Indian Journal of Virology
Open Access
  • Year: 2005
  • Volume: 16
  • Issue: 1and2

P.50. Production of TNF and IFNin Acute and Fulminant Hepatitis E virus (HEV) patients

  • Author:
  • Subrat Kumar1, R.K. Ratho1, Y. Chawla2, A. Chakraborti3
  • Total Page Count: 2
  • Page Number: 62 to 63

1Department of Virology, Post Graduate Institute of Medical Education and Research, Chandigarh.

2Hepatology, Post Graduate Institute of Medical Education and Research, Chandigarh.

3Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh.

Abstracts of Research Papers Presented during the National Symposium of Indian Virological Society at Unit of Plant Virology, Division of Plant Pathology, Indian Agricultural Research Institute, New Delhi-110 012, October 14–1.

Abstract

Human Tumor Necrosis Factor Alpha (TNFα), which is produced by activated macrophages, is one of the major proinflammatory and immunomodulatory agent. Human Interferon gamma (IFNγ), which is also a proinflammatory cytokine like TNFα, possesses antiviral activity. Levels of TNFα were found to be elevated in liver disease patients, while IFNγ has been elevated in serum of liver cirrhosis and FHF patients when compared to healthy individuals. Both these cytokines i.e., IFNγ and TNFα play a major role in cell-mediated immunity in viral diseases and are responsible for efficient virus clearance. HEV is responsible for considerable mortality and morbidity in developing world and shows a high mortality rate in pregnant women (∼30 to 40%).

The aim is to determine the Thl cytokine response in terms of IFNγ and TNFα production in the clinical outcome of patients with acute and fulminant HEV infection.

The study group comprised of 8 acute hepatitis (AH) and 2 fulminant hepatitis (FH) patients, who were positive for HEV specific IgM antibodies and had detectable HEV RNA by reverse transcriptase polymerase chain reaction (RT-PCR). 5 apparently healthy volunteers served as controls. ∼ 5ml of acute phase blood samples were collected aseptically at the first visit of the patients and controls. Serum samples were preserved in small aliquots at –70°C till tested. All the serum samples were screened for the presence of Hepatitis A virus specific antibodies (HAV IgM), hepatitis B virus surface antigen (HBsAg), Hepatitis C virus antibodies (HCVAb) and Hepatitis E IgM antibodies (HEV IgM) by Micro ELISA and samples negative for above parameters except HEV IgM were subjected to the detection of HEV RNA by RT-PCR method. Further HEV IgM and RT-PCR positive samples were subjected for serum levels of Th1 cutokines (i.e TNFα and IFNγ) by immunoenzymetric assay.

Serum TNFα level was significantly more elevated in acute and fulminant hepatitis patients when compared to healthy controls. Healthy controls have around 0–20 Pg/ml (Picogram per milliliter) and 0-1.2 IU/ml of TNFα and IFNγ levels respectively, while in acute hepatitis the TNFγ values range from 38 Pg/ml to 800 Pg/ml and IFNγ ranged between 1 IU/ml to 5.4 IU/ml. The fulminant hepatitis patients have TNFα values ranging from 48 Pg/ml to 210 Pg/ml and IFNγ values from 1 IU/ml to 1.1 IU/ml. The total serum bilirubin levels in AH patients ranged from 1.8 to 16 mg%, while in FH cases it ranged from 20.3 to 32.9 mg%. Healthy controls have serum bilirubin levels ranging from 0-0.8 mg% (within normal limit). The results suggest that serm levels of TNFα were significantly high in acute and fulminant patients when compared with the values observed in healthy controls. Both the cytokines i.e. TNFα and IFNγ levels were directly proportional to the bilirubin concentration. It clearly shows there proinflammatory role in patients with liver disease. IFNγ levels were within the normal range in acute hepatitis patients excepting one acute hepatitis case which showed an abruptly high level of IFNγ. All these patients recovered from the infection.