Dominance of hepatitis C virus (HCV) is associated with lower quantitative hepatitis B surface antigen and higher serum interferon-γ-induced protein 10 levels in HBV/HCV-coinfected patients

Wiegand, Steffen B.; Jaroszewicz, Jerzy; Potthoff, Andrej; Siederdissen, Christoph Höner zu; Maasoumy, Benjamin; Deterding, Katja; Manns, Michael P.; Wedemeyer, Heiner; Cornberg, Markus

doi:10.1016/j.cmi.2015.03.003

Cited by 50 publications

(47 citation statements)

References 37 publications

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“…We have not included the immune response in our model since there is little quantitative information about the immune response to the five viruses studied here, making it difficult to estimate the values of the extra parameters that would be necessary. Our model shows that viruses fundamentally interact through a competition for resources, but stimulating the immune response can potentially enhance or hinder the competitive advantage of one virus, with some studies suggesting that the immune response plays a role in viral interactions during coinfections [18,19,30,31].…”

Section: Limitations Of the Modelmentioning

confidence: 82%

“…Our key finding is that blocking of one virus infection by the presence of another can be explained simply through resource competition. Some studies have suggested that other mechanisms, such as the immune response [18,19,30,31] or interference through viral proteins [31,32] are responsible for the growth interference between two viruses. Our model does not include either of these mechanisms, suggesting that they are not necessary to explain the phenomenon.…”

Section: Implications Of Our Findingsmentioning

confidence: 99%

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Coinfections of the Respiratory Tract: Viral Competition for Resources

2016

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Studies have shown that simultaneous infection of the respiratory tract with at least two viruses is common in hospitalized patients, although it is not clear whether these infections are more or less severe than single virus infections. We use a mathematical model to study the dynamics of viral coinfection of the respiratory tract in an effort to understand the kinetics of these infections. Specifically, we use our model to investigate coinfections of influenza, respiratory syncytial virus, rhinovirus, parainfluenza virus, and human metapneumovirus. Our study shows that during coinfections, one virus can block another simply by being the first to infect the available host cells; there is no need for viral interference through immune response interactions. We use the model to calculate the duration of detectable coinfection and examine how it varies as initial viral dose and time of infection are varied. We find that rhinovirus, the fastest-growing virus, reduces replication of the remaining viruses during a coinfection, while parainfluenza virus, the slowest-growing virus is suppressed in the presence of other viruses.

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Section: Limitations Of the Modelmentioning

confidence: 82%

Section: Implications Of Our Findingsmentioning

confidence: 99%

Coinfections of the Respiratory Tract: Viral Competition for Resources

2016

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“…In particular, systematic reviews have shown that there is a significant clinical association between HCV and IR and/or type 2 diabetes, suggesting that HCV increases the risk of diabetes especially in predisposed individuals . To exclude confounding causes of steatosis, we excluded subjects with type 2 diabetes, although we still found that HBV‐HCV subjects had a lower prevalence of prediabetes than HCV subjects but similar to HBV subjects suggesting that HBV may interact with HCV by reducing IR as opposed to what is seen in HBV mono‐infection, although a viral interference, that is suppression of HCV replication by HBV, for example, through secretion of HCV‐induced cytokines, could also be involved. Further studies are warranted to assess this point.…”

Section: Discussionmentioning

confidence: 95%

Effect of hepatitis B virus on steatosis in hepatitis C virus co‐infected subjects: A multi‐centre study and systematic review

Goossens

Vito

Mangia

et al. 2018

Journal of Viral Hepatitis

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It remains unclear whether hepatitis B virus (HBV) infection may modify the severity of viral steatosis in patients coinfected with chronic hepatitis C virus (HCV). We examined the influence of coinfection with HBV on prevalence of steatosis in chronic hepatitis C in a multi-centre cohort of HBV-HCV subjects, and by performing a systematic review and meta-analysis of the literature. We centrally and blindly assessed steatosis prevalence and severity in a cohort of HBV-HCV coinfected subjects compared to HCV and HBV monoinfected controls and we performed a systematic review of studies addressing the prevalence of steatosis in HBV-HCV subjects compared to HCV controls. In the clinical cohort, we included 85 HBV-HCV, 69 HBV and 112 HCV subjects from 16 international centres. There was no significant difference in steatosis prevalence between the HBV-HCV and the HCV groups (33% vs 45%, P = .11). In subgroup analysis, lean HBV-HCV subjects with detectable HBV DNA had less steatosis than lean HCV subjects matched for HCV viremia (15% vs 45%, P = .02). Our literature search identified 5 additional studies included in a systematic review. Overall, prevalence of steatosis > 5% was similar in HBV-HCV infection compared to HCV (pooled odds ratio [OR] 0.91, 95% CI 0.53-1.6) although there was significant heterogeneity (I 69%, P = .007). In conclusion, although the prevalence of steatosis is similar in HBV-HCV compared to HCV subjects, our analysis suggests that there may be an inhibitory effect of HCV-induced steatogenesis by HBV in certain subgroups of patients.

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“…Hence, suppression or clearance of HCV infection with effective anti‐HCV therapy with either IFN‐ or DAA‐based therapy will remove the suppression on HBV replication and result in HBV reactivation. Recent cell culture studies further suggest that HCV suppresses HBV replication indirectly by way of IP‐10–related innate immune mechanism . In contrast to DAAs, IFN also exerts an inhibitory effect on HBV replication .…”

Section: Discussionmentioning

confidence: 99%