Infections with Cytomegalovirus and Other Herpesviruses in 121 Liver Transplant Recipients: Transmission by Donated Organ and the Effect of OKT3 Antibodies

Abstract

One hundred twenty-one adult liver transplant recipients were studied for the incidence, risk factors, and morbidity associated with herpesviruses infections after transplantation. The overall incidence of infection was 59% for cytomegalovirus (CMV), 35% for herpes simplex virus (HSV), 25% for Epstein-Barr virus (EBV), and 7% for varicella-zoster virus (VZV). Primary CMV infection occurred in 46% and reactivation CMV infection in 67% of the susceptible recipients. Symptomatic and disseminated CMV diseases were more common when patients developed primary infection (P less than .01, for both comparisons). The donor organ appeared to be the only important source of CMV infection in seronegative recipients. The use of OKT3 antibodies was associated with disseminated CMV disease in patients with primary infection (P = .04) but not with reactivation infection (P greater than .10). Although most HSV infections were oral or genital reactivations, three cases of HSV hepatitis occurred--one was a primary infection. Symptomatic reactivations of HSV were observed in 53% of HSV-seropositive recipients who received OKT3, versus 31% of seropositive recipients who did not receive OKT3 (P = .05).

Reciprocal Enhancement of Gene Expression and Viral Replication Between Human Cytomegalovirus and Human immunodeficiency Virus Type 1

“…E155 cells constantly produce HCMV proteins in 5 to 80~ of cells (higher expression if the cells are split more than once in 7 to 10 days) and a low level of infectious virus. The site of HCMV latency in vivo is not clear, but peripheral mononuclear cells (Rice et al, 1984), kidney mesangial cells (Heieren et al, 1988) and liver cells (Singh et al, 1988) have all been implicated. Infection of E155 cells with HIV-1 might mimic the situation in vivo; some cells harbour the HCMV genome in inactive or replicating form and superinfection of these cells with HIV-1 leads to more productive replication of both viruses.…”

Infectious complications after OKT3 induction in liver transplantation

“…Although extraordinarily effective in reversing established rejections, the use of OKT3 in these circumstances has been accompanied by an increase in the prevalence of infections, especially those of viral etiology. 1 In contrast, small, randomized comparative studies of OKT3 as induction immunotherapy vs. cyclosporine therapy have not documented an increase in infections with the use of OKT3 in this setting but have shown immunologic advantages such as a 20%-40% decrease in the incidence of acute rejection. [2][3][4][5] A detailed examination of infections in liver transplant recipients receiving OKT3 induction has not been published.…”

Late hepatic allograft dysfunction

“…In addition to hepatitis, CMV also causes fever, leukopenia, thrombocytopenia, atypical lymphocytosis, pneumonitis, and retinitis. [80][81][82] Of note, serologic testing has little value in the diagnosis of CMV disease and the diagnosis is made using the shell-vial technique or by polymerase chain reaction (PCR) studies. 80 Histologically, typical nuclear inclusion bodies or microabscesses are noted on liver biopsy.…”