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Patients on renal replacement therapy are recognized as a group at increased risk of infection with hepatitis C virus (HCV). While the risk has been reduced by the use of erythropoietin for treatment of anaemia and the introduction of HCV screening of blood products and potential renal transplant donors, new cases of HCV are still being documented, with patients on hospital haemodialysis appearing to be particularly at risk. The exact mode of transmission of HCV within dialysis units is unclear, although there is evidence to support nosocomial transmission between patients. Third generation HCV antibody testing was performed on all dialysis patients when a new case of HCV was identified within our unit. Stored monthly serum samples were then examined retrospectively to determine when patients became HCV RNA and HCV antibody positive. Viral typing was carried out to identify the HCV strains responsible for transmission. Four new cases of HCV infection are described within a single dialysis shift. Viral typing identified two distinct strains of HCV as being responsible for these infections, both of which had previously been identified in dialysis patients within the unit known to have HCV infection. This information, taken in conjunction with knowledge of the location of each patient for dialysis, suggests two separate episodes of nosocomial transmission of HCV between haemodialysis patients. While evidence of nosocomial transmission of HCV is accumulating, with modern dialytic procedures evidence of transmission through the dialysis machine or equipment used for dialysis is lacking. This stresses the importance of strict applications of universal precautions as the key to prevention of further transmission of HCV infection. This information is obviously applicable not only to dialysis units but all units that may potentially come in contact with HCV patients.

Citation information in Europe Pubmed Central

The time of spread of human immunodeficiency virus type 1 (HIV-1) from lymphoid to nonlymphoid tissues in the course of infection was investigated by sequence comparisons of variants infecting a range of lymphoid and nonlymphoid tissues from three individuals with AIDS in the pl7gag gene and regions flanking the V1/V2 hypervariable regions. Phylogenetic analysis in both regions revealed several lineages in each individual that contained sequences from both lymphoid and nonlymphoid tissues such as the brain. This observation contrasts strongly with the previously described organ-specific sequences in the V3 region in this study population and other investigations. Although individual pairwise comparisons of relatively short sequences such as p17gag are subject to considerable stochastic error, we found that the diversity of gag sequences in variants from lymphoid tissue was consistently lower than that found among variants amplified from the brain. By estimating mean synonymous pairwise distances in the p17gag region, we were able to make an approximate calculation of the ages of populations in different tissues. Those from lymphoid tissue ranged from 2.65 to 5.6 years in the three study subjects, compared with 4.1 to 6.2 years for variants in the brain. Indeed, variants infecting the brain were no more closely related to each other than they were to variants infecting other tissues in the body. In two of the three individuals, these times of divergence indicate that infection of the brain may have occurred as an early event in the progression to disease, preceding the onset of AIDS by several years. This study is the first in which it was possible to estimate times of diversification in different tissues in vivo and is of importance in understanding the dynamics of the spread of HIV-1 into nonlymphoid tissues and its possible adaptation for replication in different cell types.

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