Screening of Blood Donations for Zika Virus Infection - Puerto Rico, April 3-June 11, 2016.

Transfusion-transmitted infections have been documented for several arboviruses, including West Nile and dengue viruses (1). Zika virus, a flavivirus transmitted primarily by Aedes aegypti mosquitoes that has been identified as a cause of congenital microcephaly and other serious brain defects (2), became recognized as a potential threat to blood safety after reports from a 2013-2014 outbreak in French Polynesia. Blood safety concerns were based on very high infection incidence in the population at large during epidemics, the high percentage of persons with asymptomatic infection, the high proportion of blood donations with evidence of Zika virus nucleic acid upon retrospective testing, and an estimated 7-10-day period of viremia (3). At least one instance of transfusion transmission of Zika virus has been documented in Brazil after the virus emerged there, likely in 2014 (4). Rapid epidemic spread has followed to other areas of the Americas, including Puerto Rico.

Absence of detectable viremia in plasma and peripheral blood mononuclear cells from smallpox vaccinees: implications for blood safety.

BACKGROUND: Mass smallpox vaccination with live vaccinia virus has been considered as a preventive measure to counter bioterrorism involving smallpox. This has raised concerns about the possibility of vaccinia virus being transmitted from vaccinated blood donors to recipients. The results of this study could be used to define an appropriate deferral period for blood donors (vaccinated against smallpox) to ensure safety of the blood supply. STUDY DESIGN AND METHODS: A procedure was developed to culture vaccinia virus from plasma and peripheral blood mononuclear cells (PBMNCs) of vaccinees enrolled in three smallpox vaccine clinical trials. A total of 665 plasma and PBMNC samples were obtained from 95 vaccinated subjects. RESULTS: Vaccinia viremia was not detected by virus culture from plasma and PBMNC samples of healthy vaccinees 3 to 56 days after vaccination under our assay conditions. Plasma viremia assay had a sensitivity of approximately 66 plaque-forming units per mL with a Vero cell culture assay. CONCLUSION: The results of this study present evidence that in the case of mass vaccination, the risk of transmission of vaccinia virus by blood transfusion would likely be low.

Variation at NOD2/CARD15 in familial and sporadic cases of Crohn's disease in the Ashkenazi Jewish population.

OBJECTIVE: Recent reports indicate that allelic variants in NOD2/CARD15 are associated with Crohn's disease (CD) susceptibility, and that homozygosity or compound heterozygosity at this locus for any of three recently defined sequence variants confers a greatly increased risk of CD. These sequence changes include two missense mutations, R702W and G908R, and a frameshift insertion, 1007insC. The aim of this study was to determine the frequency of these NOD2/CARD15 variants in familial and sporadic CD patients in the Ashkenazi population and to determine their effects on disease susceptibility and age of disease onset (AOO). METHODS: Allele and genotype frequencies of these three variants were determined in 481 CD patients of Jewish descent and 110 Jewish controls; 169 patients had a family history of CD, and 312 were "sporadic" cases. Variants were detected by polymerase chain reaction using allele-specific primers labeled with fluorescent dye. RESULTS: Familial cases had a significantly higher frequency of the G908R variant than sporadic cases (0.127 vs 0.059, p = 0.0003) and correspondingly, a significantly higher proportion of homozygotes and compound heterozygotes (11.8% vs 4.5%, p = 0.0027). Homozygotes and compound heterozygotes had an OR for CD of 14.6 for familial cases and 5.1 for sporadic cases. There was no increased risk of CD for simple heterozygotes. The AOO was significantly lower for CD patients who were homozygotes and compound heterozygotes for NOD2/CARD15 (17.5 vs 22.4 yr, p = 0.04), but only for familial cases. CONCLUSIONS: NOD2/CARD15 contributes more to CD susceptibility in familial cases than in sporadic cases, and to an earlier AOO. There is no increased risk of CD for individuals carrying only a single copy of these NOD2/ CARD15 variants, whereas individuals carrying two copies have a 5-15-fold increased risk. The penetrance of the NOD2/CARD15 mutations was estimated at less than 1%.