During the period 1981–8 a clinical trial of a Q fever vaccine (Q-vax; Commonwealth Serum Laboratories, Melbourne) has been conducted in abattoir workers and other at-risk groups in South Australia. Volunteers in four abattoirs and visitors to the abattoirs were given one subcutaneous dose of 30 μg of a formalin-inactivated, highly-purified Coxiella burnetii cells, Henzerling strain, Phase 1 antigenic state, in a volume of 0·5 ml.

During the period, over 4000 subjects have been vaccinated and the programme continues in the abattoirs and related groups. ‘Common’ reactions to the vaccine comprised tenderness and erythema, rarely oedema at the inoculation site and sometimes transient headache. Two more serious ‘uncommon’ reactions, immune abscess at the inoculation site, were observed in two subjects, and two others developed small subcutaneous lumps which gradually dispersed without intervention.

Protective efficacy of the vaccine appeared to be absolute and to last for 5 years at least. Eight Q fever cases were observed in vaccinees, but all were in persons vaccinated during the incubation period of a natural attack of Q fever before vaccine-induced immunity had had time (≥ 13 days after vaccination) to develop. On the other hand, 97 Q fever cases were detected in persons working in, or visiting the same abattoir environments.

Assays for antibody and cellular immunity showed an 80–82% seroconversion after vaccination, mostly IgM antibody to Phase 2 antigen, in the 3 months after vaccination. This fell to about 60%, mostly IgG antibody to Phase 1 antigen, after 20 months. On the other hand, 85–95% of vaccinees developed markers of cell mediated immunity as judged by lymphoproliferative responses with C. burnetii antigens; these rates remained elevated for at least 5 years.

The Q fever vaccine, unlike other killed rickettsial vaccines, has the property of stimulating long-lasting T lymphocyte memory and this may account for its unusual protective efficacy as a killed vaccine.

An IgM capture enzyme-linked immunosorbent assay for rubella-specific IgM was used to assess the avidity of specific IgM by comparing the results obtained with and without a mild protein denaturant in the washing fluid used after incubation of IgM with rubella haemagglutinating antigen. An avidity index (AI) was calculated with AIs < 50% considered to indicate low avidity. Sera from recent primary rubella, rubella reinfection and from patients persistently reactive for specific IgM were tested. Urea and diethylamine (DEA) were compared as the protein denaturants. Twenty-six of 28 sera from cases of primary rubella gave an AI < 50% with DEA, compared with 25 of 28 with urea. Seventeen of 20 sera from cases of reinfection gave an AI > 50% with DEA whereas only 14 of 20 had a similarly high avidity with urea. Eight of 10 sera from 4 cases of persistent specific IgM reactivity gave AIs > 50% with DEA, although this was reduced to 5 when urea was used. Thus a difference has been demonstrated between the avidity of specific IgM in primary infection from that demonstrated after a secondary antigenic challenge (reinfection). This may help in serologically distinguishing primary infection from reinfection.

The immunogenicity and reactogenicity of two preparations of yeast-derived hepatitis B vaccinces were compared in healthy adult populations. The two groups were vaccinated in parallel, but they were not matched for age and sex. All subjects seroconverted, and 9 months after the first vaccine dose, all had anti HBs titres of at least 10 IU/1. The anti-HBs titres were higher in the group of subjects given 20μg vaccine antigen made by Smith Kline & RIT (GMT 2943 at 9 months) compared to those who received 10μg of vaccine made by Merck, S harp & Dohme (GMT 729 at 9 months). Adverse effects were recorded in 32·0 and 44·7% of the participants, but these were limited to minor local and general reactions. In the present study both preparations were safe and efficient.

The cross-reaction of HHV6 antibody with that to the other herpesviruses was studied in 96 blood donors whose sera were tested for IgG antibody to human herpesvirus type 6 (HHV6), cytomegalovirus (CMV), Epstein–Barr virus (EBV), varicella zostervirus (VZV) and herpes simplex virus (HSV). No correlation was found between IgG antibody to HHV6 and that to any of the other herpesviruses in these individuals. Antibodies to HHV6 and CMV were measured in patients undergoing documented serological responses to HHV6. Eleven cases of primary HHV6 infection associated with roseola infantum in babies, 1 of whom suffered from gastroenteritis as well as pyrexia and rash, are reported. Three cases of HHV6 reactivation, 1 in a 3-year-old child and 2 in adults, 1 of whom simultaneously underwent a primary CMV infection are also reported. Our results suggest that indirect immunofluorescence is a specific way of measuring HHV6 antibody, that HHV6 IgG and IgM can be detected in the absence of antibody to CMV and that HHV6 IgM is present both in primary HHV6 infections and in reactivations.

One thousand three hundred and twenty adults at risk of occupational exposure to hepatitis B were immunized using genetically engineered surface antigen and their antibody response (anti-HBs IU/1) assessed. Sex was known for all subjects and age for 1120 (range from 17–71 years). Seven hundred and sixty-four subjects were immunized in the local Department of Occupational Health, the remainder mainly by general practitioners.

Analysis of ‘good responders’ (anti-HBs > 100 IU/1) according to age and sex showed that increasing age and male sex had independent adverse effects on the likelihood of developing a satisfactory level of antibody to HBsAg. Furthermore even those most likely to respond well (young women), had a 1/5 to 1/6 failure rate to achieve > 100 IU/1 anti-HBs.

Of 63 persons who received a fourth dose of vaccine, 26 developed anti-HBs titres > 100 IU/1 when tested after 6 months. Subjects who had a low level of anti-HBs following primary immunization were more likely to develop > 100 IU/1 anti-HBs following a booster dose than were non-responders (< 10 IU/1).

A population of 488 HBsAg carrier individuals, from central Italy, classified on the basis of biochemical, clinical and histological parameters, was analysed for the presence of HBV-DNA in serum and its relationship with HBeAg/anti-HBe markers. The prevalence of HBV-DNA was 32·8% in chronic patients with biopsy-proven liver disease, and 20 and 4·3% respectively in asymptomatic carriers with and without altered ALT levels. The values in chronic patients were correlated with the histological activity.

Concordance of HBV-DNA presence and HBeAg positivity was observed in only 61·4% of cases. However HBV-DNA prevalence in sera of anti-HBe positive individuals was very low in asymptomatic carriers with normal ALT levels (2·5%). Higher values were observed in anti-HBe positive chronic patients (15·8%) and in carriers occasionally found with changes in ALT without any other clinical sign of illness (16·7%). These data would indicate that HBV-DNA is the serological marker which is most closely related to liver disease.

Patients with a clinical diagnosis of dengue but negative by serological testing were studied for rubella infection. Paired sera were obtained from 69 patients during an outbreak in Yucatán, México. The presence of specific anti-viral IgM in the acute sera was considered as diagnostic for rubella infection. The immunoglobulin was determined by measuring the difference in the inhibition of hemagglutination between the non-reduced and the reduced fractionated sera. Immunoglobulins were separated by sucrose density centrifugation. Acute rubella infection was found in 7 (10·1%) of the patients. These results demonstrate active rubella infection in patients clinically diagnosed as dengue.

During 19837 a clinical diagnosis of subacute sclerosing panencephalitis (SSPE) was confirmed by the detection of measles virus haemagglutination inhibiting antibody in the cerebrospinal fluid (CSF) in 81 subjects resident in Tamilnadu. The antibody titre (reciprocol of the endpoint dilution) in the CSF ranged from 2 to 32 and in the sera from 8 to 2048. The CSF: serum ratios of titres were 1:41:64 in 80 cases and 1:128 in one case. The median age at onset of SSPE was 10 years and 97% of cases were diagnosed at stage 2 and beyond. Based on the geographic distribution of 72 cases in an estimated population of 84 million, the annual incidence of SSPE was calculated to be 214 per million population, or 43 cases per million children below 20 years. Assuming that only 10% of all cases would have reached the level of laboratory diagnosis, the incidence may be as high as 21 cases per million population.

A competition enzyme-linked immunosorbent assay (ELISA) has been developed for the rapid identification and quantification of antibodies against African horse sickness (AHS) in sera from solipeds. The data showed the ELISA to be sensitive, specific and reliable.

More than 1600 sera from 37 different countries were examined and results compared with those obtained by agar gel immuno-diffusion (AGID) tests. In no case did any of 775 sera from countries where AHS has never been reported and where AHS vaccines are not used, record an ELISA titre greater than 4. A titre equal to or greater than 8 was considered positive. Using this criterion, 96·3% of sera tested in both assays were in agreement. Doubtful results by AGID (1·7%) were clearly defined in terms of positivity and negativity by ELISA.

This ELISA is suited for the rapid laboratory confirmation of AHS and should be considered as a replacement for the traditional AGID test.

The ability of three avian viruses to elicit antibody response in humans was surveyed for the purpose of identifying zoonotic diseases. Antibody levels in people associated with poultry were compared to those in people having limited poultry association. Antibody levels to three avian viruses: infectious bursal disease virus, a birnavirus; Newcastle disease virus, a paramyxovirus; and avian infectious bronchitis virus, a coronavirus were determined by enzyme–linked immunosorbent assays (ELISA). Differences between the two study groups were evident: people having a known association with poultry showed significantly higher levels of antibodies to Newcastle disease and avian infectious bronchitis virus. Antibodies detected may be due to virus exposure rather than zoonoses.

Outbreaks of vesicular stomatitis, serotype New Jersey, during epidemics in the United States and northern Mexico, 1982–5, were examined by backward trajectories of winds to investigate spread and possible sources. The outbreaks selected for analysis did not involve introduction of disease by infected animals. The findings indicate that wind could have been responsible for carrying infection from northern Mexico to Arizona and New Mexico and thence to Colorado and Utah and on to Wyoming, Idaho and Montana. The results of these analyses are consistent with the findings from T1 RNAse fingerprinting of virus isolates from outbreaks during the epidemics. The arrival of the trajectories was associated with the passage of a front and rain or passage of a front alone or rain alone. At the time of the trajectories temperatures of 10 °C and higher were recorded at heights up to 2500–3500 m.

Introduction by airborne particles would appear unlikely as it would have required a source of at least 105 infectious units per minute per animal. Vesicular stomatitis virus had been isolated from Simulium and Culicoides during the epidemic with amounts of virus from Simulium sufficient to suggest biological transmission. The possibility of Simulium infected with vesicular stomatitis virus being carried downwind to introduce disease is discussed in relation to the behaviour of Simulium and the pathogenesis of vesicular stomatitis in large animals.

Backward trajectories of winds were determined to identify possible sources of eastern equine encephalitis virus associated with isolation of virus from mosquitoes or birds or outbreaks in horses between 1980 and 1985 in Maryland, New Jersey, New York and Michigan, USA.

The results of the trajectory analyses suggested that eastern equine encephalitis virus could have been carried by infected mosquitoes on surface winds at temperatures 13 °C or higher from North Carolina north-eastwards along the Atlantic Coast to Maryland and New Jersey and thence to upstate New York and from western Kentucky to Michigan. Landing of mosquitoes was associated with the presence of a cold front and rain leading to variations in the location and timing of outbreaks from year to year. The mosquito responsible was most likely to have been Culiseta melanura, but Coquillettidia perturbans and Aedes sollicitans could also have been involved.

There may be a continual cycle of eastern equine encephalitis virus in mosquitoes and birds in south-eastern USA, from where the virus could be distributed by infected mosquitoes on the wind along the Gulf and Atlantic Coasts and up the Mississippi Valley.