Thank you- I was curious about that. I learn something new every day here!
All the best,
Dee
I think it very well may be what is going on with your friend. Mike
Hi- I'm not nearly as medically literate as many here, but I'm wondering if this is an example of what this article explained: I have a friend whi has decompensated cirrhosis with Hep B, C and D (the "super-virus" of Hep B- develops only with Hep B). Recently he told me that the Hep C is no longer showing up in his bloodwork- he thinks it's "gone". Is this what they mean? Just curious. Thanks! -Dee
From the same article:
"This is the first reported patient with profound suppression of chronic HCV infection and the development of chronic hepatitis B following HBV superinfection in the non-transplant setting. Although it is unknown precisely when the patient acquired HBV infection and cleared HCV, given the long-standing decompensated HCV-related liver disease, spontaneous eradication of HCV is unlikely. HBV superinfection induced suppression of HCV replication, but did not eliminate HCV entirely. The implications of persistent low-level HCV replication are unclear; however, occult HCV infection may result in protracted mild liver inflammation, as described in some patients with SVR after anti-HCV therapy.[13,15] There is also a possibility that the traces of persisting HCV may serve as a springboard for future reactivation of HCV infection."
It appears that the authors aren't convinced that "persistent" or "occult" HCV is necessarily benign. The footnotes cite the Pham and Radkowski studies/articles which I cited in the thread on eradication.
13) Radkowski M, Gallegos-Orozco J, Jablonska J. Persistence of hepatitis C virus in patients successfully treated for chronic hepatitis C. Hepatology 2005; 41: 106-14
15) Coffin CS, Pham TNQ, Urbanski SJ, et al. Persistent hepatic alterations in individuals with occult HCV infection following sustained virological response to antiviral therapy. (EASL annual meeting Vienna, Austria April 26-30, 2006). J Hepatol 2006; 44: S196.
Author Information
Carla S. Coffin,1,2 Patricia M. Mulrooney-Cousins,2 Samuel S. Lee,1 Tomasz I. Michalak,2 Mark G. Swain1
1Liver Unit, Division of Gastroenterology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada
2Molecular Virology and Hepatology Research, Faculty of Medicine, Health Sciences Centre, Memorial University, St. John's, Newfoundland, Canada
Mike
Actually, this competition between viruses has been known for some time, and is especially obvious with HIV/HCV/HBV co-infection, but as I mentioned previously in my response to jmjm, has been documented, for example to occur when measles superinfects those with HIV. It is not likely to be immune mediated and is more likely to be a direct inhibition of the replication of one virus by another.
Important information, though, ms.
Cheers,
Sonic
References
1. Moss WJ, Ryon JJ, Monze M, Cutts F, Quinn TC, Griffin DE: Suppression of human immunodeficiency virus replication during acute measles. J Infect Dis 2002, 185:1035-1042.
http://www.medscape.com/viewarticle/556641_1
"It is likely that future strategies for treating hepatitis C will involve a cocktail of multiple agents that can target both the polymerase and protease enzymes of the hepatitis C virus. In the short term, it seems likely that these agents will be used in addition to the current standard of care, combination pegylated interferon and ribavirin. Despite our tremendous enthusiasm for the potential of these new therapeutic targets in hepatitis C, many questions remain unanswered. First, how many drugs can be combined to achieve optimal response and acceptable toxicity? Second, for what duration do we need to use these combination regimens to achieve an undetectable HCV RNA that will remain sustained in the long term? Furthermore, with these new agents, will the current viral kinetic data from combination therapy (rapid virologic and early virologic response) still be applicable? It is likely that the development of new drugs will increase costs, at least temporarily, and require close monitoring of both expected and unexpected side effects.
The introduction of these targeted antiviral therapies is expected to advance our therapeutic arsenal for patients with hepatitis C, especially nonresponders to the current standard of care and the more difficult-to-treat HCV genotype 1 patients. Nevertheless, it is critical that the efficacy and safety of these drugs be established and that their cost effectiveness and their impact on a patient's health-related quality of life be carefully assessed."
Mike