hepatitis E in blood transfusions

just bringing up this issue to make sure we are aware of the potential for hepatitis E infection, with recent study highlighting blood product transmission of hep E in the UK (see hep e in UK lancet 2014​ in dropbox, or doi:10.1016/S0140-6736(14)61034-5). background:

    --hepatitis E is an RNA virus similar to hep A (first identified in 1978 as a water-borne, enterically transmitted non-A, non-B viral hepatitis, found to cause an epidemic outbreak in Kashmir). currently second most common cause of sporadic hepatitis in North Africa and Middle East, and with huge outbreak (>100K people) in China in the 1980's. spread largely by fecally-contaminated water. documented transmission in japan, germany, france by eating undercooked pork (and deer, boar) and likely can be perinatally transmitted. 3rd NHANES study (1988-94) in the US found strikingly high hep E seroprevalence at 21%!!, esp in those with pets or who consumed liver or organ meats. in the UK, hep E is the "most common infective cause of acute enterically transmitted viral hepatitis and is detected in people who have not traveled outside the UK". 4 genotypes (genotypes 1 and 2 being human viruses, 3 and 4 animal ones with zoonotic human infections, though genotype 3 is less virulent and may predominate in the US). in the UK, the vast majority (>90%) of acute hep E is from genotype 3, the rest being mostly genotypes 1 and 4.

    ​--clinically similar to hep A (acute, self-limited, rarely fulminant, does not generally become chronic -- though can be chronic in immunosuppressed), can be misclassified as other hepatitis (eg patient assumed to have drug-induced hepatic injury). can be asymptomatic, or look like severe cases of hep A (jaundice, malaise, anorexia, nausea, vomiting, abd pain, fever, hepatomegaly and 60% with cholestasis). incubation period 15-60 days. typical hepatitis lab findings (bili, ALT, AST), usually normalize after 1-6 weeks.

the Lancet study, which only looked at blood product transmission of hep E (a previously documented but relatively uncommon and inefficent mode of transmission for this virus):

    ​--assessed positive hep E RNA in 225K blood donations in southeast England from Oct 2012-Sept 2013.

    --79 donors were viremic, all with genotype 3 hep E, with RNA prevalence of one in 2848 (.04%). 56 (71%) of these were seronegative for IgG or IgM antibodies. this .04% RNA prevalence translates mathematically to 80-100K acute transfusion-associated hep E infections in England during this year of study. similar prevalences of viremia found in germany and sweden

    --these 79 donations were used to prepare 129 blood components and 62 were transfused prior to identification of hep E. 43 of the recipients were followed and 18 (42%) had evidence of infection (esp in group with negative antibody but high viral load). small numbers but it seemed that transfusion of RBCs was less likely to lead to transmission than that of other components.

    --those immunocompromized had prolonged infections, and some cleared the infection with ribivirin (also noted in other studies to be of some help)

    ​--transaminitis was common, morbidity rare, though 1 recipient developed clinical post-transfusion hepatitis.

so, hep E genotype 3 is widespread in southern England, can be spread by transfusion, rarely causes acute morbidity, but can lead to persistent infection in some immunocompromized people. one concern is that esp in immunocompromized patients, there can be persistent infection and possibility of chronic hepatitis. what are the implications of this study and other info above? at a minimum, it raises the issue of consumption of undercooked pork (which has increased, as trichinosis is not perceived to be as much of a threat). seems to me that the risk of transfusion-associated clinical hep E is pretty low (though immunocompromized individuals do disproportionately get transfusions of blood products and are more likely to have bad outcomes), that it makes sense to have accurate tracking of seroprevalence of hep E over time (as well as the genotype) and consider routine screening of blood donors if the seroprevalence/morbidity increases significantly, and that we consider testing for hep E in patients with acute hepatitis of unknown etiology.