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There is evidence of probable recent HEV infections in donors with a predicted attack rate of 2.8%.

Dear Editor,We read with interest the letter from Baylis et al., [1] reporting on the detection of hepatitis E virus (HEV) RNA and antibody in plasma fractionation pools, which originated from several regions across the globe. The authors report that 10% of the pools were HEV RNA positive and discuss the transmission risk through the use of plasmaderived medicinal products.We recently reported evidence of current HEV infection in English and Welsh blood donors indicating a turnover of the virus in the donor panel and the potential for transfusion-associated transmission [2]. To ascertain further the risk of HEV to the English blood supply, serological and molecular investigations were undertaken in plasma minipools collected in 2007. Each mini-pool was made up of 48 individual donors and had originally been prepared for hepatitis C RNA screening. Extraction and detection of HEV RNA was carried out on 880 mini-pools (equivalent to approximately 42 000 individual donors) as previously described [2]. Six of the 880 pools (0AE7%) had detectable HEV RNA. As expected, viral loads in the HEV RNApositive pools were low (£ 2000 GEq ⁄ ml). Additional HEV antibody (anti-HEV) testing found all 6 (100%) and 1 ⁄ 6 (17%) of the HEV RNA-positive pools to be anti-HEV IgG and IgM reactive respectively. Of the 100 HEV RNA-negative pools tested, 73% and 0% were HEV IgG and IgM reactive respectively.The high incidence of asymptomatic infection with HEV gives ample opportunity for blood donors to infect recipients. Studies undertaken in the general English population indicate an anti-HEV seroprevalence of 13% and estimate that 60 000 cases occur per year [3]. It is therefore perhaps unsurprising that our study demonstrates a high anti-HEV IgG prevalence in the mini-pools tested. The detection of HEV RNA and anti-HEV IgM demonstrates current HEV infections. In contrast, Baylis et al. [1] found HEV IgG only in the pools from Asia, which is very surprising given the UK seroprevalence. They also report eightfold higher rates of HEV RNA in tested pools from Europe but do not disclose the pool size. Some of these differences may be explained by variations in the make up of the pools and in the detection assays used.Collectively, these reports provide evidence of the potential to transmit HEV from blood ⁄ blood components and products. However, the extent of HEV transmission posttransfusion and the outcome of receiving HEV-containing transfusion products remain poorly explored. The risks of transfusion-associated HEV deserves due consideration in light of emerging data on the significant harm of persistent HEV in the immunosuppressed [4,5]. It is estimated that 75% of UK blood ⁄ blood components are given as haematological support to this population. The issue of HEV and blood safety therefore warrants further studies and debate. References

The hepatitis B virus (HBV) surface antigen (HBsAg) is a complex protein, and understanding accurately the impact of amino acid changes on the antigenicity of the immunodominant a determinant must take this complexity into consideration. Epitope mapping with four mAbs was used to phenotype HBsAg directly from patients' sera to investigate the effect of mutations in their native genetic backbone. The expected mAb reactivity was established initially for samples harbouring 'wild-type' HBsAg sequences across genotypes A-E. The alteration of HBsAg antigenicity, defined by mAb epitope loss, was demonstrated in a number of samples with sequence-inferred amino acid changes. Individual mutations within the mapped epitopes to which the mAbs were directed usually affected their binding. However, the loss of more than one epitope was observed as the number of mutations within a sequence increased. Conversely, not all mutations occurring in the a determinant altered the HBsAg conformation. The genotype backbone, the specific amino acid substitution and amino acid changes occurring outside the major antigenic region appeared to be important in determining expression of the predicted epitope loss. These data clearly demonstrate that sequence-based methods alone may not accurately define HBsAg phenotype. This phenotyping methodology allows for the rapid and accurate identification of antigenically altered viruses and will greatly enhance current HBV surveillance, research and diagnostic activities. The data generated can be used to inform on public health issues relating to prevalence, transmission and impact of HBsAg mutants in HBVinfected populations.

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