alcohol stimulates HCV

Additive effect of ethanol and HCV subgenomic replicon expression on COX-2 protein levels and activity

Abstract
Summary. The mechanisms by which alcohol exacerbates liver injury in patients with hepatitis C are unknown. We used the hepatitis C virus (HCV) subgenomic replicon cell system to evaluate the effect of ethanol on HCV replication and viral protein synthesis. Our results demonstrate that alcohol stimulates HCV replicon expression at both HCV-RNA and protein levels. Furthermore, we observed that ethanol treatment showed an additive effect in cyclooxygenase-2 (COX-2) protein expression and activity already induced by HCV viral proteins, and in turn increased HCV viral expression. Our results suggest that COX-2 activity is involved in ethanol-induced HCV-RNA and NS5A protein expression, because acetylsalicylic acid (ASA), a COX-1/2 inhibitor, blocked this induction and downregulated COX-2 protein expression and activity. Therefore, we suggest that ethanol increases HCV replication expression, at least in part, by upregulating a key cellular regulator of oxidative stress pathway known as COX-2 or its products.


K. Trujillo-Murillo11Department of Biochemistry, School of Medicine, UANL, Monterrey, Nuevo León, México; ,
O. Álvarez-Martínez11Department of Biochemistry, School of Medicine, UANL, Monterrey, Nuevo León, México; ,
L. Garza-Rodríguez11Department of Biochemistry, School of Medicine, UANL, Monterrey, Nuevo León, México; ,
H. Martínez-Rodríguez11Department of Biochemistry, School of Medicine, UANL, Monterrey, Nuevo León, México; ,
F. Bosques-Padilla22Gastroenterology and ,
J. Ramos-Jiménez33Infectious Diseases Service, ‘‘Dr. José E. Gonzalez’’ University Hospital, UANL, Monterrey, Nuevo León, México; and ,
H. Barrera-Saldaña11Department of Biochemistry, School of Medicine, UANL, Monterrey, Nuevo León, México; ,
A. R. Rincón-Sánchez44Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, México and
A. M. Rivas-Estilla11Department of Biochemistry, School of Medicine, UANL, Monterrey, Nuevo León, México;
1Department of Biochemistry, School of Medicine, UANL, Monterrey, Nuevo León, México; 2Gastroenterology and 3Infectious Diseases Service, ‘‘Dr. José E. Gonzalez’’ University Hospital, UANL, Monterrey, Nuevo León, México; and 4Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, México
Ana María Rivas-Estilla PhD, Department of Biochemistry, School of Medicine, UANL, Av. Madero y Av. Aguirre Pequeño s/n Col. Mitras Centro, CP 64460 Monterrey, Nuevo León, México. E-mail: ***@****
HCV, hepatitis C virus; HCC, hepatocellular carcinoma; IFN-α, interferon-alpha; COX-2, cyclooxygenase-2; ALT, alanine aminotransferase; AST, aspartate aminotransferase.

http://www.blackwell-synergy.com/doi/abs/10.1111/j.1365-2893.2006.00837.x

[mremeet]

I think Jim posted a link to another study a while back that suggested alcohol did not increase viral activity. Let the games begin! ;-)

[lanier]

Very interesting information on your post thank you.  I have done no clinical studies, but I have always felt that alcohol and viral protein synthesis were comingled.  I believe so many of these types of facts are silent clues to how we might progress from grade and stage when the time comes later in life.  I also really think that the time we have had a consistant low platelet count in years is an excent precursor for liver disease progression later in life and I would love to read more posts like this on this blog.HCV has no lobby, like viagra, or any of the other "flavor" of the month pharmacheuticals so any microbiologists who take the time to put it on their agenda will be very rich someday since the people carrying this virus will be coming out of the wood work in years to come.  

regards
Lani