For this purpose, we carried out continuous culture experiments with the diatom Thalassiosira weissflogii (Grunow) G. Fryxell & Hasle exposed to various conditions of light and N supply. The results revealed that a decrease in N acquisition occurred when a significant proportion of the

population was in mitosis. This observation suggests that N acquisition is incompatible with mitosis and therefore that its acquisition rate is not constant during the cell cycle. In addition, environmental conditions, such as light and nutrient supply disrupt the cell cycle at the level of the individual cell, which impacts synchrony of the population. “
“Coralline algae are considered among the most sensitive species to near future ocean selleck inhibitor acidification. We tested the effects of elevated pCO2 on the metabolism of the free-living coralline alga Lithothamnion corallioides (“maerl”) and the interactions with changes Mitomycin C cell line in temperature. Specimens were collected in North Brittany (France) and grown for 3 months at pCO2 of 380 (ambient pCO2), 550, 750, and 1000 μatm (elevated pCO2) and at successive temperatures

of 10°C (ambient temperature in winter), 16°C (ambient temperature in summer), and 19°C (ambient temperature in summer +3°C). At each temperature, gross primary production, respiration (oxygen flux), and calcification (alkalinity flux) rates were assessed in the light and dark. Pigments were determined by HPLC. Chl a, carotene, and zeaxanthin were the three major pigments found in L. corallioides thalli. Elevated pCO2 did

not affect pigment content while temperature slightly decreased zeaxanthin and carotene content at 10°C. Gross production was not affected by temperature but was significantly affected by pCO2 with an increase between 380 and 550 μatm. Light, dark, and diel (24 h) calcification rates strongly decreased with increasing pCO2 regardless of the temperature. Although elevated pCO2 only slightly affected gross production in L. corallioides, diel net calcification was reduced by up to 80% under learn more the 1,000 μatm treatment. Our findings suggested that near future levels of CO2 will have profound consequences for carbon and carbonate budgets in rhodolith beds and for the sustainability of these habitats. “
“As part of their strategy to infect the globally important coccolithophore, Emiliania huxleyi (Lohmann) W.W. Hay & H.P. Mohler, Coccolithoviruses trigger and regulate the host’s programmed cell death (PCD) machinery during lytic infection. The induction and recruitment of host metacaspases, specialized, ancestral death proteases that facilitate viral lysis, suggests they may be important subcellular determinants to infection. We examined the “basal” levels and patterns of caspase activity and metacaspase expression in exponentially growing resistant and sensitive E.

For this purpose, we carried out continuous culture experiments with the diatom Thalassiosira weissflogii (Grunow) G. Fryxell & Hasle exposed to various conditions of light and N supply. The results revealed that a decrease in N acquisition occurred when a significant proportion of the

population was in mitosis. This observation suggests that N acquisition is incompatible with mitosis and therefore that its acquisition rate is not constant during the cell cycle. In addition, environmental conditions, such as light and nutrient supply disrupt the cell cycle at the level of the individual cell, which impacts synchrony of the population. “
“Coralline algae are considered among the most sensitive species to near future ocean Selleckchem LDK378 acidification. We tested the effects of elevated pCO2 on the metabolism of the free-living coralline alga Lithothamnion corallioides (“maerl”) and the interactions with changes Kinase Inhibitor Library research buy in temperature. Specimens were collected in North Brittany (France) and grown for 3 months at pCO2 of 380 (ambient pCO2), 550, 750, and 1000 μatm (elevated pCO2) and at successive temperatures

of 10°C (ambient temperature in winter), 16°C (ambient temperature in summer), and 19°C (ambient temperature in summer +3°C). At each temperature, gross primary production, respiration (oxygen flux), and calcification (alkalinity flux) rates were assessed in the light and dark. Pigments were determined by HPLC. Chl a, carotene, and zeaxanthin were the three major pigments found in L. corallioides thalli. Elevated pCO2 did

not affect pigment content while temperature slightly decreased zeaxanthin and carotene content at 10°C. Gross production was not affected by temperature but was significantly affected by pCO2 with an increase between 380 and 550 μatm. Light, dark, and diel (24 h) calcification rates strongly decreased with increasing pCO2 regardless of the temperature. Although elevated pCO2 only slightly affected gross production in L. corallioides, diel net calcification was reduced by up to 80% under see more the 1,000 μatm treatment. Our findings suggested that near future levels of CO2 will have profound consequences for carbon and carbonate budgets in rhodolith beds and for the sustainability of these habitats. “
“As part of their strategy to infect the globally important coccolithophore, Emiliania huxleyi (Lohmann) W.W. Hay & H.P. Mohler, Coccolithoviruses trigger and regulate the host’s programmed cell death (PCD) machinery during lytic infection. The induction and recruitment of host metacaspases, specialized, ancestral death proteases that facilitate viral lysis, suggests they may be important subcellular determinants to infection. We examined the “basal” levels and patterns of caspase activity and metacaspase expression in exponentially growing resistant and sensitive E.

Though causes

of Lycaon mortality have been well documented, with anthropogenic mortality being recorded as a significant factor depressing populations in some systems (Woodroffe et al., 2007), the relationship between diel activity, how it could increase their conspicuousness and hence vulnerability to anthropogenic impact (Rasmussen, 1999), has not. This article investigates the hypothesis that the optimal foraging conditions for Lycaon impose high temporal niche overlap with humans, thereby putting them at greater risk than some other sympatric carnivores. To date, on the assumption that moonlight hunting does not occur, the activity Protease Inhibitor Library solubility dmso of Lycaon has been described as crepuscular to diurnal (Saleni et al., 2007). Lycaon hunt small to large ungulates (Childes, 1988; Creel & Creel, 2002; Rasmussen et al., 2008), and occasionally livestock (Rasmussen, 1999). Lycaon select for sick and weak individuals (Pole, Gordon check details & Gorman, 2003), which considering the extreme energetic cost of chasing may be a crucial life strategy (Rasmussen et al., 2008). Hyaenas Crocuta crocuta and lions Panthera leo kleptoparasitize Lycaon, with this impact being particularly significant in packs of less than six individuals (2009), so with lions also killing adults and pups, any changes in encounter with these predators is likely to have major

implications. It is plausible that changing pack dynamics will also affect diel activity, time windows utilized and encounters with competitors to include humans, which as a consequence of shooting, cars and snares, contribute selleck chemicals to 93% of all Lycaon mortality in Zimbabwean ranch land (Rasmussen, 1997). This high figure is not unusual for canids, for which anthropogenic mortality is often the greatest threat. For example, human-induced mortality in wolves ranges from 80% in America (Ballard, Whitman & Gardner,

1987; Fuller, 1989) to 92% in parts of Europe (Smietana & Wajda, 1997). Similarly, humans are responsible for most coyote, Canis latrans mortalities (Windberg, Anderson & Engeman, 1985; Gese, Rongstad & Mytton, 1989). As predators are known to respond behaviourally to levels of anthropogenic disturbance (Vila, Urios & Castroviejo, 1995; Ciucci et al., 1997; Sillero-Zubiri & Macdonald, 1997; Kitchen, Gese & Schauster, 2000; Boydston et al., 2003), it is likely that Lycaon will too. In such cases, while behavioural plasticity can facilitate survival, it will come at energetic cost. Fieldwork was conducted in two parapatric study sites separated by 150 km: Hwange National Park in the north-west of Zimbabwe, and adjacent areas, totalling 5500 km2 (April 1994 and December 2002); and the Nyamandlovu farming region totalling 1000 km2 (April 1994 until June 1997), with Lycaon densities being 0.93/100 km2 and 0.84/100 km2, respectively (Rasmussen, 1997).

We therefore conducted this study, which also aimed to validate the APASL stopping rule in our HBeAg-negative patients with CHB treated with ETV. This study used a retrospective-prospective cohort, approved by the Institutional Review Board of the Chang Gung Memorial Hospital, Taiwan. Excluding patients with coexisting HCV or HDV infection, alcoholism, autoimmune hepatitis, and malignancy, all HBeAg-negative, anti-HBe-positive patients with CHB who had been treated with ETV and were followed for a minimum of 12 months (48 weeks) after cessation

of ETV therapy by the stopping rule of APASL (undetectable LDK378 molecular weight HBV-DNA by PCR had been demonstrated on three occasions at least 6 months apart[7]) were included. After cessation of ETV therapy, serum ALT was monitored every 1-1.5 months in the first 3 months and then at least every 3 months along with serum HBV DNA assay every 3 months during off-therapy follow-up. Alfa-fetoprotein and ultrasonography were performed every 3-6 selleck chemicals llc months. If serum HBV DNA increases over 2,000 IU/mL or ALT level increases over ULN during off-therapy follow-up, HBV DNA and/or ALT were retested for confirmation and further evaluation. The “consolidation duration” was calculated from the first demonstration of undetectable HBV DNA to the end of treatment. According to the APASL guidelines, “clinical relapse” was defined as an event with an increase of serum HBV-DNA level over

2,000 IU/mL and serum ALT levels >2 × ULN, which is the AASLD and

APASL indication of anti-HBV therapy for CHB.[1, 2] Age, gender, presence of cirrhosis, prior treatment, baseline biochemical data and viral features, serum HBV DNA and ALT at the end of 3 and 6 months on therapy, serum HBsAg, HBV-DNA and ALT levels at baseline and at end of therapy, as well as treatment duration and consolidation duration were compared between patients with clinical relapse (relapsers) and those with sustained response (nonrelapsers). Since there was no APASL stopping rule for HBeAg-negative patients before 2008[7] and most of our patients have been treated with ETV after 2008, only 22 LAM-treated and 30 telbivudine (LdT)-treated HBeAg-negative patients had stopped drug therapy after a consolidation therapy >1 year and were followed for 1 year off-therapy, as the ETV cohort in the present selleck chemicals study did. The occurrences of clinical relapse in these 52 patients were searched by chart review retrospectively for comparison. The biochemical tests were performed using routine automated techniques at our clinical pathology laboratories. The serum ALT ULN was set by the laboratory at 36 U/L for both male and female. Serum hepatitis markers including HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HDV, and anti-HCV were assayed using the EIA kit (Abbott Diagnostics, North Chicago, IL). HBV genotype was determined using PCR-restriction fragment length polymorphism of the surface gene of HBV.

We therefore conducted this study, which also aimed to validate the APASL stopping rule in our HBeAg-negative patients with CHB treated with ETV. This study used a retrospective-prospective cohort, approved by the Institutional Review Board of the Chang Gung Memorial Hospital, Taiwan. Excluding patients with coexisting HCV or HDV infection, alcoholism, autoimmune hepatitis, and malignancy, all HBeAg-negative, anti-HBe-positive patients with CHB who had been treated with ETV and were followed for a minimum of 12 months (48 weeks) after cessation

of ETV therapy by the stopping rule of APASL (undetectable Pembrolizumab research buy HBV-DNA by PCR had been demonstrated on three occasions at least 6 months apart[7]) were included. After cessation of ETV therapy, serum ALT was monitored every 1-1.5 months in the first 3 months and then at least every 3 months along with serum HBV DNA assay every 3 months during off-therapy follow-up. Alfa-fetoprotein and ultrasonography were performed every 3-6 HCS assay months. If serum HBV DNA increases over 2,000 IU/mL or ALT level increases over ULN during off-therapy follow-up, HBV DNA and/or ALT were retested for confirmation and further evaluation. The “consolidation duration” was calculated from the first demonstration of undetectable HBV DNA to the end of treatment. According to the APASL guidelines, “clinical relapse” was defined as an event with an increase of serum HBV-DNA level over

2,000 IU/mL and serum ALT levels >2 × ULN, which is the AASLD and

APASL indication of anti-HBV therapy for CHB.[1, 2] Age, gender, presence of cirrhosis, prior treatment, baseline biochemical data and viral features, serum HBV DNA and ALT at the end of 3 and 6 months on therapy, serum HBsAg, HBV-DNA and ALT levels at baseline and at end of therapy, as well as treatment duration and consolidation duration were compared between patients with clinical relapse (relapsers) and those with sustained response (nonrelapsers). Since there was no APASL stopping rule for HBeAg-negative patients before 2008[7] and most of our patients have been treated with ETV after 2008, only 22 LAM-treated and 30 telbivudine (LdT)-treated HBeAg-negative patients had stopped drug therapy after a consolidation therapy >1 year and were followed for 1 year off-therapy, as the ETV cohort in the present selleck chemical study did. The occurrences of clinical relapse in these 52 patients were searched by chart review retrospectively for comparison. The biochemical tests were performed using routine automated techniques at our clinical pathology laboratories. The serum ALT ULN was set by the laboratory at 36 U/L for both male and female. Serum hepatitis markers including HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HDV, and anti-HCV were assayed using the EIA kit (Abbott Diagnostics, North Chicago, IL). HBV genotype was determined using PCR-restriction fragment length polymorphism of the surface gene of HBV.

(see statement 23). CsA is usually ceased after 3–6 months of overlap with AZA/ 6-MP or methotrexate used as monotherapy after this time. Complications of CsA include hypertension, nephrotoxicity, seizure, gingival hyperplasia and hypertension. Both CsA and IFX can be used in IV-corticosteroid refractory UC and randomized comparative study of the two agents are in progress. Rescue treatment after failure of the first agent has a 33–40% chance of inducing remission with the second agent but at the risk of developing severe septic complications.136 Tacrolimus.  Tacrolimus has a greater potency, more predictable pharmacokinetic profile and better adverse effect profile than CsA.164 Tacrolimus has steroid-sparing

effects, is rapid in onset and colectomy can be averted in a proportion of UC patients. Ogata et al. conducted a placebo-controlled study in Japanese patients with refractory UC randomizing them to high-trough http://www.selleckchem.com/products/ly2157299.html levels of 10–15 ng/mL, low-trough levels of 5–10 ng/mL versus placebo and showed

that the clinical remission rates were 19%, 9% and 5%, respectively (P < 0.001). The clinical improvement rates at 2 weeks were 62%, 36%, and 10%, respectively. Colectomy was avoided in all patients.165 Overall, the long-term colectomy rate in another tacrolimus study was 22–34%. Adverse drug effects tend to be mild and include tremor, hyperglycemia, hypertension and infection.166,167 Toxic megacolon, non-responsiveness or drug-induced adverse effects to medical buy Talazoparib treatment, high-grade dysplasia, carcinoma, steroid dependency, massive bleeding, bowel perforation and failure to thrive in the pediatric patient are indications for surgery. Level of agreement: a-100%, b-0%, c-0%, d-0%, e-0% Quality of evidence: III Classification of recommendation: C Indications for surgery.  Surgery remains an important component in the treatment algorithm of UC and early colorectal surgery consultation is recommended especially for acute severe

UC that requires hospitalization. The decision to operate is best taken by the gastroenterologist and colorectal surgeon in conjunction with the patient.168 see more The type of surgery is dependent on the acuteness of the indication and the patient’s condition. Indications for surgery include toxic megacolon, non-responsiveness or drug-induced adverse effects to medical treatment, high-grade dysplasia, carcinoma, steroid dependency, massive bleeding, and failure to thrive in the pediatric patient are indications for surgery. Toxic megacolon is defined as total or segmental non-obstructive dilatation of the colon of at least 6 cm associated with systemic toxicity. This represents severe colitis and is associated with colonic perforation. Bowel perforation is the most serious of UC complications and is associated with high morbidity and mortality. Depending on the extent of disease, oral and/or per-rectal 5-aminosalylates help maintain remission.

(see statement 23). CsA is usually ceased after 3–6 months of overlap with AZA/ 6-MP or methotrexate used as monotherapy after this time. Complications of CsA include hypertension, nephrotoxicity, seizure, gingival hyperplasia and hypertension. Both CsA and IFX can be used in IV-corticosteroid refractory UC and randomized comparative study of the two agents are in progress. Rescue treatment after failure of the first agent has a 33–40% chance of inducing remission with the second agent but at the risk of developing severe septic complications.136 Tacrolimus.  Tacrolimus has a greater potency, more predictable pharmacokinetic profile and better adverse effect profile than CsA.164 Tacrolimus has steroid-sparing

effects, is rapid in onset and colectomy can be averted in a proportion of UC patients. Ogata et al. conducted a placebo-controlled study in Japanese patients with refractory UC randomizing them to high-trough Alectinib clinical trial levels of 10–15 ng/mL, low-trough levels of 5–10 ng/mL versus placebo and showed

that the clinical remission rates were 19%, 9% and 5%, respectively (P < 0.001). The clinical improvement rates at 2 weeks were 62%, 36%, and 10%, respectively. Colectomy was avoided in all patients.165 Overall, the long-term colectomy rate in another tacrolimus study was 22–34%. Adverse drug effects tend to be mild and include tremor, hyperglycemia, hypertension and infection.166,167 Toxic megacolon, non-responsiveness or drug-induced adverse effects to medical check details treatment, high-grade dysplasia, carcinoma, steroid dependency, massive bleeding, bowel perforation and failure to thrive in the pediatric patient are indications for surgery. Level of agreement: a-100%, b-0%, c-0%, d-0%, e-0% Quality of evidence: III Classification of recommendation: C Indications for surgery.  Surgery remains an important component in the treatment algorithm of UC and early colorectal surgery consultation is recommended especially for acute severe

UC that requires hospitalization. The decision to operate is best taken by the gastroenterologist and colorectal surgeon in conjunction with the patient.168 see more The type of surgery is dependent on the acuteness of the indication and the patient’s condition. Indications for surgery include toxic megacolon, non-responsiveness or drug-induced adverse effects to medical treatment, high-grade dysplasia, carcinoma, steroid dependency, massive bleeding, and failure to thrive in the pediatric patient are indications for surgery. Toxic megacolon is defined as total or segmental non-obstructive dilatation of the colon of at least 6 cm associated with systemic toxicity. This represents severe colitis and is associated with colonic perforation. Bowel perforation is the most serious of UC complications and is associated with high morbidity and mortality. Depending on the extent of disease, oral and/or per-rectal 5-aminosalylates help maintain remission.

Members include: J. Gregory Fitz, MD, Co-Chair Gary L. Davis, MD, Co-Chair Kenneth D. Chavin, MD, PhD Mark J. Czaja, MD Adrian M. Di Bisceglie, MD, FACP Marc G. Ghany, MD Mary E. Rinella, MD Ronald J. Sokol, MD Gyongyi Szabo, MD, PhD Rebecca T. Wells, MD The overall goal of The Liver Meeting® is to provide a forum for the exchange of groundbreaking research and clinical information in diseases of the liver and biliary tract and in liver

transplantation. The Liver Meeting® 2013 is designed for physicians, surgeons, scientists, educators, nurses, physician assistants, and all other hepatology health professionals. AASLD takes responsibility for the content, quality, and scientific integrity of this CME activity.

Provide a forum for exchange of groundbreaking Roxadustat price basic and clinical research in liver disease Create an arena for the PI3K inhibitor presentation and interchange of opinions on state-of-the-art care and management of the full spectrum of patients with liver disease The American Association for the Study of Liver Diseases (AASLD) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. AASLD designates these live activities for AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Annual Meeting

(State-of-the-Art Lectures; President’s Choice; General Hepatology Update; Advances for Practitioners; Plenaries and Parallel Sessions; Global Forum; Federal Focus; and Emerging Trends) 18. 0 CME Credits Postgraduate Course 12. 0 CME Credits/***11. 75 Contact Hours Basic Research Workshop4. 0 CME Credits AASLD/IASL Program*4. 0 CME Credits Hepatology Associates Course5. 5 CME Credits/***5. 0 Contact Hours AASLD/ILTS Transplant Course* 7. 5 CME Credits/***6. 0 Contact Hours AASLD/NASPGHAN Pediatric Symposium** 3. 0 CME selleck chemicals Credits AASLD/ASGE Endoscopy Course** 6. 5 CME Credits Maintenance of Certification 2. 0 CME Credits *These activities have been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of the American Association for the Study of Liver Diseases (AASLD), and the International Liver Transplantation Society (ILTS) and the International Association for the Study of the Liver (IASL). AASLD is accredited by the ACCME to provide continuing medical education for physicians. **Co-sponsored activity: The American Association for the Study of Liver Diseases (AASLD) is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

16, 17 With this limited genome, HCV replicates in hepatocytes by relying on cellular systems, thereby co-opting cellular proteins in its life cycle. To date, HCV particles have been found to contain more than 10

host lipoproteins.11, 12 Incorporation of these host proteins into HCV virions may not be cancer metabolism inhibitor random, as other enveloped viruses selectively obtain host proteins. For example, HIV-1 selectively acquires more than 40 host proteins, but excludes some proteins such as CD4, CD45, CXCR4, CCR3, and CCR5, which are all highly expressed on HIV-1-infected cells.20 It is believed that HIV-1 acquires biologically functional RCA proteins during viral budding at the plasma membrane. HCV, however, may acquire CD59 while budding through the membranes of intracellular organelles rather than at the plasma membrane because HCV may exit the cells by way of a secretory pathway.21 FACS and western blot data in this study showed that human hepatocytes expressed high levels of intracellular and surface CD59 without a difference in their molecular weights (Fig. 1), thereby providing a possible

source for HCV to encounter and obtain CD59 in intracellular organelles such as the ER. Identifying these interactions is critical for understanding the life cycle of HCV, and may yield novel targets for development of therapeutic strategies. To date, abrogation of RCA function to regain antivirus Ab activity against enveloped viruses has only been selleck kinase inhibitor tested in vitro in artificial environments such as GVB systems.2, 5, 6, 8 These systems provide optimized conditions for complement activation in vitro, but have no clinical relevance because they do not adequately replicate in vivo conditions. In this study, CD59 blockers were directly added into patient plasma to abrogate the function of CD59 on the patient’s own viral particles,

resulting in destruction of primary virions. The enhanced virolysis was likely triggered by ADCML, as all six individuals chronically infected with HCV showed high titers of anti-E2 Abs and potent complement activity. ADCML efficacy, however, significantly varied among these samples, which may be affected by many factors including the nature of the host immune response, HCV virological features, and patient profiles, see more because they all affect the outcome of HCV infection. For example, HCV from patient Pt42 was one of the most resistant viruses to the ADCML. Accordingly, this patient had the lowest anti-HCV E2 Ab titer among all six patients examined. However, our sample size is too small to analyze the correlation between the Ab titer and virolysis. In addition, anti-HCV E1 Abs in plasma samples from these patients were not titrated. Thus, further investigations with large clinical samples are required to analyze the correlation of anti-HCV E1/E2 Ab titers and virolysis efficacy.

Yavuz Beyazit M.D.*, Murat Kekilli M.D.*, Tugrul Purnak M.D.†, Mevlut Kurt M.D.*, * Department of Gastroenterology, Turkiye Yuksek Ihtisas 20s Proteasome activity Hospital, Ankara, Turkey, † Department of Gastroenterology, Ankara Numune Education and Research Hospital, Ankara, Turkey. “
“The human hepatitis B virus (HBV) causes acute and chronic infections in humans and

chimpanzees. HBV infects its hosts at minimal inoculation doses and replicates exclusively in hepatocytes. The viral determinants for the pronounced species specificity and the high efficacy to address hepatocytes in vivo are unknown. Previous findings showed that N-terminally myristoylated peptides constituting a receptor binding domain of the HBV large envelope (L)-protein block HBV entry in vitro and in vivo. Here we investigate the ability of such peptidic receptor ligands to target the liver. Injection of radioactively labeled HBVpreS-lipopeptides resulted in rapid accumulation in livers of mice, rats, and dogs but not cynomolgus

monkeys. Without lipid moiety the peptide was excreted by renal filtration, indicating its possible retention through the lipid by serum factors. Organ distribution studies of 26 HBVpreS peptide variants revealed a correlation of HBV infection inhibition activity and the ability to target mouse livers. Together with complementary studies using primary hepatocytes of different species, we hypothesize that HBV hepatotropism is mediated through specific binding of the myristoylated N-terminal preS1-domain of the HBV L-protein to a hepatocyte specific receptor. Moreover, the restricted infectivity of HBV to human primates is selleck not generally determined click here by the absence of this binding receptor in nonsusceptible hosts

(e.g., mice) but related to postbinding step(s) (e.g., membrane fusion). Conclusion: HBVpreS-lipopeptides target to the liver. This observation has important clinical implications regarding the pharmacokinetic properties of Myrcludex B, the first entry inhibitor for HBV/HDV. In addition, this provides the basis for the application of the peptides as vehicles for hepatocyte-specific drug targeting. (HEPATOLOGY 2013) See Editorial on Page 9 DMSO, dimethylsulfoxide; ge, genome equivalent; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; HDV, hepatitis delta virus; L-protein, hepatitis B virus large surface protein; PHH, primary human hepatocytes; PTH, primary Tupaia hepatocytes; p.i., postinfection; RP-HPLC, reversed-phase high-performance liquid chromatography; SPECT/CT, single photon emission computed tomography/computed tomography. The human hepatitis B virus (HBV) causes acute and chronic liver infections. Worldwide, 350 million people are persistently infected.1 Chronic HBV will remain a major global health problem, despite the availability of vaccines. Therapies (interferon-alpha [IFNα] and five nucleoside analogs) are limited and mostly noncurative.