Department of Immunology, Sanjay Gandhi Postgraduate Institute, Lucknow- 226014, India.
Abstracts of the papers presented at the International Conference of Indian Virological Society on “Emerging and Re-emerging viral Diseases of the Tropics and Subtropics” at Indian Agricultural Research Institute, New Delhi, India, December 11–14, 2007.
Hepatitis E virus (HEV) is a frequent cause of epidemic and sporadic acute viral hepatitis in many regions of the developing world. It is important to understand the pathogenesis of liver cell necrosis and the issues related to the immune responses to viral proteins in this disease. Since HEV has not been grown in tissue culture, it is still unclear whether the virus is cytopathic. We have studied various aspects of the immune responses during this acute viral illness. We have shown that during the acute illness, there was a significant peripheral blood mononuclear cell response to HEV ORF2 proteins, and peptide mapping showed that T cell epitopes were present in the regions of aa 73–156, 289–372, 361–444 and 505–588 of HEV ORF2 protein. No association was found between specific HLA-DRB1 and HLA-DRQ1 alleles and proliferation with any peptide pool. The patients with acute HEV infection also had an expansion of the total CD4+ population accompanied by decreased numbers of NK and CD4+ NKT cells. However, the NK and NKT cells present were mostly in the activated state. Peripheral proliferative reponses to HEV ORF2 protein was accompanied by higher IFN- was unchanged. The secretion than in controls, while those of IL-2 and TNF- and IL-4?, TNF-?proportions of CD4+/CD69+ and CD8+/CD69+ cells producing IFN- in response to HEV ORF2 stimulation were similar in patients and controls. The limited immune reactivity in the peripheral blood cells of patients with acute HEV infection may be related to the sequestration of immune cells to the intra-hepatic compartment, the major site of infection.
