scholarly journals Adenosine Dioxolane Nucleoside Phosphoramidates As Antiviral Agents for Human Immunodeficiency and Hepatitis B Viruses

2013 ◽  
Vol 4 (8) ◽  
pp. 747-751 ◽  
Author(s):  
Lavanya Bondada ◽  
Mervi Detorio ◽  
Leda Bassit ◽  
Sijia Tao ◽  
Catherine M. Montero ◽  
...  
Keyword(s):  
Hepatitis B ◽  
Antiviral Agents ◽  
Nucleoside Phosphoramidates

scholarly journals A211 SPONTANEOUS HBV REMISSION AFTER HBV REACTIVATION FOLLOWING TREATMENT WITH SOFOSBUVIR AND VELPATASVIR IN A PATIENT WITH HCV AND HBV CO-INFECTION: CASE REPORT

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 242-243
Author(s):  
A Chiang ◽  
K Tsoi
Keyword(s):  
Hepatitis C ◽  
Hepatitis B ◽  
Antiviral Agents ◽  
Clinical Signs ◽  
Hbv Dna ◽  
Hcv Rna ◽  
Hbv Reactivation ◽  
Genotype 3 ◽  
Direct Acting Antiviral ◽  
Direct Acting

Abstract Background In co-infected patients with hepatitis B (HBV) and hepatitis C (HCV), the treatment of HCV with direct-acting antiviral agents (DAA) can cause HBV reactivation. However, there are no clear guidelines on the timing of treatment initiation, especially in the absence of clinical signs of flare. Aims Here we discuss the case of a 34-year-old female with HBV and HCV genotype 3 who had HBV reactivation following HCV treatment, but did not require nucleos(t)ide therapy. Methods She initially presented with chronic inactive hepatitis B and chronic hepatitis C with HBV DNA level of 67.5 IU/mL and HCV RNA level of 3.33 x 106 IU/mL. She completed a 12 week course of sofosbuvir and velpatasvir for HCV and achieved sustained virologic remission, but subsequently developed reactivation of her HBV with HBV DNA peaking at 3.41 x 104 IU/mL twelve weeks post-treatment. She did not develop any signs of hepatitis and a decision was made to monitor her clinically. Results Two years later, she spontaneously went into remission with her HBV DNA levels being <10 IU/mL. Conclusions The significance of this case is to illustrate HBV reactivation following treatment of HCV with DAAs may not necessitate immediate treatment, especially if there are no signs of flare. There have been similar reported cases, but larger prospective studies are required to determine the appropriate clinical context where monitoring may be acceptable instead of immediate treatment. Funding Agencies None

Association of intrahepatic cccDNA reduction with the improvement of liver histology in chronic hepatitis B patients receiving oral antiviral agents

2011 ◽  
Vol 83 (4) ◽  
pp. 602-607 ◽  
Author(s):  
Pin-Nan Cheng ◽  
Wen-Chun Liu ◽  
Hung-Wen Tsai ◽  
I-Chin Wu ◽  
Ting-Tsung Chang ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Antiviral Agents ◽  
Liver Histology

The effects of antiviral agents on serum hepatitis B e antigen levels in chronic type B hepatitis

1988 ◽  
Vol 3 (2) ◽  
pp. 143-152 ◽  
Author(s):  
KIYOHIKO KURAI ◽  
SHIRO IINO ◽  
KAZUHIKO KOIKE ◽  
KEIJI MITAMURA ◽  
YASUO ENDO ◽  
...  
Keyword(s):  
Hepatitis B ◽  
Antiviral Agents ◽  
Type B ◽  
Serum Hepatitis ◽  
Hepatitis B E Antigen ◽  
Chronic Type

scholarly journals The Yin and the Yang of Treatment for Chronic Hepatitis B—When to Start, When to Stop Nucleos(t)ide Analogue Therapy

Viruses ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 934 ◽  
Author(s):  
Samuel Hall ◽  
Jessica Howell ◽  
Kumar Visvanathan ◽  
Alexander Thompson
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Antiviral Agents ◽  
Standard Of Care ◽  
Current Standard ◽  
Hbsag Loss ◽  
Personalised Treatment ◽  
Treat All

Over 257 million individuals worldwide are chronically infected with the Hepatitis B Virus (HBV). Nucleos(t)ide analogues (NAs) are the first-line treatment option for most patients. Entecavir (ETV) and tenofovir disoproxil fumarate (TDF) are both potent, safe antiviral agents, have a high barrier to resistance, and are now off patent. They effectively suppress HBV replication to reduce the risk of cirrhosis, liver failure, and hepatocellular carcinoma (HCC). Treatment is continued long-term in most patients, as NA therapy rarely induces HBsAg loss or functional cure. Two diverging paradigms in the treatment of chronic hepatitis B have recently emerged. First, the public health focussed “treat-all” strategy, advocating for early and lifelong antiviral therapy to minimise the risk of HCC as well as the risk of HBV transmission. In LMICs, this strategy may be cost saving compared to monitoring off treatment. Second, the concept of “stopping” NA therapy in patients with HBeAg-negative disease after long-term viral suppression, a personalised treatment strategy aiming for long-term immune control and even HBsAg loss off treatment. In this manuscript, we will briefly review the current standard of care approach to the management of hepatitis B, before discussing emerging evidence to support both the “treat-all” strategy, as well as the “stop” strategy, and how they may both have a role in the management of patients with chronic hepatitis B.

scholarly journals Liver Fibrosis Progression and Mortality in Hepatitis B– and C–Coinfected Persons Treated With Directly Acting Antiviral Agents: Results From ERCHIVES

2019 ◽  
Vol 71 (3) ◽  
pp. 664-666 ◽  
Author(s):  
Adeel A Butt ◽  
Peng Yan ◽  
Samia Aslam ◽  
Abdul-Badi Abou-Samra ◽  
Kenneth E Sherman ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hepatitis B Virus ◽  
Liver Fibrosis ◽  
Hepatitis B ◽  
Confidence Intervals ◽  
Antiviral Agents ◽  
Virologic Response ◽  
Fibrosis Progression ◽  
B Virus

Abstract For persons with baseline Fibrosis-4 1.46–3.25, cirrhosis incidence/1000 patient-years was 49.3 among hepatitis B virus (HBV)/hepatitis C virus (HCV) coinfected and 18.2 among HCV monoinfected (P = .03). Cirrhosis risk was numerically higher but statistically nonsignificant among HBV/HCV coinfected (hazards ratio [HR] 1.51; 95% confidence intervals [CI], .37–6.05) but lower among those who attained sustained virologic response (HR, .52; 95% CI, .42–.63).

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