2000
DOI: 10.1002/lt.500060220
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Management of cytomegalovirus infection after liver transplantation

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Cited by 19 publications
(12 citation statements)
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“…Human cytomegalovirus (HCMV), a widespread human pathogen (Griffiths and Walter, 2005;Lawson, 2005;Ross and Boppana, 2005), is a prototypic β-herpesvirus, having a long replicative cycle, a restricted host range, and a cytopathic effect resulting in pronounced cell rounding and swelling (Drago et al, 2000;Griffiths and Walter, 2005;Kano and Shiohara, 2000;Sampathkumar and Paya, 2000). Sequence analysis of its ≈ 230-kb genome (Chee et al, 1990a) revealed four open reading frames (ORFs), US27, US28, UL33, and UL78 (Attwood and Findlay, 1994a,b;Chee et al, 1990b), that encode potential homologues of cellular G protein-coupled receptors (GPCRs) (Lomize et al, 1999;Pierce et al, 2002;Pin et al, 2003;Schoneberg et al, 1999;Strange, 1999), a large group of cell surface-exposed signal transducing proteins (Pierce et al, 2002;Pin et al, 2003).…”
Section: Introductionmentioning
confidence: 99%
“…Human cytomegalovirus (HCMV), a widespread human pathogen (Griffiths and Walter, 2005;Lawson, 2005;Ross and Boppana, 2005), is a prototypic β-herpesvirus, having a long replicative cycle, a restricted host range, and a cytopathic effect resulting in pronounced cell rounding and swelling (Drago et al, 2000;Griffiths and Walter, 2005;Kano and Shiohara, 2000;Sampathkumar and Paya, 2000). Sequence analysis of its ≈ 230-kb genome (Chee et al, 1990a) revealed four open reading frames (ORFs), US27, US28, UL33, and UL78 (Attwood and Findlay, 1994a,b;Chee et al, 1990b), that encode potential homologues of cellular G protein-coupled receptors (GPCRs) (Lomize et al, 1999;Pierce et al, 2002;Pin et al, 2003;Schoneberg et al, 1999;Strange, 1999), a large group of cell surface-exposed signal transducing proteins (Pierce et al, 2002;Pin et al, 2003).…”
Section: Introductionmentioning
confidence: 99%
“…Among the complications caused by CMV in transplanted patients increased long-term mortality and worsening graft survival are common [35][36][37]. Clinical disease caused by CMV is expressed by fever, malaise, myalgia, leukopenia (WBC less than 4.0000/mm 3 ), increased transaminases (hepatitis), pulmonary (pneumonitis) and/or gastrointestinal (colitis, gastritis, esophagitis) and fever being the most common manifestation, which can also occur with neurological symptomatology compatible with encephalitis but these are rarer [29,38,39].…”
Section: Clinical Manifestationsmentioning
confidence: 99%
“…During liver transplantation, primary infection tends to be more important as the CMV viremia may be limited to when virus replication is detected in peripheral blood or significant increase of specific antibodies without symptoms or viral syndrome presenting fever equal or greater than 38ºC, malaise, leukopenia, atypical lymphocytosis equal or less than 3-5% and thrombocytopenia [14,37,42,45,46]. Antiviral treatment controls the acute manifestation of the disease in most cases, but may not eradicate the CMV with recurrence reported in 26-31% of solid organ transplant recipients.. [14,36].…”
Section: Secondary Infection Occurs When the Reactivation Of Latent Imentioning
confidence: 99%
See 1 more Smart Citation
“…CMV primary infection results in life-long residence of the virus in the host, and reactivates in immunocompromised individuals frequently. Reactivation of CMV infection and development of related severe diseases and syndromes are common in solid organ recipients may lead to severe complications following transplant, such as acute rejection [5,6] . CMV may lead also to higher rates of bacterial and fungal infections in transplant recipients [7] .…”
Section: Introductionmentioning
confidence: 99%