The study of hepatitis C virus (HCV) kinetics after liver transplantation (LT) might be important to design strategies to prevent HCV infection of the graft. We analyzed HCV kinetics during and immediately after LT in 20 consecutive patients undergoing LT for HCV-related cirrhosis. HCV RNA was quantified in blood samples obtained at regular intervals before, during, and after transplantation. HCV-RNA concentrations decreased in 18 of 20 patients during the anhepatic phase (mean decay slope ؊0.92, mean HCV elimination half-life 2.2 hours). We found a significant correlation between the HCV viral load decay and the blood loss during the anhepatic phase, indicating that the observed HCV clearance rates are maximum estimates. In fact, in 1 patient with an unusually long anhepatic phase of 20 hours and with minimum blood loss, the HCV elimination half-life was 10.3 hours. Eight to 24 hours after graft reperfusion a sharp decrease in HCV viral load occurred in 19 patients (mean decay slope ؊0.34, mean HCV elimination half-life 3.44 hours). HCV RNA became undetectable in only 1 patient. During the following days, HCV-RNA concentrations increased rapidly in 10 patients (mean HCV doubling time 13.8 hours), remained at similar levels in 4, and continued to decrease in 6. The only variable associated with a second-phase viral load decay was the absence of corticosteroids as part of the immunosuppressive regimen. In conclusion, a sharp decrease in HCV viral load occurs during the anhepatic phase and immediately after graft reperfusion, most likely owing to a lack of virion production and hepatic viral clearance. HCV infection of the graft, however, is an extremely dynamic process and viral replication begins a few hours after LT. (HEPATOLOGY 2002;35: 680-687.) C irrhosis caused by hepatitis C virus (HCV) infection is the main indication of liver transplantation (LT) in most transplant programs. Infection of the liver graft after transplantation is almost universal and persistent infection leading to chronic hepatitis, cirrhosis, and graft failure is common. 1,2 In our geographic area, 30% of patients undergoing LT for HCV-related liver disease are already cirrhotic 5 years after transplantation. 3 Regretfully, prophylaxis of HCV infection of the graft is not feasible because no specific anti-HCV immune globulin is available. In addition, antiviral treatment in patients on waiting lists for LT appears to be poorly effective and may cause severe adverse effects. 4,5 Currently, treatment of hepatitis C infection after LT seems the most feasible strategy to eradicate HCV. 6-8 Treatment of HCV infection after LT can be initiated before liver damage occurs or once liver disease is already established. Treatment in the early phase of LT seems a reasonable approach because eradication of HCV would prevent liver damage. 9-11 However, there are only a few studies analyzing the efficacy of antiviral therapy in the early posttransplantation period. Interferon monotherapy is not effective in achieving sustained virologic response in ...

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It is widely agreed that hepatitis B virus immunoglobulinSeveral reports have clearly shown that liver transplantation in patients with hepatitis B virus (HBV) infection-as defined by positivity for hepatitis B surface antigen (HBsAg)-is associated with a high rate of recurrence of HBV infection after transplantation, resulting in severe graft disease in most cases and in a significant decrease in both graft and patient survival. [1][2][3][4] It is widely accepted that the risk of HBV recurrence after liver transplantation is directly proportional to the level of viral replication before transplantation, with those recipients seropositive for HBeAg and HBV DNA by hybridization technique having the highest rate of recurrence after transplantation, irrespective of the type of liver disease. 2,4 Many prophylactic strategies have been proposed to prevent HBV infection of the graft, but only long-term passive immunoprophylaxis with HBV-specific immunoglobulin (HBIG) has obtained a significant reduction in the risk of HBV graft infection and in both graft and patient mortality after liver transplantation. [4][5][6][7] The presence of serum HBV DNA before transplantation is, however, a major predictor of lack of response to this prophylactic regimen.In light of these evidences, the European Concerted Action on Viral Hepatitis (EUROHEP) recommended in 1994 to refrain from transplanting chronic HBV carriers found to be positive for either hepatitis B e antigen (HBeAg) or HBV DNA by direct hybridization. Moreover, the rest of the recipients with HBV-related disease should receive HBIG immunoprophylaxis to maintain anti-HBs levels above 100 IU/L for at least 12 months after transplantation. 6 Currently, the beneficial effect of long-term HBIG administration has become widely accepted; still no consensus has been reached regarding the optimal duration of HBIG treatment. The rate of HBV graft infection recurrence 12 months after liver transplantation seems to be much decreased but it can still undoubtedly occur. 4,6,[8][9][10] Moreover the finding of HBV DNA in peripheral mononuclear blood beyond 12 months of effective HBIG prophylaxis argues in favor of a potentially indefinite risk of graft infection. 11-13 As a consequence, most liver transplant centers are currently administering HBIG on a life-long basis. Because HBIG use is highly expensive, an alternative strategy aiming at the discontinuation of HBIG prophylaxis during the second year of treatment would be an important cost-effective measure. We present here an assessment of the efficacy of a new prophylactic strategy consisting of the discontinuation of HBIG administration followed by active immunization with HBV vaccination in patients transplanted for HBVrelated liver diseases. PATIENTS AND METHODSPatients. Between July 1990 and April 1996, 36 HBsAg-positive recipients were submitted to liver transplantation at the Hospital Abbreviations: HBV, hepatitis B virus; HBsAg, hepatitis B virus surface antigen; HBIG, hepatitis B virus immunoglobulin; HBeAg, hepatitis B vi...

A prospective study of parvovirus B19 infection during pregnancy was conducted at a large teaching hospital in Barcelona, Spain. Women (1610) who were < 28 weeks pregnant at enrollment were screened for parvovirus infection. The prevalence of IgG positivity was 35.03% (564/1610). The incidence of acute infection during pregnancy was 3.7% (60/1610). There were five abortions among the B19-infected women but only one was caused by parvovirus, as assessed by histologic examination and polymerase chain reaction assay. The incidence of fetal loss caused by parvovirus was, therefore, 1.66% (1/60). The remaining 55 pregnancies were uneventful, and at 1 year of age, none of the infants had serious abnormalities. The incidence of vertical transmission of infection was estimated at 25%. This study provides evidence that although acute parvovirus infection may occur relatively commonly during pregnancy, an adverse fetal outcome is a rare complication.

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Hepatitis B and C markers were tested in 980 pregnant women, in the infants born to infected mothers, and in a random sample of 42 and 50, respectively, children born to uninfected mothers in Tanzania. Sixty-two women (6.3%) were positive for HBsAg and 15 (24%) were HBeAg-seropositive. Anti-HCV was detected in 49 women (5%), 15 (31%) of whom had detectable viremia. HCV RNA serum levels were low and only genotype 4 was identified. Sixty-six women (6.7%) were positive for anti-HIV, six of whom were coinfected with HBV and one with HCV. Anti-HEV was negative in the 180 women tested. At 8 months of age, HBsAg was detected in 8% and 2% of children born to HBV-infected and noninfected mothers, respectively (P = 0.2). Corresponding figures at 18 months of age were 31% and 21% (P = 0.3). When tested at 2 months of age, HCV RNA was not detected in any of the 43 children born to anti-HCV-positive mothers nor in any of 50 children born to anti-HCV-negative mothers. At 18 months, only one child, born to an anti-HCV-positive mother, had detectable HCV RNA. None of the infants born to women with HIV coinfection were infected with hepatitis viruses. This study suggests that exposure to HEV does not occur in southern Tanzania. The prevalence of current HBV infection in pregnant women from rural Tanzania is lower than in other sub-Saharan areas. In early childhood, HBV infection appears to occur by horizontal rather than maternofilial mechanisms of transmission. The prevalence of HCV infection is similar to that in other African countries. The results of this study show for the first time in Africa that mother-to-infant transmission does not play a significant role in the acquisition of HCV infection.

A significant proportion of patients infected with SARS‐CoV‐2 develop severe respiratory symptoms due to an excessive immune response. Treatment of this condition may include immunosuppressive therapies, such as IL‐6 receptor antagonists and corticosteroids, which poses a risk for patients with active or past hepatitis B virus (HBV) infection. In this prospective cohort study we analyzed the risk of HBV reactivation in patients with severe COVID‐19 and resolved HBV infection undergoing immunosuppressive therapy. From March 15 th to April 30 th 2020, 600 patients with severe COVID‐19 were admitted into our Hospital and treated with immune‐modulators. Data regarding HBV infection was available in 484, of whom 69 (14%) were HBsAg negative/anti‐HBc positive. For these patients, HBV reactivation prophylaxis with entecavir was strongly recommended. Complete follow‐up was available in 61 patients: 72% were male, median age was 67 years, and anti‐HBs was >10 IU/mL in 72%. The immunosuppressive drug most used was tocilizumab (72%). Despite HBV prophylaxis recommendation, 38 (62%) patients received entecavir and 23 (38%) did not. Baseline features of both groups were similar. At follow‐up, we found no cases of HBsAg seroreversion and only 2 (3%) patients (no prophylaxis group) had detectable serum HBV‐DNA (<15 IU/mL). Both were anti‐HBs negative and had normal aminotransferase levels. Our data show that the risk of HBV reactivation in patients with severe COVID‐19 and resolved HBV infection undergoing immunosuppressive treatment is low. However, if a systematic follow‐up after hospital discharge is unfeasible in patients without anti‐HBs, a short course of antiviral prophylaxis may be a safe option.