Hepatitis C virus (HCV) and human pegivirus (HPgV), formerly GBV-C, are the only known human viruses in the Hepacivirus and Pegivirus genera, respectively, of the family Flaviviridae. We present the discovery of a second pegivirus, provisionally designated human pegivirus 2 (HPgV-2), by next-generation sequencing of plasma from an HCV-infected patient with multiple bloodborne exposures who died from sepsis of unknown etiology. HPgV-2 is highly divergent, situated on a deep phylogenetic branch in a clade that includes rodent and bat pegiviruses, with which it shares <32% amino acid identity. Molecular and serological tools were developed and validated for high-throughput screening of plasma samples, and a panel of 3 independent serological markers strongly correlated antibody responses with viral RNA positivity (99.9% negative predictive value). Discovery of 11 additional RNA-positive samples from a total of 2440 screened (0.45%) revealed 93-94% nucleotide identity between HPgV-2 strains. All 12 HPgV-2 RNA-positive cases were identified in individuals also testing positive for HCV RNA (12 of 983; 1.22%), including 2 samples co-infected with HIV, but HPgV-2 RNA was not detected in non-HCV-infected individuals (p<0.0001), including those singly infected by HIV (p = 0.0075) or HBV (p = 0.0077), nor in volunteer blood donors (p = 0.0082). Nine of the 12 (75%) HPgV-2 RNA positive samples were reactive for antibodies to viral serologic markers, whereas only 28 of 2,429 (1.15%) HPgV-2 RNA negative samples were seropositive. Longitudinal sampling in two individuals revealed that active HPgV-2 infection can persist in blood for at least 7 weeks, despite the presence of virus-specific antibodies. One individual harboring both HPgV-2 and HCV RNA was found to be seronegative for both viruses, suggesting a high likelihood of simultaneous acquisition of HCV and HPgV-2 infection from an acute co-transmission event. Taken together, our PLOS Pathogens |

Long-term use of rifaximin is associated with a decrease incidence of AKI and HRS and a decrease risk of requiring RRT in a general population of cirrhotic patients.

Introduction The liver donor risk index (LDRI), originally developed in 2006 by Feng et. al and since modified, is a method of evaluating liver grafts from deceased donors by determining the relative risk of graft failure post transplantation. Methods Online and paper surveys sent to liver transplant physicians asking about their attitudes and practices regarding decision-making in liver transplantation and the role of LDRI. Results 147 of 401 (37%) eligible respondents returned partial or complete surveys. The majority of the respondents were male (116/134 or 87%) and practiced in academic medical centers (128/138 or 93%). Transplant coordinators initially contacted the candidate with an offer in 81% of programs. Eighty-eight of 143 (62%) respondents reported that they were very familiar with LDRI, but the vast majority (114/137 or 83%) rarely or never discuss the concept of LDRI with their patients. A majority of respondents (96/132 or 73%) believe that LDRI does not adequately describe a liver’s relative risk of graft failure and that there are factors that make LDRI potentially misleading (122/138 or 88%). Nevertheless, 60 of 130 (46%) believe that LDRI would increase/improve shared decision making. Discussion The LDRI has not been widely adopted because of concerns that 1) it does not accurately reflect post-transplant survival; 2) it excludes relevant donor and recipient factors, and 3) it is too complicated for candidates to grasp. There is a need to improve it or to develop other decision making tools to help promote shared decision making. There is also great diversity in how liver offers are made to ambulatory candidates, and how transplant programs address a candidate’s refusal. Research is needed to determine evidence-based best practice.

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