Inducible nitric oxide synthase expression in chronic viral hepatitis and its relation with histological severity of disease

Kandemir, Özlem; Polat, Ayşe; Kaya, Ali

doi:10.1046/j.1365-2893.2002.00382.x

Cited by 21 publications

(19 citation statements)

References 24 publications

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“…These high NO levels are similar to those produced as a result of a systemic inflammatory response syndrome that develops when endotoxin is administered (sepsis) (8). However, the lack of increased levels of TNF-␣ in Ebola-S virus-infected patients suggests that the primary source of NO production is another cell type, possibly hepatocytes (15,21,23), and NO levels could reflect the extent of infection and pathology in the liver.…”

Section: Effects Of Ebola-s Virus Infection On Blood Cells the Develmentioning

confidence: 87%

Analysis of Human Peripheral Blood Samples from Fatal and Nonfatal Cases of Ebola (Sudan) Hemorrhagic Fever: Cellular Responses, Virus Load, and Nitric Oxide Levels

Sanchez

Lukwiya²,

Bausch

et al. 2004

J Virol

251

220

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Peripheral blood samples obtained from patients during an outbreak of Ebola virus (Sudan species) disease in Uganda in 2000 were used to phenotype peripheral blood mononuclear cells (PBMC), quantitate gene expression, measure antigenemia, and determine nitric oxide levels. It was determined that as the severity of disease increased in infected patients, there was a corresponding increase in antigenemia and leukopenia. Blood smears revealed thrombocytopenia, a left shift in neutrophils (in some cases degenerating), and atypical lymphocytes. Infected patients who died had reduced numbers of T cells, CD8؉ T cells, and activated (HLA-DR ؉ ) CD8 ؉ T cells, while the opposite was noted for patients who survived the disease. Expression levels of cytokines, Fas antigen, and Fas ligand (TaqMan quantitation) in PBMC from infected patients were not significantly different from those in uninfected patients (treated in the same isolation wards), nor was there a significant increase in expression compared to healthy volunteers (United States). This unresponsive state of PBMC from infected patients despite high levels of circulating antigen and virus replication suggests that some form of immunosuppression had developed. Ebola virus RNA levels (virus load) in PBMC specimens were found to be much higher in infected patients who died than patients who survived the disease. Similarly, blood levels of nitric oxide were much higher in fatal cases (increasing with disease severity), and extremely elevated levels (>150 M) would have negatively affected vascular tone and contributed to virus-induced shock.

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Section: Effects Of Ebola-s Virus Infection On Blood Cells the Develmentioning

confidence: 87%

Analysis of Human Peripheral Blood Samples from Fatal and Nonfatal Cases of Ebola (Sudan) Hemorrhagic Fever: Cellular Responses, Virus Load, and Nitric Oxide Levels

Sanchez

Lukwiya²,

Bausch

et al. 2004

J Virol

251

220

View full text Add to dashboard Cite

show abstract

“…26 Nitric oxide has been implicated in the pathogenesis of chronic hepatitis C, mainly via peroxinitrite; a potential oxidant that is produced by the reduction of superoxide anion with nitric oxide. 27 Recently, cooperation between TNF and SLC11A1 genes was shown to result in raised nitric oxide production following cytokine stimulation. 28 This mechanism could explain the advanced fibrosis found in patients carrying the 3/3 SLC11A1 genotype and the A/G 2238 TNF mutation.…”

Section: Discussionmentioning

confidence: 99%

SLC11A1 promoter gene polymorphisms and fibrosis progression in chronic hepatitis C

Romero‐Gómez

Montes-Cano²,

Otero-Fernández³

et al. 2004

Gut

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“…PAH has also been reported in patients with hepatitis B. HBV has been shown to produce the HBV X protein, which is necessary for virus infection and has also been implicated in the development of hepatocellular carcinoma [98,99]. HBV X protein has also been shown to induce the expression of inducible nitric oxide synthase, TGF-b and VEGF [100,101]. The X protein also stabilizes hypoxia-inducible factor (HIF)-1a and induces the expression of angiopoietin [102].…”

Section: Other Viruses and Diseases Associated With Pahmentioning

confidence: 99%

Viral infection and pulmonary hypertension: is there an association?

Voelkel

Bull

2011

Expert Review of Respiratory Medicine

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Pulmonary arterial hypertension (PAH) may be idiopathic, familial or associated with various disease processes. The vascular lesions common to all are the plexiform lesions. It is well documented that the plexiform lesions are angioproliferative, but what leads to this angioproliferation is not so clear. Here, we consider the association of viruses, including HIV, human herpesvirus-8, hepatitis B and hepatitis C, with angioproliferation and the development of PAH. The pathogenesis of viral infections often involves proangiogenic and prosurvival signals, similar to the signals found in the phenotypically abnormal endothelial cells of PAH. However, viral infections alone are unlikely to lead to PAH because - much like the viral induction of cancers - additional cofactors, including genetic predisposition, are undoubtedly required for the development of disease. In this article, we also discuss how a dysregulated immune system, in conjunction with a viral infection, could cause PAH. Both autoimmune diseases and viruses are associated with defects in the immune regulatory system, primarily in the T-cell system. These T-cell defects may be a common pathway for the formation of plexiform lesions. Regardless of the route by which viruses may lead to PAH, it is important to recognize their role in this rare disease. Studies of viral pathways in angioproliferation - both in vitro and in animal models - may lead to novel therapeutic targets in PAH.

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Inducible nitric oxide synthase expression in chronic viral hepatitis and its relation with histological severity of disease

Cited by 21 publications

References 24 publications

Analysis of Human Peripheral Blood Samples from Fatal and Nonfatal Cases of Ebola (Sudan) Hemorrhagic Fever: Cellular Responses, Virus Load, and Nitric Oxide Levels

Analysis of Human Peripheral Blood Samples from Fatal and Nonfatal Cases of Ebola (Sudan) Hemorrhagic Fever: Cellular Responses, Virus Load, and Nitric Oxide Levels

SLC11A1 promoter gene polymorphisms and fibrosis progression in chronic hepatitis C

Viral infection and pulmonary hypertension: is there an association?

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