alexa Increased Expressions Of NKp44, NKp46 On NK/NKT Like Cells Are Associated With Impaired Cytolytic Function In Self-limiting Hepatitis E Infection | 23644
ISSN: 1948-5964

Journal of Antivirals & Antiretrovirals
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4th World Congress on Virology

Anuradha Tripathy
Accepted Abstracts: J Antivir Antiretrovir
DOI: 10.4172/1948-5964.S1.022
Abstract
Hepatitis E virus is the major cause of acute viral hepatitis in several developing countries. Growing evidence indicates the involvement of innate immune response in self-limiting Hepatitis E infection. We have characterized the NK/NK T like (NKT-like) cells in patients with self limiting Hepatitis E infection. The distribution of peripheral NK/NK T-like cells, expressions of activation receptors, cytotoxic potential & effector function of NK/NKT-like cells from fresh PBMCs of 86 acute patients, 101 recovered and 54 control individuals were assessed. Activated NKT?like (CD16+ CD56+CD3+) cells were high in the patient groups. On CD56+CD3?cells, NKp44 & NKp46 expressions were high in the acute patients whereas NKp30, NKp44, NKp46 & NKG2D were high in the recovered individuals. On CD56+CD3+ cells, NKp44, NKp46 and NKG2D expressions were high in the recovered but NKp30 was low in both the patient groups. Collectively the current study elucidates the role of NK/NK T-like cells demonstrating phenotypic alterations of activated NKT- like cells & activation receptors, lack of CD107a expression and functional impairment of peripheral NK/NKT-like cells in self- limiting Hepatitis E infection.
Biography
Anuradha Tripathy has completed his Ph.D from the All India Institute of Medical Sciences, New Delhi, India and postdoctoral studies from the school of life sciences, JNU, New Delhi. Currently, she is holding the post of Scientist D, at the National Institute of Virology, Pune., India. She has published more than 25 papers in reputed international journals Her area of specialization include understand the immunopathogenesis, involvement of host genetics in viral diseases and assessment of vaccine induced immune response.
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