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SEN virus (SEN-V) is a blood-borne, single-stranded, nonenveloped DNA virus. Although its prevalence varies by geographic region, it has been detected in as many as 30 percent of postoperative transfusion recipients, compared to 3 percent of postoperative patients who did not receive transfusions. A significant association has been observed between transfusion volume and the occurrence of SEN-V infection. Transmission by transfusion also has been confirmed by the detection of greater than 99 percent homology between SEN-V in donor and recipient sera. Concurrent infections with SEN-V and hepatitis B virus, hepatitis C virus, or human immunodeficiency virus type 1 have been documented, and these observations probably reflect the blood-borne transmission of these viruses as well as SEN-V. Although SEN-V was discovered as part of a search for causes of posttransfusion hepatitis, there is no firm evidence so far that SEN-V infection either causes hepatitis or worsens the course of coexistent liver disease. Nevertheless, SEN-V appears to be transmitted by transfusion, and further studies may reveal more about its role in the future.

During the past 50 years, most US-licensed plasma derivatives have maintained an impressive record of not transmitting HBV, HCV, or HIV Albumin (50-year history) has never transmitted these viruses. PPF (40-year history) transmitted HBV on only one occasion, which was associated with a design flaw in one manufacturing plant. IGIM has never transmitted any of these viruses since the requirement of sensitive serologic screening tests for HBV (24 years). IGIV (17-year history) transmitted HCV in only one outbreak involving the product of one manufacturer. Even AHF and FIX have not transmitted these viruses since effective virus-inactivation processes in manufacturing were developed. In summary, there has been no transmission of HBV, HCV, or HIV by US-licensed plasma derivatives since the introduction of effective virus-inactivation procedures. This means, essentially, that there has been no transmission of these viruses since the end of 1987; the sole exception is IGIV, by which there has been no transmission since 1994.

BACKGROUND: A study was designed to estimate relative analytic sensitivity and window-period (WP) closure and to project incremental yield of newer HBsAg tests, pooled-sample NAT, and single-sample NAT, compared to currently licensed HBsAg tests. STUDY DESIGN AND METHODS: HBV DNA and HBsAg test results for 23 HBV seroconversion (SC) panels were first analyzed to construct a model of primary HBV viremia. One-hundred representative samples were then selected from 10 panels and coded with 28 analytical controls. All 128 samples were tested by seven HBsAg tests and by four pooled-sample and three single-sample NAT assay formats. Results were analyzed to obtain differential times to HBV detection and combined with HBV incidence rates to project comparative yields. RESULTS: HBV doubling time during the ramp-up phase was estimated at 2.56 days. HBsAg concentrations at cutoff for new tests ranged from 0.07 to 0.12 ng per mL, compared with 0.13 to 0.62 ng per mL for licensed tests. Estimated viral load at cutoff ranged from 102 to 267 IU per mL for new tests and from 363 to 1069 IU per mL for licensed tests. HBsAg tests detected 31 to 63 percent of early ramp-up phase samples in the 100-member seroconversion panel study, while pooled-sample NAT detected 55 to 71 percent and single-sample NAT, 82 to 99 percent. Compared with currently licensed HBsAg assays, newer HBsAg assays would reduce the WP by 2 to 9 days; pooled-sample NAT would reduce the WP by 9 to 11 days; and single-sample NAT would reduce the WP by 25 to 36 days. CONCLUSION: Newer HBsAg tests would be expected to detect an additional 15 to 21 infected units per 107 donations, compared to licensed HBsAg tests. Sensitivity, WP closure, and yield projections for newer HBsAg assays and pooled-sample NAT are comparable. Single-sample NAT would increase yield by 13 to 15 units per 107 donations over pooled-sample NAT and newer HBsAg assays and by 35 to 50 units per 107 donations over currently licensed HBsAg assays.

BACKGROUND: It was reported recently that sequences corresponding to the human T-lymphotropic virus type I (HTLV-I) tax gene were detected in peripheral blood mononuclear cells from 8 to 11 percent of healthy blood donors without detectable antibodies to HTLV-I. A multicenter blind study was conducted to determine if these results could be independently confirmed. STUDY DESIGN AND METHODS: Specimens were collected from 100 anti-HTLV-I-negative healthy blood donors and from 11 anti-HTLV-I- or anti-HTLV-II-positive individuals. All samples were coded and distributed to each of four independent testing laboratories for polymerase chain reaction analysis to detect sequences of the HTLV-I or HTLV-II tax gene, using detailed procedures specified by the laboratory reporting the original observation. Each laboratory also tested a dilution panel of a plasmid containing HTLV-I tax to determine the analytical sensitivity of the procedure. RESULTS: The analytical sensitivity of the screening methods permitted detection of as few as 1 to 10 copies of the tax gene. However, HTLV-I tax sequences could not be detected in any of the anti-HTLV-I-negative blood donors at more than one test site. CONCLUSION: HTLV-I tax sequences appear not to be present in this population of 100 blood donors negative for anti-HTLV-I.

The use of autologous blood for transfusion in increasing rapidly. However, the issue of donor safety is more complicated when the blood donor is a pregnant woman. Autologous blood is now often collected during pregnancy from mothers whose medical histories include a risk factor that may lead to a need for a transfusion at delivery. The effect of maternal blood donation on the developing fetus has not been well studied. Systematic studies of maternal blood donation in many more pregnant patients are needed

Sera and questionnaires were evaluated retrospectively from 128 volunteer blood donors whose blood had been implicated in cases of clinically recognized post-transfusion hepatitis in recipients of one- or two-unit blood transfusion between 1971 and 1977. Serologic markers of hepatitis B virus (HBV) infection were found in 23 percent, compared to 9.7 percent of 3,230 prospective blood donors. The prevalence of antibody to hepatitis A virus was similar among implicated donors (44%), prospective donors (58%), and among those implicated donors with (41%) and without (44%) HBV markers. Among implicated donors, none had a history at the time of donation of having had clinically recognizable hepatitis, 93 percent had no history of prior blood transfusion, and 80 percent had normal hepatic enzymes. Data from this study confirm that non-A, non-B hepatitis has been a common form of posttransfusion hepatitis in recent years, since 77 percent of these implicated donors had no HBV serologic markers. In addition, these donors could not be distinguished by age, race, sex, history of clinical hepatitis or of prior blood transfusion, or in most cases by hepatic enzyme levels.

Sera from 200 volunteer blood donors and 200 paid blood donors, all positive for hepatitis B surface antigen (HBsAg), were tested for the presence of hepatitis B e antigen (HBeAg). HBeAg was detected in 31 HBsAg-positive paid donors (15%), and in 11 HBsAg-positive volunteer donors (5%) by agar gel diffusion. The presence of HBeAg was associated with higher titers of HBsAg. No significant difference was found in the prevalence of antibody to HBeAg (anti-HBe) in the two donor groups. Rheumatoid factor was not associated with the presence or absence of HBeAg or anti-HBe, indicating that HBeAg is probably not an anti-IgG. These data support the epidemiological evidence that paid blood donors appear to be more likely than volunteer donors to transmit hepatitis B virus infection to recipients of their blood.

Evidence supporting the existence of two agents of human non-A, non-B hepatitis was obtained by the inoculation of chimpanzees sequentially with serum from a chronically infected human (Inoculum I) and with fibrinogen prepared from pooled plasma (Inoculum IV), each of which had transmitted non-A, non-B hepatitis to humans. Passage inoculations of serum samples obtained during the acute stages of chimpanzee infections transmitted by either the agent in Inoculum I or IV also transmitted non-A, non-B hepatitis to additional chimpanzees. Transmission and passage of the agent in Inoculum IV were conducted in chimpanzees which previously had recovered from infection by the agent in Inoculum I. Cytoplasmic tubules in hepatocytes, which have been described during non-A, non-B hepatitis, were observed by electron microscopy in liver biopsies obtained during all infections transmitted by the agent in Inoculum I. These cytoplasmic tubules were not detected in liver biopsies from chimpanzees infected by Inoculum IV, except in one chimpanzee inoculated by Inoculum IV without prior exposure to the agent in Inoculum I. The cytoplasmic tubules observed in this study were found to be composed of transverse bands arranged with a periodicity of approximately 17 nm. These studies suggest that two different agents or distinct serotypes of human non-A, non-B hepatitis may have been present in these inocula, although reactivation of latent infection or reinfection could not be ruled out completely.

Sera and questionnaires from 3,230 prospective U.S. volunteer blood donors were obtained in an earlier study to determine the prevalence of serologic markers of hepatitis B virus (HBV) and hepatitis A virus (HAV) among prospective blood donors with or without a history of either hepatitis or blood transfusion. These sera were reevaluated using a radioimmunoassay for antibody to hepatitis B core antigen (anti-HBc). Anti-HBc in the absence of hepatitis B surface antigen (HBsAg) or its antibody (anti-HBs) was detected in 30 of 1,151 (2.6%) prospective donors with a history of hepatitis, compared to four of 1,086 (0.4%) with no history of hepatitis (p less than 0.001). Although end-point dilution titers of anti-HBc greater than or equal to 1:100 and the presence of IgM anti-HBc were more frequently detected among donors with a history of hepatitis than among donors with no history of hepatitis, the difference was not statistically significant. Unlike a history of hepatitis, a history of transfusion or a history of exposure to persons with hepatitis had no significant association with the detection of anti-HBc in the absence of other HBV serologic markers.