Globalization and the Changing Epidemiology of Hepatitis A Virus

Jacobsen, Kathryn H.

doi:10.1101/cshperspect.a031716

Cited by 129 publications

(198 citation statements)

References 64 publications

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“…Paradoxically, in low endemic countries most children and adults remain susceptible to symptomatic infection and disease burden is high[ 11 ]. Global distribution is depicted in Figure 1 [ 12 ].…”

Section: Epidemiology Of Viral Hepatitismentioning

confidence: 99%

Update on global epidemiology of viral hepatitis and preventive strategies

Jefferies

Rauff

Rashid

et al. 2018

WJCC

294

199

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Viral hepatitis is one of the major public health concerns around the world but until recently it has drawn little attention or funding from global health policymakers. Every year 1.4 million people die from viral hepatitis-related cirrhosis and liver cancer. However, the majority of the infected population are unaware of their condition. This population have significant obstacles to overcome such as lack of awareness, vulnerability, increased migration, disease stigma, discrimination, as well as poor health resources, conflict in policy development and program implementation. Despite implementing infection control measures over the last few decades eradication or significant disease reduction remains elusive. This study aims to present the current global prevalence status and examines potential elimination strategies. The information for this research were obtained through a systematic review, published scientific literatures, the official websites of various government organisations, international public health organisations and internationally recognised regulatory bodies over a period of 40 years between 1978 and 2018.

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Section: Epidemiology Of Viral Hepatitismentioning

confidence: 99%

Update on global epidemiology of viral hepatitis and preventive strategies

Jefferies

Rauff

Rashid

et al. 2018

WJCC

294

199

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“…H epatitis A virus (HAV) is an unusual hepatotropic picornavirus. Classified within the genus Hepatovirus, it is an ancient human pathogen that remains a common cause of enterically transmitted hepatitis globally (1). It infects susceptible individuals in a stealth-like manner, replicating efficiently in the liver and releasing newly replicated virus through the biliary track to the intestines from which it is shed in feces (2,3).…”

mentioning

confidence: 99%

Redundant Late Domain Functions of Tandem VP2 YPX ₃ L Motifs in Nonlytic Cellular Egress of Quasi-enveloped Hepatitis A Virus

González‐López

Rivera-Serrano

et al. 2018

J Virol

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The quasi-envelopment of hepatitis A virus (HAV) capsids in exosome-like virions (eHAV) is an important but incompletely understood aspect of the hepatovirus life cycle. This process is driven by recruitment of newly assembled capsids to endosomal vesicles into which they bud to form multivesicular bodies with intraluminal vesicles that are later released at the plasma membrane as eHAV. The endosomal sorting complexes required for transport (ESCRT) are key to this process, as is the ESCRT-III-associated protein, ALIX, which also contributes to membrane budding of conventional enveloped viruses. YPXL late domains in the structural proteins of these viruses mediate interactions with ALIX, and two such domains exist in the HAV VP2 capsid protein. Mutational studies of these domains are confounded by the fact that the Tyr residues (important for interactions of YPXL peptides with ALIX) are required for efficient capsid assembly. However, single Leu-to-Ala substitutions within either VP2 YPXL motif (L1-A and L2-A mutants) were well tolerated, albeit associated with significantly reduced eHAV release. In contrast, simultaneous substitutions in both motifs (L1,2-A) eliminated virus release but did not inhibit assembly of infectious intracellular particles. Immunoprecipitation experiments suggested that the loss of eHAV release was associated with a loss of ALIX recruitment. Collectively, these data indicate that HAV YPXL motifs function as redundant late domains during quasi-envelopment and viral release. Since these motifs present little solvent-accessible area in the crystal structure of the naked extracellular capsid, the capsid structure may be substantially different during quasi-envelopment. Nonlytic release of hepatitis A virus (HAV) as exosome-like quasi-enveloped virions is a unique but incompletely understood aspect of the hepatovirus life cycle. Several lines of evidence indicate that the host protein ALIX is essential for this process. Tandem YPXL "late domains" in the VP2 capsid protein could be sites of interaction with ALIX, but they are not accessible on the surface of an X-ray model of the extracellular capsid, raising doubts about this putative late domain function. Here, we describe YPXL domain mutants that assemble capsids normally but fail to bind ALIX and be secreted as quasi-enveloped eHAV. Our data support late domain function for the VP2 YPXL motifs and raise questions about the structure of the HAV capsid prior to and following quasi-envelopment.

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“…Due to the improvement in socioeconomic levels in many South American countries, a decrease in HAV seroprevalence rates is estimated to occur . Therefore, the risk of hepatitis A outbreaks may increase as a consequence of a growing number of susceptible individuals …”

Section: Introductionmentioning

confidence: 95%

Poor response to hepatitis A vaccination in hematopoietic stem cell transplant recipients

Adati

Silva

Sumita

et al. 2020

Transplant Infectious Dis

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Background Hepatitis A virus (HAV) infection is highly prevalent in developing countries. In countries experiencing a shift from intermediate/high endemicity to low endemicity, the World Health Organization recommends the incorporation of HAV vaccine into the national vaccination calendar for children aged ≥1 year. Since HAV antibodies wane over time, most HSCT revaccination guidelines advise vaccination as optional, following the country recommendation. However, no study has evaluated the serological response to HAV vaccine in allogeneic HSCT recipients. Methods We conducted a prospective study in 46 HSCT recipients who received two doses of inactivated HAV vaccine. Blood samples were taken before vaccination to determine HAV prevalence rates, and before and 4‐6 weeks after the second dose. Specific anti‐HAV antibodies were detected by a competitive commercial enzyme immune assay. Results Patients received the first dose of vaccine at a median of 332.5 (120‐4134) days after HSCT. Median absolute lymphocyte count at vaccination was 1947 (696‐12 500)/mm3. The seroprevalence rate was 93.5% at inclusion. Although safe and well tolerated, the serological response to HAV vaccine in susceptible patients was poor (33%), and no boost effect was observed in seropositive patients. Conclusions In areas with intermediate/high seroprevalence of HAV, serology should be recommended prior to referral to vaccination. The mechanisms of antibody interference and how to overcome T‐cell function deficiency need to be better understood in transplant populations receiving HAV vaccine. Alternative schedules of HAV vaccination should be evaluated in prospective trials.

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Globalization and the Changing Epidemiology of Hepatitis A Virus

Cited by 129 publications

References 64 publications

Update on global epidemiology of viral hepatitis and preventive strategies

Update on global epidemiology of viral hepatitis and preventive strategies

Redundant Late Domain Functions of Tandem VP2 YPX ₃ L Motifs in Nonlytic Cellular Egress of Quasi-enveloped Hepatitis A Virus

Poor response to hepatitis A vaccination in hematopoietic stem cell transplant recipients

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Globalization and the Changing Epidemiology of Hepatitis A Virus

Cited by 129 publications

References 64 publications

Update on global epidemiology of viral hepatitis and preventive strategies

Update on global epidemiology of viral hepatitis and preventive strategies

Redundant Late Domain Functions of Tandem VP2 YPX 3 L Motifs in Nonlytic Cellular Egress of Quasi-enveloped Hepatitis A Virus

Poor response to hepatitis A vaccination in hematopoietic stem cell transplant recipients

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Redundant Late Domain Functions of Tandem VP2 YPX ₃ L Motifs in Nonlytic Cellular Egress of Quasi-enveloped Hepatitis A Virus