markers using an exclusion threshold of LOD < or = -2. Similarly for the AUNN dataset, we established exclusion at lambdaAV = 1.9. For the combined dataset we estimate exclusion of lambda = 1.6. We did not identify significant linkage in either the sib-pairs or the AUNN dataset nor when datasets were stratified for the presence/absence of the HLA-DRB1*15 allele or for paternal or maternal transmission. This comprehensive scrutiny of the X-chromosome suggests that it is unlikely to harbour an independent susceptibility locus or one which interacts with the HLA. Complex interactions including epigenetic ones, and masking by balanced polymorphisms are mechanisms not excluded by the approach taken.

Parental transmission of MS in a population-based Canadian cohort.

OBJECTIVE: Genetic and environmental factors have important roles in multiple sclerosis (MS) susceptibility. The precise nature of these factors and mode of inheritance remains unknown. A female predominance is universally found. Recently, offspring of affected fathers were reported to be more likely to have MS than those of affected mothers. This was attributed to the Carter effect, which is seen in polygenic disorders. The Carter effect predicts that affected parents of the sex lesser affected by a disease/trait are more genetically loaded for risk alleles and thus transmit these more often to their offspring. This hypothesis was tested in a population-based Canadian MS cohort. METHODS: Using the longitudinal Canadian database, we identified 3,088 nuclear families with one affected parent and a total of 8,401 offspring, of which 798 had MS. Transmission to daughters and sons from affected mothers and fathers was compared. RESULTS: There was equal transmission of MS from affected fathers vs affected mothers (9.41% vs 9.76%). Stratifying by gender of affected parent there were no differences in the female:male sex ratio of affected (2.46% vs 2.41%, p = 0.88) or unaffected offspring (0.91% vs 0.95%, p = 0.46). CONCLUSIONS: We observed equal disease transmission to offspring from affected mothers and affected fathers, no difference in the female:male sex ratio of affected offspring, and previously no difference in sibling recurrence risk by gender of parent affected. These findings show no evidence for the Carter effect and do not support the hypothesis of polygenic inheritance of multiple sclerosis susceptibility by parent.

The role of hereditary spastic paraplegia related genes in multiple sclerosis. A study of disease susceptibility and clinical outcome.

Multiple sclerosis (MS) is a common inflammatory disease of the central nervous system unsurpassed for its variability in disease outcome. It has been observed that axonal loss in MS is significant and that irreversible clinical disability relates to such axonal loss. The clinical similarities between Hereditary Spastic Paraplegia (HSP) and progressive MS, along with their analogous profiles of axonal loss in the long tracts, make the genes known to cause HSP biologically relevant candidates for the study of clinical outcome in MS. A cohort of sporadic MS cases and a set of unaffected controls were used to determine the role of HSP genes on MS susceptibility and disease severity. The MS cases were taken from opposite extremes of the putative distribution of long-term outcome using the most stringent clinical criteria to date. Genotyping the two sets of MS patients and controls could not provide any evidence to suggest that genes involved in the pathogenesis of HSP (Paraplegin, NIPA1, KIF5A, HSPD1, Atlastin, Spartin, Spastin, PLP1, L1CAM, Maspardin and BSCL2) play a role in susceptibility to, or modifying the course of, MS, although small effects of these genes cannot be ruled out.

No effect of APOE and PVRL2 on the clinical outcome of multiple sclerosis.

Multiple sclerosis (MS) is a common inflammatory disease of the central nervous system unsurpassed for its variability in disease outcome. Apolipoprotein E (APOE) is involved in neuronal remodelling and several studies have attempted to examine the effect of APOE on MS disease severity, but its function in modifying the course of MS is controversial. It has been suggested recently that PVRL2, not APOE, is the locus on chromosome 19 which influences clinical outcome of MS. A cohort of sporadic MS cases, taken from opposite extremes of the putative distribution of long-term outcome using the most stringent clinical criteria to date, was used to determine the role of APOE and PVRL2 on MS disease severity. The MS cases selected represent the prognostic best 5% (benign MS) and worst 5% (malignant MS) of cases in terms of clinical outcome assessed by the EDSS. Genotyping the two sets of MS patients (112 benign and 51 malignant) and a replication cohort from Sardinia provided no evidence to suggest that APOE or PVRL2 have any outcome modifying activity. We conclude that APOE and PVRL2 have little or no effect on the clinical outcome of MS.

Follow-up investigation of 12 proposed linkage regions in multiple sclerosis.

Multiple sclerosis (MS) is an autoimmune disease with overwhelming evidence for genetic determination, and for which a maternal parent-of-origin effect has been reported. As with many complex diseases, multiple suggestive linkage signals have been observed. However, the only unambiguous association and linkage identified to date is with alleles of the human lymphocyte antigen (HLA) class II region. We have now carried out high-density microsatellite genotyping for 12 of the most promising regions (1p, 1q, 2q, 4q, 5p, 9q, 10p, 11p, 12q, 17q, 18p, 19p) from a whole-genome scan in 552 affected sibling pairs. This has been carried out in 194 families containing avuncular pairs. These permit examination of parent-of-origin effects in non-colineal pairs when divided into likely maternal and paternal trait transmission. The results do not confirm any non-major histocompatibility complex linkage in the overall subset nor in the maternal, paternal or HLA-DRB1*1501 subsets. We were able to establish exclusion for a locus with lambda(AV) > or = 1.3 for all the previously suggested regions. These results again raise the possibility that the paradigm of multiple genes of small individual effect used to justify genome searches in MS is incorrect.

Self-reported symptoms associated with West Nile virus infection in RNA-positive blood donors.

BACKGROUND: In 2003, West Nile virus (WNV) nucleic acid amplification testing (NAT) was implemented to detect potentially infected donors. Of more than 5.3 million donations screened prospectively by the American Red Cross during the epidemic periods of 2003 and 2004, 974 were NAT-reactive and 519 confirmed-positive. A subset of both the confirmed-positive and the false-positive groups was assessed for demographic characteristics, symptoms, and symptom reporting relative to date of donation. STUDY DESIGN AND METHODS: All donors with initial WNV NAT-reactive results were invited to participate in a study that included a demographic, symptom, and date-of-symptom questionnaire. WNV confirmed-positive cases were compared to false-positive controls for comparison of frequency of symptom reporting before, on the day of, and after donation. RESULTS: Enrolled cases and controls were similar in all characteristics except cases were more likely to live in rural areas. Symptoms were reported by 61 percent of cases versus 20 percent of controls, with 74 percent of symptoms reported by cases within the 14 days after donation. The frequency of headache and fever reported together in the 7 days before donation was not significantly different between cases and controls; only the individual frequencies of headache, eye pain, and new rash during this time were significantly different. The most commonly reported symptoms, after adjustment for symptom reporting by controls, were headache, new rash, and generalized weakness; these symptoms were reported by 25 percent of cases. CONCLUSIONS: The demographic characteristics of infected donors reflected the rural nature of the 2003 to 2004 WNV epidemics. This study suggests that asking donors about predonation headache and fever had no detectable contribution to blood safety.

Risk factors for HCV infection among blood donors confirmed to be positive for the presence of HCV RNA and not reactive for the presence of anti-HCV.

BACKGROUND: In 1999, NAT of blood donations was implemented to detect "window-period" infections. Blood donors who have confirmed NAT results positive for the presence of HCV in the absence of anti-HCV are likely to have been recently infected. Of over 26.8 million donations tested between March 3, 1999, and March 31, 2003, 810 were HCV-reactive by NAT. A subset of these donors was assessed for recent exposure risk. STUDY DESIGN AND METHODS: All anti-HCV- blood donors with reactive, unconfirmed HCV NAT results were invited to participate in a study that included an extensive demographic and risk questionnaire. Confirmed HCV+ cases were compared to HCV- (falsely positive) controls for histories of potential risk factors during the 6 months before donation. RESULTS: Recent injection drug use (IDU) was independently associated with HCV infection (29.2% vs. 0% of cases vs. controls, p < 0.001). In addition, likely sources were identified for three other cases (4.6%), including occupational exposure, sexual contact with an HCV-infected partner (who was an IDU), and perinatal exposure, none of which was known to the donors at the time of donation. Incarceration was independently associated with HCV infection among the group not reporting IDU and after removal of the three donors with likely sources of risk (14.6% vs. 1.3% of cases vs. controls, p < 0.001). CONCLUSIONS: A likely risk, primarily IDU, was found for 43 percent of HCV+ donors whose infections were identified solely by NAT. Because the maximum efficiency of the donor history questions may have been reached, NAT will continue to be an important measure to interdict recently infected blood donors.

Simian foamy virus infection in a blood donor.

BACKGROUND: Infections with simian foamy virus (SFV) are widely prevalent in nonhuman primates. SFV infection was confirmed in a worker, occupationally exposed to nonhuman primates, who donated blood after the retrospectively documented date of infection. Human-to-human transmission of SFV through transfusion and its pathogenicity have not been studied. STUDY DESIGN AND METHODS: Recipients of blood from this donor were identified and blood samples from such recipients were tested for SFV infection by Western blot and PCR assay. RESULTS: One recipient of RBCs and another recipient of FFP had died; retroviral infections were not implicated. One platelet recipient could not be tested. Recipients of RBCs (two), a WBC-reduced RBC unit (one), and a platelet unit (one) tested SFV-negative 19 months to 7 years after transfusion. Tested recipients had transfusions 3 to 35 days after blood donation. Samples of one lot of albumin and three lots of plasma protein fraction (manufactured from recovered plasma from two donations) tested negative both for antibodies and for viral RNA. CONCLUSION: SFV transmission through transfusion was not identified among four recipients of cellular blood components from one SFV-infected donor. Derivatives containing plasma from that donor tested negative for SFV.

IgE is present on peripheral blood monocytes and B cells in normal dogs and dogs with atopic dermatitis but there is no correlation with serum IgE concentrations.

Blood was collected from 29 dogs, 14 with atopic dermatitis (AD) and 15 controls. Total serum IgE was quantitated. Peripheral blood monocytes were harvested and labeled with leucocyte markers and anti-canine IgE before analysis by flow cytometry. There was no statistically significant difference between the atopic and control groups when the mean number of cells in the monocyte (CD14), antigen presenting cell (CD1c) or B cell (CD21) populations were examined. However, the variation in cell numbers was significant and much greater in the atopic group for CD1c and CD14 labeled cells. The mean percentage of double labeled cells, CD1c/IgE and CD14/IgE was significantly lower in the atopic population compared with the controls. More variation was observed in the numbers of monocytes of atopic dogs (CD14/IgE) and antigen presenting cells (CD1c/IgE) of control dogs. The mean percentage of B cells expressing IgE was 65 and 51% in the atopic and control groups respectively which is greater than that reported in humans. There was no statistically significant difference. Total serum IgE concentrations were similar in each group and did not correlate with cell bound IgE in any of the leucocyte populations studied. Canine AD is associated with more variability in circulating monocyte numbers and lower numbers of monocytes expressing IgE than control dogs. Unlike in humans, there is no correlation between circulating and cell bound IgE. Furthermore, high levels of IgE in the dog may be related to a greater number of B cells in the circulation committed to IgE production.