Histologic, viral, and molecular correlates of dengue fever infection of the liver using highly sensitive immunohistochemistry.
Diagn Mol Pathol
; 15(4): 223-8, 2006 Dec.
Article
em En
| MEDLINE
| ID: mdl-17122650
The mechanism by which the virus associated with dengue fever can cause a fatal hepatitis is not well understood. The purpose of this study was to examine 9 cases of fatal dengue hemorrhagic fever-associated hepatitis, and to correlate the histologic findings with viral detection and cytokine response. The histologic changes were nonspecific and included massive hepatic necrosis and a pauci-cellular acute hepatitis. Viral cDNA detection by reverse transcriptase in situ polymerase chain reaction demonstrated that the fatal hepatitis was due to infection on average of >90% of hepatocytes and many Kupffer cells. Similar results were obtained using immunohistochemistry for viral protein using an automated highly sensitive system. Immunohistochemical analysis for tumor necrosis factor alpha, and interleukin-2, showed rare positive Kupffer cells. In comparison, fatal cases of hepatitis C associated liver failure demonstrated far fewer infected hepatocytes and a concomitant strong up-regulation of many cytokines, notably tumor necrosis factor alpha and interleukin-2. It is concluded that fatal dengue hemorrhagic fever is associated with acute, severe liver damage due primarily to massive direct infection of hepatocytes and Kupffer cells with minimal cytokine response. The infection can be readily detected in a few hours using an automated system that has a sensitivity equivalent to reverse transcriptase in situ polymerase chain reaction.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Imuno-Histoquímica
/
Dengue Grave
/
Vírus da Dengue
/
Hepatite Viral Humana
/
Fígado
Tipo de estudo:
Diagnostic_studies
/
Etiology_studies
Limite:
Humans
Idioma:
En
Revista:
Diagn Mol Pathol
Assunto da revista:
BIOLOGIA MOLECULAR
/
PATOLOGIA
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Brasil
País de publicação:
Estados Unidos