Transfusional risk of HHV-8 infection

Abstract

David J Blackbourn and colleagues,1Blackbourn DJ Ambroziak J Lennette E Adams M Ramachandran B Levy JA Infectious human herpesvirus 8 in a healthy North American blood donor.Lancet. 1997; 349: 609-611Summary Full Text Full Text PDF PubMed Scopus (152) Google Scholar reporting the presence of human herpesvirus eight (HHV-8) sequences in a blood donor, suggested that the virus could be transmitted by blood transfusions. Indeed, HHV-8, which is present in a high percentage of cases of Kaposi sarcoma, has been found in the peripheral blood mononuclear cells (PBMCs) of healthy individuals, and the fact that some individuals may carry this agent without symptoms2Moore PS Chang Y Detection of herpesvirus-like DNA sequence in Kaposi's sarcoma in patients with and those without HIV infection.N Engl J Med. 1995; 332: 1181-1185Crossref PubMed Scopus (1081) Google Scholar raises the possibility that HHV-8, like hepatitis virus and HIV, could be transmitted by blood transfusion. HHV-8 prevalence data in blood donors have been limited by the lack of a specific and validated serological assay, and by the difficulty in undertaking large-scale PCR studies. However, HHV-8, being a transmissible agent, must be present in at least a small proportion of the general population and thus in blood donors. Although it is reassuring that epidemiological studies have shown that the AIDS-associated Kaposi sarcoma is rare in patients who were HIV-infected through transfusion or intravenous drug use, and that Kaposi sarcoma cases fail to emerge in recipients of blood products, the possibility of HHV-8 transmission through transfusion cannot be excluded. For this reason, we looked for the presence of HHV-8 DNA sequences in PBMCs of 19 patients who had received a large number of blood components during their life: ten had homozygous thalassaemia and nine had sickle-cell disease. They had received a mean total of 326·2 white-blood-cell-reduced packed red cells per patient (total 6525, range 50–700), and 12 were male. Mean age was 21 years (range 4·56). No patient was infected with HIV; four were positive for antibody to hepatitis C virus; eight had a positive marker of GBV-C/hepatitis G virus infection (viral RNA or anti-E2 antibody). The lymphocyte samples studied were coded for blind analysis and tested in duplicate by PCR according to a previously described procedure,3Lefrère JJ Mehohas MC Mariotti M Meynard JL Thauvin M Frottier J Detection of human herpesvirus 8 DNA sequences before the appearance of Kaposi's sarcoma in human immunodeficiency virus (HIV)-positive subjects with a known date of HIV seroconversion.J Infect Dis. 1996; 174: 283-287Crossref PubMed Scopus (51) Google Scholar with a specific primer pair (KS1 and KS2) amplifying a sequence of 233 base pairs designated KS330233, that specifically hybridised to the internal probe KSS.4Chang Y Cesarman F Pessin MS et al.Identification of new human herpes virus-like DNA sequences in AIDS-associated Kaposi sarcoma.Science. 1994; 266: 1865-1869Crossref PubMed Scopus (4951) Google Scholar Controls included lymphocyte samples from 17 HHV-8 DNA-positive AIDS patients with Kaposi sarcoma and four HHV-8 DNA positive healthy HIV-negative homosexual men (positive controls), and lymphocyte samples of 15 healthy HIV-negative individuals at low risk of HIV infection (negative controls). The 19 multiply-transfused recipients were all negative for HHV-8 DNA by PCR. Positive and negative controls gave results as expected. With respect to transfusional risk of HHV-8 infection, the at-risk recipients are mainly immunodepressed patients, or individuals likely to be immunodepressed later in life, who could, at some point, develop HHV-8-linked Kaposi sarcoma. Most individuals known to have received cellular components from hepatitis viruses or HIV-infected donors became infected. Our failure to detect HHV-8 DNA sequences in our patients suggests that HHV-8 is not transmitted with a high frequency in individuals receiving white-blood-cell-reduced components. Our patients, having received only such products over their whole life, could not reflect the transfusional risk of HHV-8 infection through non-white-blood-cell-reduced products. One can only suppose that if HHV-8 is highly cell-associated, it could lose its efficacy for transfusional transmission after filtration done for white-blood-cell reduction. Before having more data on HHV-8 prevalence in blood donors and on the parenteral risk of HHV-8 transmission, white-blood-cell reduction seems a prudent preventive measure. Recently, the French Ministry of Health decided that all transfused individuals would henceforth receive only such cellular products.