Can influenza H1N1 vaccination lead to the membranous glomerulonephritis?

In 2009 winter, Influenza A (H1N1) monovalent split virus vaccine was used prevalently in the whole world as a result of the pandemic caused by Influenza (H1N1) virus. The vaccine's adverse effects were observed closely and vaccination has been found as safe in most studies. But some reports about immune response related diseases after influenza vaccinations are remarkable. The close relationship between membranous glomerulonephritis and antigens is known, particularly in seconder forms which occur after viral infections and vaccinations. So this case report is about a 56-year-old man, who developed membranous glomerulonephritis 23 days after the vaccination against Influenza A (H1N1) virus.     

Emergence of H274Y oseltamivir-resistant A(H1N1) influenza viruses in Japan during the 2008–2009 season

BackgroundA substantial increase in oseltamivir-resistant A(H1N1) influenza viruses was reported in Europe in late 2007.ObjectivesTo monitor the antiviral susceptibility profile of human A(H1N1) influenza viruses in Japan during the 2007–2008 and 2008–2009 seasons.Study designViruses were obtained from respiratory samples of patients with influenza collected in Japan between December 2007 and April 2008 (n = 1046) and between December 2008 and April 2009 (n = 1789). Oseltamivir resistance was determined by an H274Y-specific real-time PCR cycling probe assay and a neuraminidase inhibition assay. Amantadine resistance was assessed by sequencing the M2 gene. Sequencing of the hemagglutinin and NA genes was performed to infer phylogenetic relationships between different strains.ResultsThree of 687 (0.4%) A(H1N1) viruses from the 2007–2008 season and 745 of 745 (100%) viruses from the 2008–2009 season carried the NA–H274Y substitution and demonstrated a >300-fold reduction in oseltamivir susceptibility. All oseltamivir-resistant viruses from the 2008–2009 season possessed an A193T substitution in the receptor-binding domain of the hemagglutinin. Amantadine resistance was detected in 431 of 687 (62.7%) and 0 of 745 (0.0%) of the A(H1N1) viruses from the 2007–2008 and 2008–2009 seasons, respectively.ConclusionsA dramatic surge in oseltamivir-resistant A(H1N1) viruses possessing the NA–H274Y substitution was detected in Japan during the 2008–2009 season. The emergence of oseltamivir-resistant viruses was facilitated by mutations in the viral genome. Intensified surveillance, including phenotypic assays and sequencing of the hemagglutinin, neuraminidase, and M2 gene would allow monitoring of the spread and evolution of drug-resistant influenza virus variants.     

A review of the dynamics and severity of the pandemic A(H1N1) influenza virus on Réunion Island, 2009

On Reunion Island, in response to the threat of emergence of the pandemic influenza A(H1N1)2009 virus, we implemented enhanced influenza surveillance from May 2009 onwards in order to detect the introduction of pandemic H1N1 influenza and to monitor its spread and impact on public health. The first 2009 pandemic influenza A(H1N1) virus was identified in Réunion on July 5, 2009, in a traveller returning from Australia; seasonal influenza B virus activity had already been detected. By the end of July, a sustained community pandemic virus transmission had been established. Pandemic H1N1 influenza activity peaked during week 35 (24–30 August 2009), 4 weeks after the beginning of the epidemic. The epidemic ended on week 38 and had lasted 9 weeks. During these 9 weeks, an estimated 66 915 persons who consulted a physician could have been infected by the influenza A(H1N1)2009 virus, giving a cumulative attack rate for consultants of 8.26%. Taking into account the people who did not consult, the total number of infected persons reached 104 067, giving a cumulative attack rate for symptomatics of 12.85%. The crude fatality rate (CFR) for influenza A(H1N1)2009 and the CFR for acute respiratory infection was 0.7/10 000 cases. Our data show that influenza pandemic did not have a health impact on overall mortality on Réunion Island. These findings demonstrate the value of an integrated epidemiological, virological and hospital surveillance programme to monitor the scope of an epidemic, identify circulating strains and provide some guidance to public health control measures.     

Virus interference. Did rhinoviruses activity hamper the progress of the 2009 influenza A (H1N1) pandemic in Norway?

During summer and autumn 2009 Norway, like several other European countries, experienced an unexpected delay in the progress of the 2009 pandemic influenza A (H1N1) virus. It is considered whether interference with other respiratory viruses, in particular rhinoviruses, may have hampered the development of the influenza pandemic, and if interference phenomena are common in the development of outbreaks with epidemic viruses. If so, cytokines, in particular interferon, are the most probable executor of this effect.     

H1N1v at a seroepidemiological glance: is the nightmare over?

When the second wave of pandemic influenza A H1N1v 2009 (H1N1v) emerged in the winter of 2010/2011, public health authorities were afraid of dangerous implications and severe clinical courses again. As further H1N1v waves might appear, achievement of sufficient herd immunity is a matter of urgency. The objective of this study was to determine the seroprevalence of antibodies against H1N1v by hemagglutination-inhibition test (HI) after the second wave. We compared our recent findings with our data obtained after the first pandemic in 2009/2010. Between March and May 2011 we collected serum samples from 600 persons aged 1 to 84?years admitted to University Hospital Frankfurt/Main and analysed the titres of anti-H1N1v by HI. The overall seroprevalence of anti-H1N1v has risen from 36.9% (95% confidence interval (95%CI), 33-41) in unvaccinated persons after the first wave to 57.3% (95%CI, 53.1-61.2) in vaccinated and unvaccinated. The highest rate of seropositivity was detected in the age group of 10-19?years (66%; 95%CI, 55.8-75.2), whereas the lowest was found in the age group 40-59?years (51%; 95%CI, 40.8-61.1). Although seroprevalence has significantly increased, sufficient herd immunity is still not achieved. Therefore, general vaccination programs have to be propagated continuously by public health authorities.     

甲型H1N1流感疫苗接种研究概况

2009年3月中下旬北美墨西哥暴发新型流行性感冒,4月中旬美国疾病预防控制中心确认本次大流行的病毒株为猪来源的甲型H1N1流感病毒。2010年10月,我国首先在全球范围内开展甲型H1N1流感疫苗接种。目前关于甲型H1N1流感疫苗的接种研究进展尚总结得不多,本文现综述如下。     

中国甲型H1N1流感疫苗质量分析

目的 通过对甲型H1N1流感疫苗批签发中的检测数据进行分析和比较,了解我国甲型H1N1流感疫苗的总体质量状况.方法 按照各企业注册标准对甲型H1N1流感疫苗进行资料审查和全项检定,对关键项目检测结果进行分析和比较.结果 甲型H1N1流感疫苗批签发总体合格率为99.8%,有效成分血凝素含量在标示量的90%～103%范围内,甲醛、卵清蛋白和内毒素含量等安全性指标均符合规定.结论 我国甲型H1N1流感疫苗各项检测总体情况良好,能充分保证疫苗的安全性和有效性,中国食品药品检定研究院的独立检验和批签发对保证上市疫苗的质量发挥了重要作用.

Abstract：

Objective To analyze the laboratory testing data of 2009 pandemic influenza A (H1N1) vaccines during lot release procedure, thus to know the overall quality status of this vaccines.Methods National Institutes for Food and Drug Control(NIFDC) carried out the laboratory test according to the specifications of each manufacture, and the results was analyzed and compared between manufacturer and NIFDC. Results 99.8% of vaccines batches were released by NIFDC, haemagglutinin contents were between 90% to 103 % of labeled values, and testing results slightly differ between manufactures and NIFDC,other items related to safety were all meet specifications. Conclusion The quality of H1N1 vaccines in China were satisfying, the lot release and independent test by NIFDC play important roles to ensure the vaccines' quality.     

甲型H1N1流感的小知识

甲型H1N1流感又称为A（H1N1）型流感,人感染猪流感。其病原体为甲型H1N1流感病毒,该病毒包含有禽流感、猪流感和人流感三种流感病毒的核糖核酸基因片断。中国卫生部2009年4月30日发布2009年第8号公告,明确将甲型H1N1流感纳入传染病防治法规定管理的乙类传染病,并采取甲类传染病的预防、控制措施。     

季节性流感与甲型H1N1流感

流行性感冒（流感）是由流感病毒引起的急性呼吸道传染病。流感病毒传染性强,传播速度快。主要通过呼吸道传播,接触患者的呼吸道分泌物、体液和被污染的物品也可造成传播。     

甲型H1N1流感疫苗接种研究概况

2009年3月中下旬北美墨西哥暴发新型流行性感冒,4月中旬美国疾病预防控制中心确认本次大流行的病毒株为猪来源的甲型H1 N1流感病毒.2010年10月,我国首先在全球范围内开展甲型H1N1流感疫苗接种.目前关于甲型H1N1流感疫苗的接种研究进展尚总结得不多,本文现综述如下.     

Seasonal H1N1 2007 influenza virus infection is associated with elevated pre‐exposure antibody titers to the 2009 pandemic influenza A (H1N1) virus

The new influenza strain detected in humans in April 2009 has caused the first influenza pandemic of the 21st century. A cross‐reactive antibody response, in which antibodies against seasonal H1N1 viruses neutralized the 2009 pandemic influenza A (H1N1) virus (2009 pH1N1), was detected among individuals aged >60 years. However, factors other than age associated with such a cross‐reactive antibody response are poorly documented. Our objective was to examine factors potentially associated with elevated pre‐exposure viro‐neutralization and hemagglutination‐inhibition antibody titers against the 2009 pH1N1. We also studied factors associated with antibody titers against the 2007 seasonal H1N1 virus. One hundred subjects participating in an influenza cohort were selected. Sera collected in 2008 were analysed using hemagglutination inhibition and viro‐neutralization assays for the 2009 pH1N1 virus and the 2007 seasonal H1N1 virus. Viro‐neutralization results were explored using a linear mixed‐effect model and hemagglutination‐inhibition results using linear‐regression models for interval‐censored data. Elevated antibody titers against 2009 pH1N1 were associated with seasonal 2007 H1N1 infection (viro‐neutralization, p 0.006; hemagglutination‐inhibition, p 0.018). Elevated antibody titers were also associated with age in the viro‐neutralization assay (p <0.0001). Seasonal 2007 H1N1 infection is an independent predictor of elevated pre‐exposure antibody titers against 2009 pH1N1 and may have contributed to lowering the burden of the 2009 pH1N1 pandemic.     

Will the next human influenza pandemic be caused by the virus of the avian flu A/H5N1? Arguments pro and counter

In 1997, the avian influenza A subtype H5N1 that caused big outbreaks of fowl pest in mass poultry farming had emerged in Hong Kong. Its spread throughout Eurasia had given rise to concerns in terms of the possible imminence of the next human influenza pandemic. In this article, epidemiological and virological arguments supporting or declining this fear are outlined and discussed with regard to viral infectivity and pathogenicity.     

The interaction of influenza H5N1 viral hemagglutinin with sialic acid receptors leads to the activation of human γδT cells

Highly pathogenic avian influenza H5N 1 epidemics are a significant public health hazard. Genetically engineered H5N 1 viruses with mammalian transmission activity highlight the potential risk of a human influenza H5N 1 pandemic. Understanding the underlying principles of the innate immune system in response to influenza H5N 1 viruses will lead to improved prevention and control of these potentially deadly viruses, γδT cells act as the first line of defense against microbial infection and help initiate adaptive immune responses during the early stages of viral infection. In this study, we investigated the molecular mechanisms of γδ T cells in response to influenza H5N1 viral infection, We found that recombinant hemagglutinin （rHA） derived from three different strains of influenza H5N 1 viruses elicited the activation of γδ T cells cultured in peripheral blood mononuclear cells （PBMCs）. Both the cell surface expression of CD69, an early activation marker on γδ T cells, and the production of interferon-y （IFN-y） were significantly increased. Notably, the rHA protein-induced γδ T-cell activation was not mediated by TCRγδ, NKG2D or pattern recognition receptors （PRRs） or NKp46 receptors. The interaction of rHA proteins with sialic acid receptors may play a critical role in γδ T-cell activation. Our data may provide insight into the mechanisms underlyingγδT-cell activation in response to infection with H5N1 viruses.     

唐山市甲型H1N1流感病毒血凝素基因序列分析

目的 分析2010—2016年唐山市甲型H1N1流感病毒血凝素(hemagglutinin,HA)基因序列进化特征.方法 选取唐山市3家哨点医院流感样病例分离到的24株甲型H1N1病毒,通过RT-PCR和测序方法获得HA基因的全长序列,运用分子生物学软件和统计学软件对序列进行拼接、比对和分析.结果 同源进化分析显示,24株甲型H1N1流感病毒HA基因与疫苗株A/California/7/2009的核苷酸和氨基酸的同源性分别为97.0%~99.0%和97.0%~98.5%.进化分析显示,2010—2016年唐山地区流行的甲型H1N1流感病毒属于1、7、6三个基因分支,其中6分支毒株分为6C、6B、6B.1和6B.2亚支.氨基酸位点分析显示,不同毒株与疫苗株比较存在8~16处氨基酸位点改变,其中7个变异涉及3个抗原表位:H138Q/Y和S203T突变位于Ca区,N125S、K153E、S162N、K163T/Q突变位于Sa区,S185T突变位于Sb区同时也位于受体结合部位;2015—2016流行季6B.1分支毒株抗原位点S162N突变增加了新的潜在糖基化位点.结论 与疫苗株比较,随着时间推移唐山地区甲型H1N1流感病毒发生了抗原漂变,未来仍应关注6B分支流行株的变化.     

汕头市濠江区甲型H1N1流感病毒感染状况

目的了解汕头市濠江区甲型H1N1流感感染状况,为防控措施提供科学依据。方法在2010年1-9月期间,开展3次人群甲型H1N1流感病毒感染状况横断面调查,采用血凝抑制法检测居民甲型H1N1流感病毒血清抗体,对结果进行统计分析。结果 3次人群甲型H1N1流感病毒感染血清学检测,共检测480人,总阳性率为15%,各月份阳性率逐次下降（1月为20%、3月为15.2%、9月为9.4%）;各年龄组人群中,6～岁组阳性率（30.2%）最高,16～岁组阳性率（15.1%）次之,0～岁组幼儿阳性率（8.3%）再次之,≥60岁老人组阳性率（6.3%）最低。结论濠江区人群甲型H1N1流感病毒感染率较低,人群免疫屏障尚未完全建立,适当接种甲流疫苗仍有必要。     

人感染甲型H1N1流感病毒的研究进展

2009年4月以来,包括墨西哥、美国和加拿大在内的许多国家发生了人感染甲型H1N1流感病毒疫情,WHO已于2009年4月29日将此次流感流行的预警级别不断提升至5级。现已基本明确,引起此次流感疫情的甲型H1N1流感病毒是猪流感病毒（swine influenza virus,SIV）的一种新型变异株。