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The study of HCV has been hampered by the narrow host range of HCV.<ref>{{cite pmid | 19891557}}</ref> The use of [[Replicon (genetics)|replicons]] has been successful but these have only been recently discovered.<ref name="pmid19344246">{{cite journal | author = Meier V, Ramadori G | title = Hepatitis C virus virology and new treatment targets | journal = Expert Rev Anti Infect Ther | volume = 7 | issue = 3 | pages = 329–50 | year = 2009 | month = April | pmid = 19344246 | doi = 10.1586/eri.09.12 | url = http://www.future-drugs.com/doi/abs/10.1586/eri.09.12?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dncbi.nlm.nih.gov| accessdate = 2009-04-16}}</ref> HCV, as with most all [[RNA]] viruses, exists as a [[viral quasispecies]], making it very difficult to isolate a single strain or receptor type for study.<ref>{{cite journal |author=Manns MP, Foster GR, Rockstroh JK, Zeuzem S, Zoulim F, Houghton M |title=The way forward in HCV treatment—finding the right path |journal=Nat Rev Drug Discov |volume=6 |issue=12 |pages=991–1000 |year=2007 |month=December |pmid=18049473 |doi=10.1038/nrd2411 }}</ref>
A possible association between low Vitamin D leves and a poor response to treatment has been reported.<ref name=Lange2011>Lange CM, Bojunga J, Ramos-Lopez E, von Wagner M, Hassler A, Vermehren J, Herrmann E, Badenhoop K, Zeuzem S, Sarrazin C (2011) Vitamin D deficiency and a CYP27B1-1260 promoter polymorphism are associated with chronic hepatitis C and poor response to interferon-alfa based therapy. J Hepatol 54(5):887-893</ref> In vitro work has shown that Vitamin D may be able to reduce viral replication.<ref name=Gal-Tanamy2011>Gal-Tanamy M, Bachmetov L, Ravid A, Koren R, Erman A, Tur-Kaspa R, Zemel R (2011) Vitamin D: an innate antiviral agent suppressing hepatitis C virus in human hepatocytes. Hepatology 54(5):1570-9. doi: 10.1002/hep.24575.</ref> While this work looks promising the results of clinical trials are awaited.
==Stability in the environment==
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