Publications by authors named "Lisa Sandmann"

20 Publications

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New Treatments for Chronic Hepatitis B Virus/Hepatitis D Virus Infection.

Clin Liver Dis 2021 Nov 8;25(4):831-839. Epub 2021 Aug 8.

Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Carl-Neuberg-Str. 1, Hannover 30625, Germany; German Center for Infection Research (DZIF), Partner Side Hannover/Braunschweig. Electronic address:

Chronic hepatitis D virus (HDV) infection is the most severe form of viral hepatitis with high rates of end-stage liver disease and hepatocellular carcinoma. Therefore, effective antiviral treatment strategies are needed desperately. Until recently, antiviral treatment was limited to pegylated interferon-alpha. With the conditional approval of the entry inhibitor bulevirtide by the European Medicines Agency, new treatment options are now available. In addition, multiple other antiviral compounds are currently tested in clinical phase II and III trials and represent promising agents for the treatment of chronic HDV infection.
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http://dx.doi.org/10.1016/j.cld.2021.06.011DOI Listing
November 2021

HBcrAg Levels Are Associated With Virological Response to Treatment With Interferon in Patients With Hepatitis Delta.

Hepatol Commun 2021 Sep 24. Epub 2021 Sep 24.

Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.

Standard treatment of hepatitis delta virus (HDV) infection remains pegylated-interferon alfa (peg-IFNα) in most centers, which is not only associated with rather low efficacy but several adverse events. Hepatitis B core-related antigen (HBcrAg) is linked to intrahepatic covalently closed circular DNA levels and has previously been suggested as response predictor in IFN-based treatment of hepatitis B virus (HBV) mono-infection. This study aimed to investigate the value of HBcrAg in the management of patients with HBV/HDV co-infection undergoing peg-IFNα treatment. The Hep-Net-International-Delta-Hepatitis-Intervention Trial-2 study included 120 patients co-infected with HBV/HDV. Patients were treated for 96 weeks with peg-IFNα and either tenofovir or placebo. Ninety-nine patients with HDV-RNA results 24 weeks after end of treatment (FU24) were included in this analysis, of whom 32 patients (32.3%) had undetectable HDV RNA at FU24. HBcrAg was measured at baseline, week 12, 24, 48, 96, and FU24. HBcrAg levels showed no significant correlation with HDV RNA but were significantly linked to treatment outcome. HBcrAg levels < 4.5 log IU/mL at baseline, week 24, and week 48 had high negative predictive value (NPV) for achieving undetectable HDV RNA at FU24 (81.8%, 87.1% and 95.0%, respectively). Similarly, HBcrAg levels at week 96 were significantly higher in patients with viral relapse until FU24 (3.0 vs. 3.63 log IU/mL; P = 0.0089). Baseline, week 24, and week 48 HBcrAg levels were also associated with the likelihood of achieving HBsAg level < 100 IU/mL at FU24 (HBcrAg < 3.0 log IU/mL: NPV 91.7%, 90.4% and 92.3%, respectively). Test statistics improved when combining HBcrAg with additional viral and clinical parameters. Conclusion: HBcrAg is linked to treatment response to peg-IFNα in patients with HBV/HDV co-infection and could be a promising marker to determine treatment futility.
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http://dx.doi.org/10.1002/hep4.1821DOI Listing
September 2021

Towards eradication of HBV: Treatment approaches and status of clinical trials.

Curr Opin Pharmacol 2021 Oct 30;60:232-240. Epub 2021 Aug 30.

Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School Hannover, Germany; Centre for Individualised Infection Medicine (CiiM), a Joint Venture of Helmholtz Centre for Infection Research and Hannover Medical School, Hannover, Germany; German Center for Infection Research (DZIF), Partner-Site Hannover-Braunschweig, Hannover, Germany. Electronic address:

Chronic hepatitis B virus (HBV) infection and its sequelae remain a global health challenge. Current treatments are effective in controlling HBV replication, but complete eradication or 'cure' of HBV remains a rare event and is difficult to assess because of the intrahepatic reservoir of covalently closed circular DNA. Based on the understanding of the HBV life cycle and the deciphering of immune responses to HBV, therapeutic strategies to target HBV eradication are in principle possible. This article reviews current developments in new therapies aimed at HBV cure.
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http://dx.doi.org/10.1016/j.coph.2021.07.008DOI Listing
October 2021

Reaching the Unreachable: Strategies for HCV Eradication in Patients With Refractory Opioid Addiction-A Real-world Experience.

Open Forum Infect Dis 2021 Aug 17;8(8):ofab325. Epub 2021 Jun 17.

Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.

To achieve global hepatitis C virus (HCV) eradication, barriers prohibiting treatment access need to be overcome. We established a strategy to initiate antiviral therapy in patients with severe, refractory heroin addiction. All patients achieved sustained virological response. Outreach programs of hepatologists might be a reasonable way to overcome barriers to HCV treatment.
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http://dx.doi.org/10.1093/ofid/ofab325DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8339280PMC
August 2021

Experimental Drugs for the Treatment of Hepatitis D.

J Exp Pharmacol 2021 16;13:461-468. Epub 2021 Apr 16.

Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.

Chronic hepatitis D virus infection is the most severe form of viral hepatitis. Antiviral treatment is urgently needed to prevent patients from developing end stage liver disease or hepatocellular carcinoma. Treatment options were limited to off-label use of pegylated interferon alfa until conditional approval of bulevirtide by the EMA (European Medicines Agency) in July 2020. However, several other antiviral compounds are currently investigated and represent promising agents for the treatment of chronic HDV infection.
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http://dx.doi.org/10.2147/JEP.S235550DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8057838PMC
April 2021

Hypophosphatemia in people with HIV: no benefit when switching from tenofovir disoproxil fumarate to tenfovir alafenamide.

AIDS 2021 07;35(9):1516-1518

Department of Rheumatology and Immunology, Hannover Medical School, Hannover.

Treatment with tenofovir disoproxil fumarate (TDF) has been associated with hypophosphatemia mainly because of injury of the renal proximal tubulus. Studies on the impact of tenfovir alafenamide (TAF) on phosphate homeostasis in people with HIV (PWH) are limited. Prompted by a patient with phosphate wasting under tenofovir but no other evidence for tubular dysfunction, a retrospective cohort analysis with 102 PWH revealed that hypophosphatemia remained largely unchanged after switching from TDF to TAF.
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http://dx.doi.org/10.1097/QAD.0000000000002905DOI Listing
July 2021

The transplant cohort of the German center for infection research (DZIF Tx-Cohort): study design and baseline characteristics.

Eur J Epidemiol 2021 Feb 25;36(2):233-241. Epub 2021 Jan 25.

German Center for Infection Research, Hannover-Braunschweig Site, Brunswick, Germany.

Infectious complications are the major cause of morbidity and mortality after solid organ and stem cell transplantation. To better understand host and environmental factors associated with an increased risk of infection as well as the effect of infections on function and survival of transplanted organs, we established the DZIF Transplant Cohort, a multicentre prospective cohort study within the organizational structure of the German Center for Infection Research. At time of transplantation, heart-, kidney-, lung-, liver-, pancreas- and hematopoetic stem cell- transplanted patients are enrolled into the study. Follow-up visits are scheduled at 3, 6, 9, 12 months after transplantation, and annually thereafter; extracurricular visits are conducted in case of infectious complications. Comprehensive standard operating procedures, web-based data collection and monitoring tools as well as a state of the art biobanking concept for blood, purified PBMCs, urine, and faeces samples ensure high quality of data and biosample collection. By collecting detailed information on immunosuppressive medication, infectious complications, type of infectious agent and therapy, as well as by providing corresponding biosamples, the cohort will establish the foundation for a broad spectrum of studies in the field of infectious diseases and transplant medicine. By January 2020, baseline data and biosamples of about 1400 patients have been collected. We plan to recruit 3500 patients by 2023, and continue follow-up visits and the documentation of infectious events at least until 2025. Information about the DZIF Transplant Cohort is available at https://www.dzif.de/en/working-group/transplant-cohort .
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http://dx.doi.org/10.1007/s10654-020-00715-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7987595PMC
February 2021

Treatment of Chronic Hepatitis C: Efficacy, Side Effects and Complications.

Visc Med 2019 Jun 21;35(3):161-170. Epub 2019 May 21.

Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.

Background: Chronic hepatitis C virus (HCV) infection can lead to liver cirrhosis and its complications. Viral eradication is essential to prevent disease progression and reduces liver-related mortality and morbidity. Since the availability of direct-acting antivirals (DAA), HCV treatment has changed significantly. Current treatment strategies for different groups of patients as well as potential risks and caveats will be discussed in this review.

Summary: Interferon-free (IFN-free) treatment not only shortens treatment duration, but also achieves high rates of viral clearance and is overall well tolerated. Genotype-restricted but also pangenotypic combinations are available. Usually two DAA of different drug classes are combined. For the majority of the patients, treatment duration ranges from 8 to 12 weeks. Liver and kidney function as well as prior treatment experience and potential drug-drug interactions influence substance choices and treatment duration. However, modern IFN-free treatment is not only safer, but also overall far more simplified and effective. Global HCV eradication might be an ambitious but not completely unrealistic goal to pursue.

Key Messages: IFN-free antiviral treatment is safe and well tolerated. Patients can be treated almost independently of liver function or concomitant disease. Viral eradication is associated with reduced morbidity and mortality and better quality of life.
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http://dx.doi.org/10.1159/000500963DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6616049PMC
June 2019

Utility of viral kinetics in HCV therapy - It is not over until it is over?

Liver Int 2019 05;39(5):815-817

Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.

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http://dx.doi.org/10.1111/liv.14047DOI Listing
May 2019

Treatment strategies for patients with decompensated liver cirrhosis due to hepatitis C virus infection eligible for liver transplantation: real-life data from five German transplant centers.

Eur J Gastroenterol Hepatol 2019 Aug;31(8):1049-1056

Department of Gastroenterology, Hepatology and Endocrinology, Hanover Medical School, Hannover.

Background: Even with highly effective direct-acting antivirals (DAAs) treatment of patients with decompensated hepatitis C (HCV) cirrhosis remains challenging. Clinical deterioration and the need for liver transplantation (LT) may arise despite previous antiviral treatment. It is unclear whether in patients with high Model for End-Stage Liver Disease (MELD) antiviral treatment is too risky and should thus be deferred until after LT. Treatment choices that are currently made in the real-world setting are unclear.

Methods: We performed a retrospective multicenter data analysis of patients with decompensated HCV cirrhosis (MELD ≥15) that presented to liver transplant centers that are part of the German Center for Infection Research when highly active DAA therapy was available. Choice of treatment strategy (DAA first vs. transplantation first) was analyzed and correlated with baseline and outcome parameters.

Results: Thirty-five patients fulfilled the inclusion criteria and their mean MELD score was 18.5±3.78 (median: 17, interquartile range=16-19). In the majority of patients (85.7%) DAA therapy was initiated before LT; survival rates and change in MELD were numerically better in this group compared with those where DAA therapy was withheld (82.1 vs. 40%, P=0.078; ΔMELD: -2.68±6.2 vs. 5.8±14.4, P=0.157). However, DAA treatment was more often initiated in patients with better liver function (MELD: 18±3.54 vs. 21.8±3.9, P=0.008). Three patients discontinued DAA treatment because of clinical deterioration; these patients all had a MELD score above 20 at the start of therapy.

Conclusion: At liver transplant centers in Germany DAA before LT is attempted in the majority of cases. It appears to be associated with an improved outcome and seems safe at least in individuals with MELD below or equal to 20.
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http://dx.doi.org/10.1097/MEG.0000000000001386DOI Listing
August 2019

Role of BK polyomavirus (BKV) and Torque teno virus (TTV) in liver transplant recipients with renal impairment.

J Med Microbiol 2018 Oct 23;67(10):1496-1508. Epub 2018 Aug 23.

5​German Center for Infection Research, DZIF, Germany.

Purpose: Renal impairment is a common complication after liver transplantation (LT). While BK polyomavirus (BKV) has been linked to renal failure in kidney transplant recipients, Torque teno virus (TTV) is a surrogate marker for immunosuppression that does not have a clear association with any human disease. The impact of BKV and TTV on renal impairment after LT is unknown.

Methodology: In this retrospective study, urine and serum samples from 136 liver transplant recipients were screened for BKV and TTV by quantitative PCR. In addition, serum was screened for BKV-specific antibodies and the VP1 typing region was sequenced for BKV genotyping. All parameters were correlated with clinical data.Results/Key findings. BK viruria was detected up to 21 years after transplantation in 16.9 % of cases. BK viraemia was detected in 8.7 % of patients with BK viruria up to 4 years after LT. BKV-specific antibodies were detected in 93.6 % of all LT recipients and correlated with BKV viral load in urine. There was no correlation between renal impairment and the detection of BK DNA in urine (OR 0.983). TTV DNA was detected in 84.6 % of serum samples and in 66.6 % of urine samples. The TTV viral load in serum correlated with the BKV viral load but had no impact on renal impairment.

Conclusion: Our data indicate that the detection of BKV and TTV is not a risk factor for renal impairment after LT. A correlation of TTV and BKV viral load seems to be an indicator for the immune status of the host.
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http://dx.doi.org/10.1099/jmm.0.000823DOI Listing
October 2018

Mice Expressing Minimally Humanized CD81 and Occludin Genes Support Hepatitis C Virus Uptake In Vivo.

J Virol 2017 02 31;91(4). Epub 2017 Jan 31.

Princeton University, Department of Molecular Biology, Lewis Thomas Laboratory, Princeton New Jersey, USA

Hepatitis C virus (HCV) causes chronic infections in at least 150 million individuals worldwide. HCV has a narrow host range and robustly infects only humans and chimpanzees. The underlying mechanisms for this narrow host range are incompletely understood. At the level of entry, differences in the amino acid sequences between the human and mouse orthologues of two essential host factors, the tetraspanin CD81 and the tight junction protein occludin (OCLN), explain, at least in part, HCV's limited ability to enter mouse hepatocytes. We have previously shown that adenoviral or transgenic overexpression of human CD81 and OCLN facilitates HCV uptake into mouse hepatocytes in vitro and in vivo In efforts to refine these models, we constructed knock-in mice in which the second extracellular loops of CD81 and OCLN were replaced with the respective human sequences, which contain the determinants that are critical for HCV uptake. We demonstrate that the humanized CD81 and OCLN were expressed at physiological levels in a tissue-appropriate fashion. Mice bearing the humanized alleles formed normal tight junctions and did not exhibit any immunologic abnormalities, indicating that interactions with their physiological ligands were intact. HCV entry factor knock-in mice take up HCV with an efficiency similar to that in mice expressing HCV entry factors transgenically or adenovirally, demonstrating the utility of this model for studying HCV infection in vivo IMPORTANCE: At least 150 million individuals are chronically infected with hepatitis C virus (HCV). Chronic hepatitis C can result in progressive liver disease and liver cancer. New antiviral treatments can cure HCV in the majority of patients, but a vaccine remains elusive. To gain a better understanding of the processes culminating in liver failure and cancer and to prioritize vaccine candidates more efficiently, small-animal models are needed. Here, we describe the characterization of a new mouse model in which the parts of two host factors that are essential for HCV uptake, CD81 and occludin (OCLN), which differ between mice and humans, were humanized. We demonstrate that such minimally humanized mice develop normally, express the modified genes at physiological levels, and support HCV uptake. This model is of considerable utility for studying viral entry in the three-dimensional context of the liver and to test approaches aimed at preventing HCV entry.
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http://dx.doi.org/10.1128/JVI.01799-16DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5286898PMC
February 2017

Host cell mTORC1 is required for HCV RNA replication.

Gut 2016 12 14;65(12):2017-2028. Epub 2015 Aug 14.

Department of Gastroenterology, Hepatology and Endocrinology, Medizinische Hochschule Hannover, Hannover, Germany.

Objective: Chronically HCV-infected orthotopic liver transplantation (OLT) recipients appear to have improved outcomes when their immunosuppressive regimen includes a mammalian target of rapamycin (mTOR) inhibitor. The mechanism underlying this observation is unknown.

Design: We used virological assays to investigate mTOR signalling on the HCV replication cycle. Furthermore, we analysed HCV RNA levels of 42 HCV-positive transplanted patients treated with an mTOR inhibitor as part of their immunosuppressive regimen.

Results: The mTOR inhibitor rapamycin was found to be a potent inhibitor for HCV RNA replication in Huh-7.5 cells as well as primary human hepatocytes. Half-maximal inhibition was observed at 0.01 µg/mL, a concentration that is in the range of serum levels seen in transplant recipients and does not affect cell proliferation. Early replication cycle steps such as cell entry and RNA translation were not affected. Knockdown of raptor, an essential component of mTORC1, but not rictor, an essential component of mTORC2, inhibited viral RNA replication. In addition, overexpression of raptor led to higher viral RNA replication, demonstrating that mTORC1, but not mTORC2, is required for HCV RNA replication. In 42 HCV-infected liver-transplanted or kidney-transplanted patients who were switched to an mTOR inhibitor, we could verify that mTOR inhibition decreased HCV RNA levels in vivo.

Conclusions: Our data identify mTORC1 as a novel HCV replication factor. These findings suggest an underlying mechanism for the observed benefits of mTOR inhibition in HCV-positive OLT recipients and potentiate further investigation of mTOR-containing regimens in HCV-positive recipients of solid organ transplants.
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http://dx.doi.org/10.1136/gutjnl-2014-308971DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5136730PMC
December 2016

Modulation of HCV reinfection after orthotopic liver transplantation by fibroblast growth factor-2 and other non-interferon mediators.

Gut 2016 06 23;65(6):1015-23. Epub 2015 Mar 23.

Department of Gastroenterology, Hepatology and Endocrinology, Medizinische Hochschule Hannover, Hannover, Germany German Center for Infection Research (DZIF), Hannover, Germany Institute for Molecular Biology, Medizinische Hochschule Hannover, Hannover, Germany.

Objective: In HCV infected individuals graft infection occurs shortly after orthotopic liver transplantation (OLT). We aimed to describe the composition of the inflammatory response at this time, how it affects the HCV replication cycle and identify novel proviral and antiviral factors.

Design: We used a Luminex assay to quantify 50 inflammatory mediators in sera before and shortly after OLT. In vitro grown HCV based on the JFH-1 isolate were used to characterise the effects of patient sera and individual mediators on HCV.

Results: Although the mediator composition is highly variable between individuals, sera drawn immediately post-OLT significantly enhance HCV infectivity compared with control sera from before OLT in about half of the cases. Among 27 non-interferon inflammatory mediators fibroblast growth factor (FGF)-2 stood out as it enhanced HCV RNA replication and release of infectious particles. The effect was concentration-dependent and detectable in dividing and non-dividing cells. Moreover, pharmacological inhibition of FGF-2 receptor signalling abrogated the enhancing effect of FGF-2 and inhibited HCV replication in the absence of serum FGF-2 suggesting that HCV replication is dependent on basal activation of the FGF-2 triggered signalling pathway. Finally, in individuals with chronic HCV infection with high viral load, serum FGF-2 was significantly higher compared with those with low viral load.

Conclusions: Although no single mediator may account for this effect, serum shortly post-OLT enhances HCV infection. FGF-2 is a novel endogenous driver of HCV replication and a potential therapeutic target.
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http://dx.doi.org/10.1136/gutjnl-2014-308003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4893125PMC
June 2016

Primary biliary acids inhibit hepatitis D virus (HDV) entry into human hepatoma cells expressing the sodium-taurocholate cotransporting polypeptide (NTCP).

PLoS One 2015 3;10(2):e0117152. Epub 2015 Feb 3.

Institut für Molekularbiologie, Medizinische Hochschule Hannover, Hannover, Germany; Klinik für Gastroenterologie, Hepatologie und Endokrinologie, Medizinische Hochschule Hannover, Hannover, Germany.

Background: The sodium-taurocholate cotransporting polypeptide (NTCP) is both a key bile acid (BA) transporter mediating uptake of BA into hepatocytes and an essential receptor for hepatitis B virus (HBV) and hepatitis D virus (HDV). In this study we aimed to characterize to what extent and through what mechanism BA affect HDV cell entry.

Methods: HuH-7 cells stably expressing NTCP (HuH-7/NTCP) and primary human hepatocytes (PHH) were infected with in vitro generated HDV particles. Infectivity in the absence or presence of compounds was assessed using immunofluorescence staining for HDV antigen, standard 50% tissue culture infectious dose (TCID50) assays and quantitative PCR.

Results: Addition of primary conjugated and unconjugated BA resulted in a dose dependent reduction in the number of infected cells while secondary, tertiary and synthetic BA had a lesser effect. This effect was observed both in HuH-7/NTCP and in PHH. Other replication cycle steps such as replication and particle assembly and release were unaffected. Moreover, inhibitory BA competed with a fragment from the large HBV envelope protein for binding to NTCP-expressing cells. Conversely, the sodium/BA-cotransporter function of NTCP seemed not to be required for HDV infection since infection was similar in the presence or absence of a sodium gradient across the plasma membrane. When chenodeoxycolic acid (15 mg per kg body weight) was administered to three chronically HDV infected individuals over a period of up to 16 days there was no change in serum HDV RNA.

Conclusions: Primary BA inhibit NTCP-mediated HDV entry into hepatocytes suggesting that modulation of the BA pool may affect HDV infection of hepatocytes.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0117152PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315608PMC
January 2016

Barriers of hepatitis C virus interspecies transmission.

Virology 2013 Jan;435(1):70-80

Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University, New York, NY 10065, USA.

Hepatitis C virus (HCV) is a major causative agent of severe liver disease including fibrosis, cirrhosis and liver cancer. Therapy has improved over the years, but continues to be associated with adverse side effects and variable success rates. Furthermore, a vaccine protecting against HCV infection remains elusive. Development of more effective intervention measures has been delayed by the lack of a suitable animal model. Naturally, HCV infects only humans and chimpanzees. The determinants of this limited host range are poorly understood in part due to difficulties of studying HCV in cell culture. Some progress has been made elucidating the barriers for the HCV lifecycle in non-permissive species which will help in the future to construct animal models for HCV infection, immunity and pathogenesis.
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http://dx.doi.org/10.1016/j.virol.2012.09.044DOI Listing
January 2013

Anti-retroviral drugs do not facilitate hepatitis C virus (HCV) infection in vitro.

Antiviral Res 2012 Oct 24;96(1):51-8. Epub 2012 Jul 24.

Klinik für Gastroenterologie, Hepatologie und Endokrinologie, Medizinische Hochschule Hannover, Hannover, Germany.

An estimated 4 to 5 million people are co-infected with HIV/HCV worldwide. Recently observed outbreaks of acute HCV infection among HIV-positive men who have sex with men (MSM) have been linked to behavioral factors such as high risk sexual practices and recreational drug use. However, at the molecular level, many drugs such as glucocorticoids or cyclosporine A have been found to modulate viral replication. Thus, it is conceivable that drugs used in highly active antiretroviral therapy (HAART) may heighten susceptibility to HCV infection and contribute to the recent outbreaks. We therefore performed a comprehensive screen of antiretroviral drugs covering all available drug classes both individually and in typical combinations used during HAART to probe for direct effects on HCV cell entry, replication, new particle assembly and release. Importantly, no significant enhancement or inhibition of HCV cell entry, replication or new particle production was detected. While raltegravir and ritonavir boosted atazanavir reduce HCV replication, a tenfold reduction of HCVcc entry by the CCR5 antagonist maraviroc was observed. In conclusion, commonly used HAART agents do not specifically enhance HCV replication. Thus recent epidemic outbreaks of acute HCV in HIV-infected MSM are unlikely to be related to enhancing effects of HAART drugs.
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http://dx.doi.org/10.1016/j.antiviral.2012.07.005DOI Listing
October 2012
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