Detección de anticuerpos contra el virus de la hepatitis C en donantes de sangre voluntarios Translated title: Detection of antibodies against hepatitis C virus in volunteer blood donors

Nucleic acid testing (NAT) for human immunodeficiency virus (HIV) and hepatitis C virus (HCV) was introduced for blood donation screening in the United States in 1999. This study analyzes temporal trends of these two infections since NAT introduction. Donation data from 1999 to 2008 were analyzed; each donation was tested for antibodies and viral RNA for HIV and HCV. Incidence for first-time (FT) donors was derived by multiplying that among repeat (RP) donors by the ratio of NAT yield rates between FT and RP donors. Incidence for all donors was the weighted mean based on percentage of FT and RP donors. Residual risk (RR) was determined using the window-period model. During the 10-year period approximately 66 million donations were screened with 32 HIV (1:2 million) and 244 HCV (1:270,000) NAT yield donations identified. HCV prevalence among FT donors decreased by 53% for 2008 compared to 1999. HIV and HCV incidence among RP donors increased in 2007 through 2008 compared to 2005 through 2006. During 2007 through 2008, HIV incidence was 3.1 per 10(5) person-years (py), with an RR estimate of 0.68 per 10(6) (1:1,467,000) donations; HCV incidence was 5.1 per 10(5) py, with an RR estimate of 0.87 per 10(6) (1:1,149,000). The increase in HIV incidence was primarily among 16- to 19-year-old, male African American donors and that in HCV was primarily among Caucasian donors of 50 or more years. Donors from the Southern United States had higher incidence rates. HCV prevalence decreased significantly since NAT introduction. The increase in HIV and HCV incidence in 2007 through 2008 warrants continued monitoring and investigation.

Chronic delta hepatitis (CDH) represents a severe form of chronic viral hepatitis, induced by the hepatitis delta virus (HDV) in conjunction with the hepatitis B virus (HBV). Delta hepatitis may lead to disease in humans through co-infection. The former leads to acute hepatitis which clinically can range from mild hepatitis to fulminant hepatitis and death. Severe or fulminant hepatitis is more often observed with HBV-HDV co-infection compared to HBV mono-infection. Chronic infection after acute hepatitis B + D co-infection is infrequent and similar to the rate in mono-infected patients. CDH develops in 70-90% of patients with superinfection. CDH runs a more progressive course than chronic hepatitis B and may lead to cirrhosis within 2 years in 10-15% of patients. However, as with any immune-mediated disease, different patterns of progression, ranging from mild to severe progressive disease, are observed. Active replication of both HBV and HDV may be associated with a more progressive disease pattern. Further, different HDV and HBV genotypes may contribute to various disease outcomes. CDH may be frequently associated with hepatocellular carcinoma development although recent studies provided conflicting results. The only established therapy for CDH is treatment with interferons for a duration of at least 1 year. On treatment, 6 month HDV RNA assessment may give clues as to whether to stop treatment at 1 year or continue beyond 1 year. New approaches to treatment of CDH are an urgent need of which the use of prenylation inhibitors appears the most promising. © 2010 Blackwell Publishing Ltd.

Although hepatitis C virus (HCV) transmission through tissue transplantation has been rarely reported, a donor with undetected viremia may infect several recipients. A patient developed acute hepatitis C shortly after tissue transplantation. Ninety-one tissues or organs had been recovered from the donor. To determine whether the donor was the source of infection and the extent of transmission to other organ and tissue recipients. Descriptive epidemiologic study; serum testing for HCV infection. Recipients were located in 16 states and 2 other countries. Donor and graft recipients. Hepatitis C virus infection was defined as the presence of anti-HCV or HCV RNA. The authors determined the genetic relatedness of viral isolates from the donor and recipients by genotype comparison and quasi-species analysis. The donor was anti-HCV-negative but was HCV RNA-positive (genotype 1a). Forty persons received transplants during 22 months. Five persons were HCV-infected before transplantation or had a genotype other than 1a, and 5 persons had no post-transplantation serum specimens available. Of the remaining 30 recipients, HCV infection occurred in 8 recipients: 3 of 3 organ recipients, 1 of 2 saphenous vein recipients, 1 of 3 tendon recipients, and 3 of 3 tendon with bone recipients. These 8 recipients had viral isolates genetically related to those of the donor. No cases occurred in recipients of skin (n = 2), cornea (n = 1), or irradiated bone (n = 16). Post-transplantation serum specimens were unavailable for 5 recipients. An anti-HCV-negative donor was the source of HCV infection for 8 recipients of organs or tissues. Although HCV transmission from anti-HCV-negative donors is probably uncommon, changes in donor screening to include routine testing for HCV RNA merit further consideration to improve the safety of transplantation.