It appears that superinfection with HBV played an important role in HCV suppression in this patient. Although the patient was most likely immunocompromised because of his chronic illnesses, i.e., renal failure and decompensated liver disease, this should unlikely lead to suppression of HCV infection, rather than to upregulation or reactivation of HCV replication. We assume that the inhibitory effect of HBV superinfection on HCV replication was probably indirect and mediated through activation of the host's immune system by HBV. Thus, we hypothesize that vigorous HBV-specific and/or HBV-induced non-specific immune responses, including induction of antiviral cytokines such as INF, were sufficient to suppress active HCV infection, although unable to inhibit HBV infection concurrently or completely eradicate HCV. However, it cannot be excluded that inhibition of HCV replication could also occur because of a direct interference between HCV and HBV. This possibility has recently been investigated in patients with chronic HCV and occult HBV infection characterized by low levels of HBV DNA occurring in the serum and/or the liver in the absence of serum HBsAg. The authors found that HCV and HBV can coinfect the same hepatocytes. Furthermore, HCV RNA levels were significantly lower in coinfected cells than in those infected only with HCV.
In summary, this study demonstrates for the first time that HBV superinfection can induce profound suppression of chronic hepatitis C. This may have significant implications for understanding the interplay between these two viruses and their immune responses.
"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."
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.
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.
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.
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
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
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