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01000naa a22002652 4500 |
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NLM147873290 |
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DE-627 |
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20231223044322.0 |
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tu |
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231223s2004 xx ||||| 00| ||eng c |
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|a (NLM)15093547
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|a DE-627
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|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Eisen-Vandervelde, Audrey L
|e verfasserin
|4 aut
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| 245 |
1 |
4 |
|a The molecular basis of HCV-mediated immune dysregulation
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| 264 |
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1 |
|c 2004
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| 336 |
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|a Text
|b txt
|2 rdacontent
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| 337 |
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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| 338 |
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|a Band
|b nc
|2 rdacarrier
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| 500 |
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|a Date Completed 27.05.2004
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| 500 |
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|a Date Revised 14.11.2007
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|a published: Print
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|a Citation Status MEDLINE
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| 520 |
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|a Chronic hepatitis C virus (HCV) infection, which occurs in over 85% of patients and causes mild to severe liver disease, is a growing burden to health systems worldwide. The propensity of HCV to establish persistent infection suggests that the virus, which is non-cytopathic, has evolved one or more mechanisms aimed at evading host immunity. In addition to the appearance of quasispecies, which may arise under selective pressure during B and T cell responses, HCV gene products interact with host proteins in order to subvert immune surveillance. Gaining insight into these interactions may provide the basis for novel therapies aimed at preventing chronic HCV infection
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| 650 |
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, U.S. Gov't, P.H.S.
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| 650 |
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|a Review
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| 650 |
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7 |
|a Viral Core Proteins
|2 NLM
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| 700 |
1 |
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|a Yao, Zhi Qiang
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Hahn, Young S
|e verfasserin
|4 aut
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| 773 |
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8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 111(2004), 1 vom: 01. Apr., Seite 16-21
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|x 1521-7035
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|g volume:111
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|a GBV_ILN_350
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| 951 |
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|a AR
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| 952 |
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|d 111
|j 2004
|e 1
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|c 04
|h 16-21
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