Historical Trends in the Hepatitis C Virus Epidemics in North America and Australia

Rodrigo, Chaturaka; Eltahla, Auda A.; Bull, Rowena A.; Grebely, Jason; Dore, Gregory J.; Applegate, Tanya; Page, Kimberly; Bruneau, Julie; Morris, Meghan D.; Cox, Andrea L.; Osburn, William O.; Kim, Arthur Y.; Schinkel, Janke; Shoukry, Naglaa H.; Lauer, Georg M.; Maher, Lisa; Hellard, Margaret; Prins, Maria; Estes, Chris; Razavi, Homie; Lloyd, Andrew R.; Luciani, Fabio

doi:10.1093/infdis/jiw389

Cited by 18 publications

(14 citation statements)

References 39 publications

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“…Full protection was achieved until one day before vaccination and decreased to 17% until one day after challenge, while administration three days after challenge did not show protection. 113 Interestingly, similarly to observations made by Marzi et al in an EBOV post-exposure vaccine model, 74 an rVSV vector vaccine control also mediated partial protection when given one day pre-challenge. 113 Antibody generation was associated with protection 113 and a serumtransfer experiment confirmed that protection was antibodydependent.…”

Section: Nipah Virussupporting

confidence: 62%

“…Surprisingly, however, post-exposure prophylaxis with an rVSV-vectored vaccine against Marburg virus conferred similar protection against EVD, and the authors argued that VSV-driven innate immune activation as well as filovirus-specific immune responses may play a role in protection from EVD. 74 Of note, compared to the disease course in humans, the onset of clinical disease is faster and its manifestation more severe in the NHP model, with a lethality of close to 100%. When NHPs were challenged with Sudan ebolavirus (SUDV), which leads to lethal disease in NHP later than does EBOV, 100% of NHP were protected when vaccinated with rVSV-SUDV 20-30 min p.i.…”

Section: Correlates Of Protection and Duration Of Immune Responsesmentioning

confidence: 99%

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Recombinant vesicular stomatitis virus vector vaccines for WHO blueprint priority pathogens

Fathi

Dahlke

Addo

2019

Human Vaccines & Immunotherapeutics

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The devastating Ebola virus (EBOV) outbreak in West Africa in 2013-2016 has flagged the need for the timely development of vaccines for high-threat pathogens. To be better prepared for new epidemics, the WHO has compiled a list of priority pathogens that are likely to cause future outbreaks and for which R&D efforts are, therefore, paramount (R&D Blueprint: https://www.who.int/blueprint/priority-diseases/en/). To this end, the detailed characterization of vaccine platforms is needed. The vesicular stomatitis virus (VSV) has been established as a robust vaccine vector backbone for infectious diseases for well over a decade. The recent clinical trials testing the vaccine candidate VSV-EBOV against EBOV disease now have added a substantial amount of clinical data and suggest VSV to be an ideal vaccine vector candidate for outbreak pathogens. In this review, we discuss insights gained from the clinical VSV-EBOV vaccine trials as well as from animal studies investigating vaccine candidates for Blueprint pathogens. ARTICLE HISTORY

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Section: Nipah Virussupporting

confidence: 62%

Section: Correlates Of Protection and Duration Of Immune Responsesmentioning

confidence: 99%

Recombinant vesicular stomatitis virus vector vaccines for WHO blueprint priority pathogens

Fathi

Dahlke

Addo

2019

Human Vaccines & Immunotherapeutics

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“…94.7% of Australian sequences in clade 1 contained Q80 in NS3 and clustered in a strongly supported sub-cluster with other NS3 Q80 sequences, likely representing previously described sub-clade 1C [ 51 ]. Phylogenetic separation has been reported for subtype 1a sequences from North America and Australia [ 53 ], and Bayesian estimates place the origin of the epidemics for both continents around the early 20 th century coinciding with World War I [ 54 ]. Geographical separation of the continents likely resulted in genetically distinct sequences due to a founder effect in the two regions, which may also explain the relative absence of the NS3 Q80K polymorphism in the Australian sequences.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C virus genetic diversity by geographic region within genotype 1-6 subtypes among patients treated with glecaprevir and pibrentasvir

et al. 2018

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Hepatitis C virus (HCV) is genetically diverse and includes 7 genotypes and 67 confirmed subtypes, and the global distribution of each HCV genotype (GT) varies by geographic region. In this report, we utilized a large dataset of NS3/4A and NS5A sequences isolated from 2348 HCV GT1-6-infected patients treated with the regimen containing glecaprevir/pibrentasvir (GLE/PIB) to assess genetic diversity within HCV subtypes by geographic region using phylogenetic analyses, and evaluated the prevalence of baseline amino acid polymorphisms in NS3 and NS5A by region/country and phylogenetic cluster. Among 2348 NS3/4A and NS5A sequences, phylogenetic analysis identified 6 genotypes and 44 subtypes, including 3 GT1, 8 GT2, 3 GT3, 13 GT4, 1 GT5, and 16 GT6 subtypes. Phylogenetic analysis of HCV subtype 1a confirmed the presence of two clades, which differed by geographic region distribution and NS3 Q80K prevalence. We detected phylogenetic clustering by country in HCV subtypes 1a, 1b, 2a, 2b, and 5a, suggesting that genetically distinct virus lineages are circulating in different countries. In addition, two clades were detected in HCV GT4a and GT6e, and NS5A amino acid polymorphisms were differentially distributed between the 2 clades in each subtype. The prevalence of NS3 and NS5A baseline polymorphisms varied substantially by genotype and subtype; therefore, we also determined the activity of GLE or PIB against replicons containing NS3/4A or NS5A from HCV GT1-6 clinical samples representing 6 genotypes and 21 subtypes overall. GLE and PIB retained activity against the majority of HCV replicons containing NS3/4A or NS5A from HCV GT1-6 clinical samples, with a median EC50 of 0.29 nM for GLE and 1.1 pM for PIB in a transient replicon assay. The data presented in this report expands the available data on HCV epidemiology, subtype diversity by geographic region, and NS3 and NS5A baseline polymorphism prevalence.

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“…Hence, the outcome of Spanish efforts to control HCV1a spread is also dependent on reducing the prevalence in the groups that are at most risk in other European countries and North America. Given that PWID are the major source of ongoing HCV transmission in these countries [26], this calls for an intensification of close follow-up and treatment in this population, as well as needle exchange and opioid substitution programmes. Of note, the absence of clear phylogenetic structuring of other HCV subtypes in European PWID by geographical region indicates that the pattern that we recovered for subtype 1a may be a general one [27].…”

Section: Discussionmentioning

confidence: 99%

“…During the second half of the 20th century, there was a continuous improvement in medical procedures, paralleled by other societal changes that resulted in a shift from mostly iatrogenic spread to an epidemic with injecting drug use as the main risk factor for HCV1a transmission in resource rich settings [26], including Spain [12]. Unfortunately, we could not directly assess this because data on risk behaviour were not available.…”

Section: Discussionmentioning

confidence: 99%

Increasing importance of European lineages in seeding the hepatitis C virus subtype 1a epidemic in Spain

Pérez¹,

Vrancken

Chueca³

et al. 2019

Eurosurveillance

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Background Reducing the burden of the hepatitis C virus (HCV) requires large-scale deployment of intervention programmes, which can be informed by the dynamic pattern of HCV spread. In Spain, ongoing transmission of HCV is mostly fuelled by people who inject drugs (PWID) infected with subtype 1a (HCV1a). Aim Our aim was to map how infections spread within and between populations, which could help formulate more effective intervention programmes to halt the HCV1a epidemic in Spain. Methods Epidemiological links between HCV1a viruses from a convenience sample of 283 patients in Spain, mostly PWID, collected between 2014 and 2016, and 1,317, 1,291 and 1,009 samples collected abroad between 1989 and 2016 were reconstructed using sequences covering the NS3, NS5A and NS5B genes. To efficiently do so, fast maximum likelihood-based tree estimation was coupled to a flexible Bayesian discrete phylogeographic inference method. Results The transmission network structure of the Spanish HCV1a epidemic was shaped by continuous seeding of HCV1a into Spain, almost exclusively from North America and European countries. The latter became increasingly relevant and have dominated in recent times. Export from Spain to other countries in Europe was also strongly supported, although Spain was a net sink for European HCV1a lineages. Spatial reconstructions showed that the epidemic in Spain is diffuse, without large, dominant within-country networks. Conclusion To boost the effectiveness of local intervention efforts, concerted supra-national strategies to control HCV1a transmission are needed, with a strong focus on the most important drivers of ongoing transmission, i.e. PWID and other high-risk populations.

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Historical Trends in the Hepatitis C Virus Epidemics in North America and Australia

Cited by 18 publications

References 39 publications

Recombinant vesicular stomatitis virus vector vaccines for WHO blueprint priority pathogens

Recombinant vesicular stomatitis virus vector vaccines for WHO blueprint priority pathogens

Hepatitis C virus genetic diversity by geographic region within genotype 1-6 subtypes among patients treated with glecaprevir and pibrentasvir

Increasing importance of European lineages in seeding the hepatitis C virus subtype 1a epidemic in Spain

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