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SUMMARY The hepatitis E virus (HEV) is a major cause of acute hepatitis globally. Genotypes 1 and 2 (G1 and G2) are obligate human pathogens transmitted faeco-orally, leading to epidemics in developing countries. In contrast, genotypes 3 and 4 (G3 and G4) have a wider host range, including humans, but are primarily porcine viruses and are transmitted from animals to humans as a food-borne zoonosis when meat from an infected animal is consumed. HEV is increasingly recognised as a problem in developed countries, including countries in Europe. G3 HEV is now the most common cause of acute viral hepatitis in the UK and cases continue to rise. The majority of these infections are acquired within the UK and thought to be from insufficiently cooked meat, predominantly processed pork meat. Previously thought to only cause self-limiting disease, HEV infection can persist in immunosuppressed patients, which may lead to chronic hepatitis and the rapid development of cirrhosis. Of particular interest to the transfusion community has been the possibility of transfusion-transmitted HEV, which has been reported from countries classically considered HEV-endemic but also non-endemic countries in Europe and Japan. This has prompted some countries to introduce screening for HEV in blood donations.

Thirteen patients with AIDS or ARC on continuous zidovudine therapy (800–1200 mg daily), who developed severe anaemia (median Hb 7.9g dl−1 range 4.9–9.4) after 66 days of treatment (median, range 35–258) were then treated with an intermittent regimen in an open study. The regimen consisted of cycles of 4 weeks on treatment (600–100 mg daily) followed by 2 weeks off. Intermittent treatment was tolerated for a significantly longer period of time (median 257 days range 72–603) and a higher cumulative does ( P < 0.001). Four patients discontinued intermittent therapy in the period of follow-up, three due to bone marrow suppression. Eight of 13 patients needed red cell transfusions on continuous therapy compared to only one on the intermittent regimen. On intermittent therapy median haemoglobin concentration and neutrophil counts remained stable (Hb median 11.9g dl−1 range 9.1–14.8, neut. median 1.7 × 109I−1 range 0.6–4.3). Ten patients had detectable levels of P24 antigen which decreased from a median of 128 pg ml−1 (range 15–242) to 24 pg ml−1 (range 0–53) on continuous therapy. Subsequently, in eight of these patients on the intermittent regimen, levels of P24 Ag remained below 50% of initial pretreatment values (median 28 pg ml−1 range 0–178) or below 50 pg ml−1.

Background and Objectives Certain patient ethnic groups may require blood components from donors under-represented in the UK donor population. Selective recruitment of Afro-Caribbean donors is therefore necessary but was considered to pose an increased risk of human T-cell leukaemia/lymphoma virus (HTLV) infection. To assess this a seroprevalence study of HTLV was undertaken in Afro-Caribbean and Caucasian donors.Materials and Methods Sera from 1100 Afro-Caribbean and 1100 Caucasian donors were tested for antibody to HTLV. Reactive samples were confirmed for specificity using an algorithm comprising two additional assays and polymerase chain reaction (PCR) where possible.Results Six Afro-Caribbean donors (0.55%) were considered to be infected with HTLV I.Conclusion Donor selection in this case caused a significantly elevated prevalence of HTLV infection and serves as a warning of the need for care in the design policies for selective donor recruitment.

SUMMARYBetween March and June 2008, 12 cases of hepatitis A were notified in Winchester. Cases were from a primary school and a nursery school with no direct linkage. Hepatitis A virus (HAV) RNA sequenced from nine cases confirmed the strain in both schools to be identical. The outbreak could have affected three other schools and a maternity unit and was controlled by immunization and screening of neonates in the maternity unit by dried blood spots. No neonates were infected and no further cases were reported until 5 months later when the index case's mother became infected with same strain of virus associated with the outbreak despite vaccination. Neither the source of the outbreak or the subsequent infection of the index case's mother was identified; however, with the timing of the cases continued transmission in the community by children with asymptomatic infection or a recurrent source cannot be ruled out.

SummaryRubella vaccination histories were taken from 333 young women working in the head office of a retail organization: 29% said they had had vaccine and 47% said they had not. The remainder did not know. Forty-six per cent of those ≤ 25 years old (who should have been offered vaccine at school), and 6% of those > 25 years old, said they had been vaccinated. When screened for immunity to rubella by radial haemolysis (RH) 3% had a low level of antibody (< 15 i.u./ml) and 11% had no antibody. After immunization with Cendevax the specific rubella IgM response was measured by an IgM antibody capture radioimmunassay (MACRIA). It was only detectable in the group without RH antibody, and was present in 26/31 of them. The Ig M response to Cendevax was strongest in specimens taken 20–39 days after immunization, but in 10 out of 11 cases tested was still present at around 71 days. The specific Ig M responses to Cendevax were very similar to those in women given Almevax in an earlier study, when measured in parallel tests.Taking both vaccines together, specific Ig M was present in 35 out of 36 vaccinees without pre-existing antibody tested between 40 and 77 days post-immunization. Detection of specific IgM by MACRIA would therefore be an effective means of determining susceptibility retrospectively in rubella vaccinees found to be pregnant.

SUMMARYEight sera from 125 cases of infectious mononucleosis (IM) were reactive for rubella-specific IgM in an M-antibody capture radioimmunoassay. The reactivity of individual sera varied depending upon the source of the rubella antigen used in the assay. One serum gave strongly positive results with some rubella haemagglutinating antigens but negative results with others and may have contained an IgM antibody which was capable of distinguishing between strains of rubella virus.If the diagnosis of rubella is based solely on detection in solid-phase immunoassay of rubella-specific IgM, IM should be excluded.

Summary Studies in animals have determined the importance of specific receptors to the action of many hormones and drugs. In man, a non-invasive external counting technique has been used and absence of receptor function has been demonstrated in a patient with nephrogenic diabetes insipidus using radioactively labelled arginine vasopressin. This is in contrast to the findings in a patient with pituitary diabetes insipidus and a normal control. These results suggest a model for the study of hormone and drug kinetics in man avoiding multiple samplings of biological fluids.

The aetiology of acute anterior uveitis (AAU) in the great majority of cases is unclear. Various infective agents have been postulated, however, as playing a direct or indirect part in the disease process, possibly via an immune-complex vasculitis. In an earlier study we concluded that, contrary to a previous report, hepatitis B virus (HBV) played only a small role, if any, in the pathogenesis of uveitis in Great Britain. Since we did not look for other markers of HBV infection other than hepatitis B surface antigen (HBsAg), it is possible that some cases of recent HBV infection may have been missed. In the present study 49 patients with AAU were tested for markers of hepatitis B infection. Sera from all patients tested were found to be negative for HBsAg and for antibody to the HBV core (anti-HBc), excluding HBV as a significant cause of AAU in this country. Since the quest for an infective agent in AAU may remain unproductive, future research on the aetiopathogenesis of AAU should include the study of tissue 'vulnerability' and the local and systemic immunoregulatory factors which modulate inflammatory responses.

A renal transplant patient was infected by a transfusion of blood from a chronic carrier of hepatitis B and he also became a symptomless carrier. Stored sera enabled detailed retrospective measurement of the rate of decline of passively transferred HBsAg, anti-HBc, and anti-HBe. Active HBsAg production was detected after two months and anti-HBc after six months; neither HBe nor anti-HBe was actively produced although there were many 42 nm HBV particles in the patient's serum.

SummaryRadial haemolysis (RH) was used to test sera for immunity to rubella from 1317 patients attending a general practice. One hundred and forty-one (10·7%) were treated as susceptible and offered an attenuated virus vaccine (RA 27/3). Pre-immunization sera from 43% of these patients were reactive at low levels in RH (< 15 international units rubella antibody per ml).Pre- (S1) and post- (S2) immunization sera from 66 vaccinees were studied in detail. Antibody was detected by RH, haemagglutination inhibition (HI) and enzyme-linked immunosorbent assay (ELISA), and the specific IgM response was measured by a solid-phase M-antibody capture radioimmunoassay (MACRIA). The vaccine-induced IgM response was only detected if the S1 serum was non-reactive by all tests for rubella antibody. It was weaker than that seen following wild virus infection. It could be detected reliably for six weeks, and in most cases for nine weeks, after immunization. In contrast, patients with S1 specimens reactive by RH, HI or ELISA never showed an IgM response in the S2 specimen despite ‘significant’ antibody rises often being present.It was considered that an IgM response to RA 27/3 was the best indicator of pre-immunization susceptibility to rubella. The failure of many vaccinees to make an IgM response implied that a significant proportion were already immune. It is suggested that the threshold for a report of immunity to rubella could be lowered from 15 i.u. antibody per ml and so fewer women immunized without vaccine being withheld from those who need it.

By November 7, 1983, 24 cases of AIDS in the United Kingdom had been reported to the Communicable Disease Surveillance Centre. At the same time an increasing number of homosexual men with unexplained lymphadenopathy syndrome (LAS) have been seen in our department. Between December 1982 and July 1983, 14 homosexual men with LAS and 11 healthy homosexual men were studied. Patients with LAS had a high number of lifetime episodes of sexually transmitted diseases, a history of recent sexual activity in the United States (9 of 14), sexual contact with British AIDS patients or other persons with LAS (7 of 14), and hypergammaglobulinemia. Low T-helper/T-suppressor ratios (less than 0.8), due mainly to a decrease in T-helper cells, were found in both groups. Lymph node biopsies showed follicular hyperplasia and hypocellular pattern. All 25 patients studied had antibodies to Epstein-Barr virus capsid antigen (anti-VCA) and 11 had antibodies to early antigen (anti-EA); 13 of 17 were excreting the virus; and two showed no Epstein-Barr-virus-specific regression. Peripheral blood immunoglobulin-producing B-cells from six patients with hypergammaglobulinemia were negative for the Epstein-Barr virus nuclear antigen (EBNA). Five lymph node biopsies showed no EBNA-positive cells. Epstein-Barr virus reactivation is common in the patients with LAS and healthy homosexual men in London, but would not seem to be the cause of the polyclonal B-cell activation or lymphadenopathy.

Serological markers for hepatitis B virus infection have been examined in 34 patients with acute hepatitis B, 17 of whom developed fulminant hepatic failure. Hepatitis B surface antigen concentrations were significantly lower and hepatitis Be antigen was less frequently detectable in patients with fulminant hepatic failure compared with those with acute hepatitis (median 0.64 micrograms, range 16-0 and median 32 micrograms and range 100-4 micrograms respectively, p less than 0.001; HBeAg detected in 12% and 88% respectively, p less than 0.001). The IgM component of hepatitis B core antibody was significantly higher in the patients with fulminant hepatic failure with median values of 500 IU/ml compared with those with uncomplicated hepatitis (median 202 IU/ml, p less than 0.05 Wilcoxon's rank test). Three patients who developed a fulminant course had detectable levels of either anti-HBs or anti-HBe. These results are consistent with enhanced antibody responses to all three hepatitis B virus antigens and more rapid clearance of the latter during fulminant hepatic failure.