Superinfection of hepatitis A virus in hepatocytes infected with hepatitis B virus

Win, Nan Nwe; Ogawa, Masahiro; Nakamoto, Shingo; Haga, Yuki; Sasaki, Reina; Nakamura, Masato; Wu, Shuang; Matsumoto, Naoki; Matsuoka, Satoshi; Kato, Naoya; Shirasawa, Hiroshi; Yokosuka, Osamu; Okamoto, Hiroaki; Moriyama, Mitsuhiko

doi:10.7150/ijms.32795

Cited by 9 publications

(8 citation statements)

References 17 publications

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“…Moreover, evidence suggests that HAV internal ribosomal entry-site (IRES) is an attractive target of antiviral agents against HAV and the JAK2 inhibitor AZD1480 can inhibit IRES activity and HAV replication [75,76]. Recently, Japanese miso extracts have been reported to have inhibitory effects on HAV replication not only in patients infected with HAV but also in patients superinfected with HAV and HBV [9].…”

Section: Discussionmentioning

confidence: 99%

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The global trends and regional differences in incidence and mortality of hepatitis A from 1990 to 2019 and implications for its prevention

et al. 2021

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Background and purpose Despite decades of improved sanitation and hygiene measures and vaccine introduction, hepatitis A has been spread through numerous outbreaks globally. We used data from the Global Burden of Disease (GBD) study to quantify hepatitis A burden at the global, regional and national levels. Methods Annual incident cases, deaths, age-standardized incidence rates (ASIRs), and age-standardized mortality rates (ASMRs) of hepatitis A between 1990 and 2019 were derived from the GBD study 2019. Percentage changes of cases and deaths, and estimated annual percentage changes (EAPCs) of ASIRs and ASMRs were calculated to quantify their temporal trends. Results Global hepatitis A incident cases increased by 13.90% from 139.54 million in 1990 to 158.94 million in 2019. ASIR of hepatitis A remained stable (EAPC = 0.00, 95% CI −0.01 to 0.01), whereas ASMR decreased (EAPC = −4.63, 95% CI −4.94 to −4.32) between 1990 and 2019. ASIR increased in low (EAPC = 0.09, 95% CI 0.04 to 0.14) and low-middle (EAPC = 0.04, 95% CI 0.03 to 0.06) socio-demographic index (SDI) regions. For GBD regions, the most significant increases of ASIR were detected in high-income Asia Pacific (EAPC = 0.53, 95% CI 0.41 to 0.66), Oceania (EAPC = 0.31, 95% CI 0.25 to 0.36), and Australasia (EAPC = 0.28, 95% CI 0.13 to 0.44). EAPC of ASIR was positively associated with SDI value in countries and territories with SDI value ≥ 0.7 (ρ = −0.310, p < 0.001). Conclusion There is an unfavorable trend that hepatitis A is still pending in hyperendemic regions and is emerging in low endemic regions. These highlight the need of targeted and specific strategies to eliminate hepatitis A, such as sanitation measures and a comprehensive plan for surveillance and vaccination against hepatitis A.

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Section: Discussionmentioning

confidence: 99%

“…HAV infection is the second largest cause of fulminant viral hepatitis characterized by massive hepatocyte necrosis and inflammatory infiltrate after hepatitis B virus (HBV) infection [ 8 ]. In addition, superinfection of HAV with HBV is also a health problem in regions with high endemicity levels both of HAV and HBV [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

The global trends and regional differences in incidence and mortality of hepatitis A from 1990 to 2019 and implications for its prevention

et al. 2021

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“…We demonstrated that the HAV replication is similar between HepG2.2.15 and HepG2, 96 h after HAV infection. However, HBV replication is inhibited in HAV-infected HepG2.2.15, compared to HepG2.2.15 without HAV infection [ 73 ].…”

Section: Coinfection Of Hav With Hbvmentioning

confidence: 99%

“…We also observed that the replication of both HAV and HBV is suppressed in human hepatocyte PXB cells superinfected with HAV and HBV, compared to those mono-infected with HAV or HBV [ 73 ]. Thus, HAV infection seems to inhibit HBV replication.…”

Section: Coinfection Of Hav With Hbvmentioning

confidence: 99%

“…Japanese rice-koji miso extracts enhanced GRP78 expression and inhibited HAV HA11-1299 genotype IIIA strain replication in the human hepatocytes, Huh7 and PXB cells [ 97 ]. We investigated the effect of miso extracts on virus replication in HepG2.2.15 cells infected with the HAV HA11-1299 strain [ 73 ]. It is noteworthy that miso extracts have an inhibitory effect on HAV replication but no inhibitory effect on HBV replication.…”

Section: Prevention Of Hav Infection In Patients With Chronic LIVmentioning

confidence: 99%

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Co-Occurrence of Hepatitis A Infection and Chronic Liver Disease

Sasaki

Masuzaki

Takahashi

et al. 2020

IJMS

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Hepatitis A virus (HAV) infection occasionally leads to a critical condition in patients with or without chronic liver diseases. Acute-on-chronic liver disease includes acute-on-chronic liver failure (ACLF) and non-ACLF. In this review, we searched the literature concerning the association between HAV infection and chronic liver diseases in PubMed. Chronic liver diseases, such as metabolic associated fatty liver disease and alcoholic liver disease, coinfection with other viruses, and host genetic factors may be associated with severe hepatitis A. It is important to understand these conditions and mechanisms. There may be no etiological correlation between liver failure and HAV infection, but there is an association between the level of chronic liver damage and the severity of acute-on-chronic liver disease. While the application of an HAV vaccination is important for preventing HAV infection, the development of antivirals against HAV may be important for preventing the development of ACLF with HAV infection as an acute insult. The latter is all the more urgent given that the lives of patients with HAV infection and a chronic liver disease of another etiology may be at immediate risk.

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