The Prevalence and Serological Association of Hepatitis D Virus Genotypes in Taiwan.

Keva Joseph,Jee-Fu Huang,Tyng-Yuan Jang,Shu-Chi Wang,Ming-Lung Yu,Chia-Yen Dai,Wan-Long Chuang,Chung-Feng Huang,Ciniso Sylvester Shabangu

doi:10.3390/pathogens10101227

Abstract

Hepatitis Delta Virus (HDV) is an RNA virus that requires the presence of hepatitis B surface antigen (HBsAg) to propagate into hepatocytes, with Genotype I being more prevalent globally. However, the prevalence of HDV genotypes in Taiwan is unknown. Accordingly, a cohort including 24 chronic HBV patients who received nucleos(t)ides (NUCs) between January 2002 and July 2018 was used to determine HDV genotypes and genotype specific serological association in chronic HBV carriers. HDV-positive genotypes in 18/24 (75%) males and 6/24 (25%) females were identified among chronic HBV patients. Viremia was lower in HDV-IV patients than in patients affected with other HDV genotypes (1.34 log10 copies/mL vs. 3.30 log10 copies/mL; p = 0.009). A logistics regression analysis revealed that HDV-IV was inversely proportional to HDV RNA (odds ratio [OR]/95% confidence intervals [CI]: 0.370/0.164–0.830; p = 0.017). The serologic association study indicated lower levels of creatinine (p = 0.047) and HDV-RNA (p = 0.009) in the HDV-IV group than the non-HDV-IV group but did not indicate any significant differences in the AST, ALT, bilirubin levels or other laboratory test factors. The three genotypes evident in Taiwan were HDV-I (4/24, 16.7%), HDV-II (6/24, 25.0%), and HDV-IV (14/24, 58.3%), and HDV-IV is the predominant HDV genotype in Taiwan. These results anticipate a clear understanding of HDV genotype serological association in chronic HBV carriers.

Highlights

The hepatitis delta virus (HDV) was discovered and detected in the nuclei of hepatocytes of patients who tested seropositive for hepatitis B virus (HBV) surface antigen (HBsAg) [1]
It is referred to as a defective RNA virus [4]. This notwithstanding, key modified pathways related to fibrosis, epigenetic changes, immune response, specific dysregulation of long non-coding RNA, and proteomic changes have all been suggested to promote hepatocellular carcinoma (HCC) development [5,6]
Hepatitis Delta Virus (HDV) has two clinical presentations: co-infection and superinfection with HBV, where co-infection is the ability of HDV and HBV to infect a host simultaneously in an acute phase, and superinfection refers to chronic

Summary

Introduction

The hepatitis delta virus (HDV) was discovered and detected in the nuclei of hepatocytes of patients who tested seropositive for hepatitis B virus (HBV) surface antigen (HBsAg) [1]. Is approximately 35–37 nm in diameter with a small, single circular RNA genome approximating 1672–1700 nucleotides, enveloped by HBsAg—a key feature that perpetuates the ability of the virus to hijack the machinery of the hosts’ cellular functions [2,3]. It is, referred to as a defective RNA virus [4]. HDV has two clinical presentations: co-infection and superinfection with HBV, where co-infection is the ability of HDV and HBV to infect a host simultaneously in an acute phase, and superinfection refers to chronic

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