Little is known about the innate immune response to severe acute respiratory syndrome (SARS) coronavirus (CoV) infection. Mannose-binding lectin (MBL), a key molecule in innate immunity, functions as an anteantibody before the specific antibody response. Here, we describe a case-control study that included 569 patients with SARS and 1188 control subjects and used in vitro assays to investigate the role that MBL plays in SARS-CoV infection. The distribution of MBL gene polymorphisms was significantly different between patients with SARS and control subjects, with a higher frequency of haplotypes associated with low or deficient serum levels of MBL in patients with SARS than in control subjects. Serum levels of MBL were also significantly lower in patients with SARS than in control subjects. There was, however, no association between MBL genotypes, which are associated with low or deficient serum levels of MBL, and mortality related to SARS. MBL could bind SARS-CoV in a dose-and calcium-dependent and mannan-inhibitable fashion in vitro, suggesting that binding is through the carbohydrate recognition domains of MBL. Furthermore, deposition of complement C4 on SARSCoV was enhanced by MBL. Inhibition of the infectivity of SARS-CoV by MBL in fetal rhesus kidney cells (FRhK-4) was also observed. These results suggest that MBL contributes to the first-line host defense against SARS-CoV and that MBL deficiency is a susceptibility factor for acquisition of SARS.Severe acute respiratory syndrome (SARS), a newly emerged infectious disease of humans, has affected 125 countries, with 8098 cases and 774 deaths reported to the World Health Organization (WHO) during the first half of 2003 [1]. The most affected locations were mainland China, Hong Kong, Taiwan, Singapore, and To-

In the subtropics, influenza is an important cause of hospitalization among children, with rates exceeding those reported for temperate regions.

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Objective. The programmed death 1 (PD-1) molecule is a negative regulator of T cells, and a genetic association between PD-1 and systemic lupus erythematosus and rheumatoid arthritis (RA) in Caucasians has been reported. The aim of this study was to investigate the association of PDCD1 polymorphisms and haplotypes with RA in the Chinese population.Methods. Three single-nucleotide polymorphisms (SNPs), PD-1.1 G/A, PD-1.3 G/A, and PD-1.5 C/T, were genotyped in 180 patients with RA and 647 healthy controls in a case-control association study. Analyses of the association of genotypes and alleles with disease, haplotype construction, and linkage disequilibrium (LD) were performed.Results. We constructed haplotypes with the alleles of markers PD-1.1 G/A and PD-1.5 C/T and found that the GT haplotype was overrepresented in patients with RA (31%) compared with controls (23%) (P ‫؍‬ 0.001, odds ratio [OR] 1.54, 95% confidence interval [95% CI] 1.18-1.99). Among GT double homozygotes the risk of RA was increased even further (OR 2.31, 95% CI 1.31-4.08, P ‫؍‬ 0.006). We also observed that the AA genotype of SNP PD-1.1 was associated with a decreased risk for developing RA (OR 0.38, 95% CI 0.15-0.99, P ‫؍‬ 0.034). No association for SNP PD-1.5 in RA was found, and SNP PD-1.3 was nonpolymorphic in the Chinese population.Conclusion. Our results support the involvement of PDCD1 as a susceptibility gene for RA in the Chinese population.

There is a worldwide belief that the prevalence of asthma and other allergic diseases is increasing but the measures used in many studies are susceptible to systematic errors. We examined the trend of asthma, allergic rhinitis and eczema prevalence in school children aged 6-7 years in Hong Kong from 1995 to 2001 using standardized ISAAC methodology. There were 4448 and 3618 children participating in 2001 and 1995, respectively. The prevalence of life-time rhinitis (42.4% vs. 38.9%, p < 0.01), current rhinitis (37.4% vs. 35.1%, p < 0.03), current rhinoconjunctivitis (17.2 vs. 13.6%, p < 0.01) and life-time eczema (30.7% vs. 28.1%, p = 0.01) increased significantly. There was no significant change in prevalence of life-time asthma, life-time wheeze and current wheeze albeit a significant increase in severe asthma symptoms. We investigated a number of potential risk factors including sex, family history of atopy, sibship size, birth weight, respiratory tract infections, pet ownership and exposure to tobacco smoke. However, the increases in prevalence of rhinitis and eczema could not be entirely explained by the change of prevalence of these risk factors. The odds ratio OR for the study period remained significantly associated with current rhinitis (OR 1.31, 95% confidence intervals CI 1.17-1.46), current rhinoconjunctivitis (OR 1.63, 95% CI 1.41-1.87) and life-time eczema (OR 1.30, 95% CI 1.16-1.45) after adjustment for these confounding variables using logistic regression model. Further study is warranted to elucidate the factors contributing to the observable change in the prevalence of rhinitis in our population.

SummaryObjective To examine the association of air pollutants with hospital admission for childhood asthma in Hong Kong. Methods Data on hospital admissions for asthma, influenza and total hospital admissions in children aged 418 years at all Hospital Authority hospitals during 1997-2002 were obtained. Data on daily mean concentrations of particles with aerodynamic diameter o 10 mm (i. e. PM 10 ) and o 2.5 mm (i. e. PM 2.5 ), nitrogen dioxide (NO 2 ), sulphur dioxide (SO 2 ), and ozone (O 3 ) and data on meteorological variables were associated with asthma hospital admissions using Poisson's regression with generalized additive models for correction of yearly trend, temperature, humidity, day-of-week effect, holiday, influenza admissions and total hospital admission. The possibility of a lag effect of each pollutant and the interaction of different pollutants were also examined. Results The association between asthma admission with change of NO 2 , PM 10 , PM 2.5 and O 3 levels remained significant after adjustment for multi-pollutants effect and confounding variables, with increase in asthma admission rate of 5.64% (3.21-8.14) at lag 3 for NO 2 , 3.67% (1.52-5.86) at lag 4 for PM 10 , 3.24% (0.93-5.60) at lag 4 for PM 2.5 and 2.63% (0.64-4.67) at lag 2 for O 3 . Effect of SO 2 was lost after adjustment. Conclusion Ambient levels of PM 10 , PM 2.5 , NO 2 and O 3 are associated with childhood asthma hospital admission in Hong Kong.

Food allergy is defined as an adverse immune response towards food proteins or as a form of a food intolerance associated with a hypersensitive immune response. It should also be reproducible by a double-blind placebo-controlled food challenge. Many reported that food reactions are not allergic but are intolerances. Food allergy often presents to clinicians as a symptom complex. This review focuses on the clinical spectrum and manifestations of various forms of food allergies. According to clinical presentations and allergy testing, there are three types of food allergy: IgE mediated, mixed (IgE/Non-IgE), and non-IgE mediated (cellular, delayed type hypersensitivity). Recent advances in food allergy in early childhood have highlighted increasing recognition of a spectrum of delayed-onset non-IgE-mediated manifestation of food allergy. Common presentations of food allergy in infancy including atopic eczema, infantile colic, and gastroesophageal reflux. These clinical observations are frequently associated with food hypersensitivity and respond to dietary elimination. Non-IgE-mediated food allergy includes a wide range of diseases, from atopic dermatitis to food protein-induced enterocolitis and from eosinophilic esophagitis to celiac disease. The most common food allergies in children include milk, egg, soy, wheat, peanut, treenut, fish, and shellfish. Milk and egg allergies are usually outgrown, but peanut and treenut allergy tends to persist. The prevalence of food allergy in infancy is increasing and may affect up to 15-20 % of infants. The alarming rate of increase calls for a public health approach in the prevention and treatment of food allergy in children.

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