Acute adenovirus hepatitis in liver transplant recipients

Cames, B; Rahier, Jacques; Burtomboy, G; Goyet, Jean de Ville de; Reding, Raymond; Lamy, M; Otté, Jean-Bernard; Sokal, Étienne

doi:10.1016/s0022-3476(05)80593-1

Cited by 92 publications

(50 citation statements)

References 11 publications

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“…3G, K, and S) that was histologically similar to human adenovirus hepatitis in immunocompromised patients (6,7,44). MT and Btk Ϫ/Ϫ mice infected with 700 PFU succumbed with hepatic necrosis and mild cellular inflammation ( Fig.…”

Section: Discussionmentioning

confidence: 94%

Fatal Disseminated Mouse Adenovirus Type 1 Infection in Mice Lacking B Cells or Bruton's Tyrosine Kinase

Moore

McKissic

Brown

et al. 2004

J Virol

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Human adenoviruses are associated with self-limiting respiratory, conjunctival, and gastrointestinal disease. In immunocompromised people, human adenovirus infection can result in pneumonia, hepatitis, encephalitis, pancreatitis, gastroenteritis, or disseminated disease involving multiple organs (8, 43). Disseminated human adenovirus infection usually results in death. The incidence of disseminated human adenovirus disease is increasing with the increased number of immunocompromised children, and pediatric bone marrow transplant recipients are most at risk (5,12,13,16).Due to species specificity, human adenovirus pathogenesis is poorly understood. Study of mouse adenovirus type 1 (MAV-1) permits the analysis of a replicating adenovirus in vivo. The outcome of infection depends on the virus dose and mouse strain (15,26,33,40). In outbred and C57BL/6 (B6) mouse strains, MAV-1 infects cells of the monocyte-macrophage lineage and endothelial cells (10,20,33). The highest levels of virus are found in the spleen and brain (20,26,39). MAV-1-specific cytotoxic T cells peak at 10 days postinfection (d.p.i.) and then decline (18). T cells cause acute immunopathology and are required for survival 9 to 16 weeks postinfection in MAV-1-induced encephalomyelitis (33). Inbred mouse strains susceptible and resistant to MAV-1 are available, and sublethal irradiation of resistant mice renders them susceptible (40). Mice with a severe combined immunodeficiency (SCID) mutation are susceptible to MAV-1 (10, 35).Here we report findings that survival of acute MAV-1 infection is B-cell dependent and T-cell independent. We postulated that Bruton's tyrosine kinase (Btk) plays a role in protection from MAV-1. Loss of Btk in mice results in the X-linked immunodeficiency (Xid) phenotype (22). Btk Ϫ/Ϫ mice have reductions in serum immunoglobulin (natural antibody), conventional B cells, and peritoneal B-1 cells relative to control mice (22). Here we demonstrate that Btk is required for survival of MAV-1 infection. We present data indicating that early T-cell-independent antiviral immunoglobulin M (IgM) plays a pivotal role in protection against disseminated MAV-1 infection. MATERIALS AND METHODSVirus and mice. Wild-type MAV-1 was propagated and titrated in 3T6 cells (9). The mice used are indicated in Table 1 (11,14,23,24,(29)(30)(31). A ␤ bϪ/Ϫ and Jh mice were purchased from Taconic. C57BL/6NCr (B6) and BALB/CAnNCr mice were purchased from the National Cancer Institute. All other mice were purchased from Jackson Laboratory. The 50% lethal dose (LD 50 ) was determined as described previously (37). Sera were heat inactivated at 57°C for 45 min before passive transfer.Quantitation of virus. Organ homogenates were prepared as described previously (40) or in phosphate-buffered saline (PBS) with 1-mm glass beads (BioSpec Products, Bartlesville, Okla.) in 2 ml/well 96-well plates (Axygen, Union City, Calif.) with a Mini Beadbeater (BioSpec) and the manufacturer's protocol. Virus was titrated by plaque assay as described previously (9). The means of...

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Section: Discussionmentioning

confidence: 94%

Fatal Disseminated Mouse Adenovirus Type 1 Infection in Mice Lacking B Cells or Bruton's Tyrosine Kinase

Moore

McKissic

Brown

et al. 2004

J Virol

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“…Risk factors for severe disease included identification of virus at multiple sites and prolonged excretion. Adenovirus-induced hepatitis in liver transplant patients is associated with significant mortality (ϳ40%) and can result in massive hepatic necrosis (18). Various therapies have been tried in the past, including reductions in immunosuppression and ganciclovir.…”

Section: Adenovirusesmentioning

confidence: 99%

Nosocomial Spread of Viral Disease

2001

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Viruses are important causes of nosocomial infection, but the fact that hospital outbreaks often result from introduction(s) from community-based epidemics, together with the need to initiate specific laboratory testing, means that there are usually insufficient data to allow the monitoring of trends in incidences. The most important defenses against nosocomial transmission of viruses are detailed and continuing education of staff and strict adherence to infection control policies. Protocols must be available to assist in the management of patients with suspected or confirmed viral infection in the health care setting. In this review, we present details on general measures to prevent the spread of viral infection in hospitals and other health care environments. These include principles of accommodation of infected patients and approaches to good hygiene and patient management. They provide detail on individual viral diseases accompanied in each case with specific information on control of the infection and, where appropriate, details of preventive and therapeutic measures. The important areas of nosocomial infection due to blood-borne viruses have been extensively reviewed previously and are summarized here briefly, with citation of selected review articles. Human prion diseases, which present management problems very different from those of viral infection, are not included

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“…Species C adenoviruses also cause significant morbidity and mortality among immunosuppressed individuals, including recipients of bone marrow (4,16,59), liver (7,41), kidney (45), heart (53), and lung (6,46) transplants, as well as in children with immunodeficiency diseases (24). Among transplant recipients, the incidence of adenoviral disease is much higher in children than in adults (16,26).…”

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confidence: 99%