No abstract

This article describes a widespread outbreak of hepatitis A virus (HAV) infection amongst drug abusers in Finland. Although attempts to demonstrate the virus in amphetamines failed, the infection was assumed to be linked to intravenous use of the drug. The unusual mode of transmission prompted us to analyse possible atypical clinical features as well as the spread of the virus to the general population, nowadays practically without protective immunity. Serologically verified cases that occurred in Helsinki were interviewed, their hospital records were analysed and their contacts were serology tested. Amphetamine lots, as well as faecal samples from patients, were examined with RT-PCR. Detailed information was obtained from 238 subjects, among whom 131 admitted drug abuse and 67 cases were classified as secondary cases. Phylogenetic analysis of virus strains from HAV-infected cases suggested a common origin, and epidemiological observations linked it with particular lots of amphetamine. Three cases died, and 3 presented with severe clinical disease. Icterus was more common among i.v. drug abusers than others. Infection with hepatitis A virus was probably related to the faecal contamination of amphetamine associated with the transportation of the drugs in the gastrointestinal tract.

IgM rheumatoid factor (RF), an autoantibody to the Fc fragment of IgG, was determined by solid-phase enzyme immunoassay (EIA). RF levels were significantly higher in patients with rubella virus infection than in patients with infections due to influenza virus, cytomegalovirus, respiratory syncytial virus, parainfluenza virus, adenovirus, mumps virus, or herpes simplex virus. To evaluate the role of RF in EIA determinations of viral antibodies, IgM RF from IgM-IgG cryoglobulin or control IgM was added to patient sera before assay for viral antibodies. IgM RF inhibited virus-specific IgG and IgA reactions and gave nonspecific IgM reactions in EIA for antibodies to rubella and influenza viruses, but had little or no effect on antibodies to cytomegalovirus. The minimal effective amounts of RF were 100-500 ng/ml for inhibition of IgG, 300-1,000 ng/ml for IgA, and 25-500 ng/ml for IgM. The control IgM preparation gave no such effects. These studies reinforce the need to eliminate RF interference in solid-phase EIA.

A quantitative PCR test, the Cobas Amplicor CMV Monitor, was used for the monitoring of viral load in the peripheral blood of 27 individual liver transplant patients and correlated with cytomegalovirus (CMV) pp65 antigenemia. Altogether, 243 specimens were analyzed. During the first 3 months, 20 patients showed PCR positivity which correlated with pp65 antigenemia. Of those, 13 patients developed symptomatic CMV infection 27 to 52 days after transplantation, with a significantly higher peak viral load in PCR and in pp65 assay compared with the seven asymptomatic infections (median 10,200 versus 2,240 copies/ml, P < 0.05, and median 100 versus 30 pp65-positive cells/50,000 leukocytes, P < 0.01). Five were primary infections of D؉/R؊ cases (donor CMV seropositive and recipient seronegative) and demonstrated, except in one case, a high peak viral load (>10,000 copies/ml; range, 10,200 to 21,600 copies, and >50 positive cells, range, 50 to 800 cells). The peak viral loads of the six D؉/R؉ patients with symptomatic infection varied widely (range, 2,290 to 126,000 copies and 50 to 300 positive cells). Two D؊/R؉ patients developed symptomatic infection with a lower viral load (range, 1,120 to 6,510 copies and 25 to 100 positive cells). All symptomatic infections were successfully treated with ganciclovir. The asymptomatic infections all in D؉/R؉ patients with low copy numbers (<5,500 copies) were monitored until CMV disappeared. One of the seven PCR-negative patients had one sample with low antigenemia, but the subsequent specimens were all negative. The time-related correlation of the two methods was also good. In summary, quantitative PCR could equally well be used as the CMV pp65 assay for the monitoring of viral load in individual transplant patients.Cytomegalovirus (CMV) infection is a common complication after liver transplantation. A variety of clinical manifestations of CMV, such as fever, leukopenia, thrombocytopenia, colitis, pneumonia, and hepatitis, have been described (16). Immunosuppressed organ transplant patients are usually frequently monitored for CMV and treated with antiviral agents. The antiviral treatment is based on the clinical symptoms and/or rapid laboratory diagnosis. Also, preemptive therapy, which is commonly used to prevent the development of CMV disease after transplantation, is based on monitoring the viral load of the patients (5,6,15,20).For more than 10 years, the CMV-pp65 antigenemia assay has been the most commonly used method for monitoring the appearance of CMV infection in transplant patients (2,8,22,25). The antigenemia test is quantitative and can also be used to assess viral load and to monitor the response to antiviral treatment. Although there have been attempts to standardize the assay (8, 23), the great variety of in-house and commercial modifications of the method make it difficult to compare the results and run clinical trials based on this technique. Quantitative PCR techniques, which are easy to standardize, are less laborious for laboratory personnel, and can be autom...