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As well as being an important clinical pathogen, HCV is also interesting in terms of fundamental research as it is one of the most variable pathogens known to infect humans.
Anti-envelope antibody responses in individuals at high risk of hepatitis C virus who resist infection.
Tracking TCRAY sequence clonotype expansions during antiviral therapy using high-throughput sequencing of the hypervariable region. Hepatitis C virus induced degradation of cell death-inducing DFFA-like effector B leads to hepatic lipid dysregulation. Polyprotein driven formation of two interdependent sets of complexes supporting hepatitis C virus genome replication. Cohort study of the impact of direct acting antiviral therapy in patients with chronic hepatitis C and decompensated cirrhosis.
Broad anti-HCV antibody responses are associated with improved clinical disease parameters in chronic HCV infection.
Inhibition of hepatitis C virus RNA replication by ISG15 does not require its conjugation to protein substrates by the HERC5 E3 ligase. Spatiotemporal reconstruction of the introduction of hepatitis C virus into Scotland and its subsequent regional transmission.
Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection. The mechanism of interferon refractoriness during hepatitis C virus Infection and Its reversal with a peroxisome proliferator-activated receptor I± agonist.
Waiting time and transplantation for hepatocellular cancer: a balance between tempus fugit and carpe diem. Elevated interferon-stimulated gene transcription in peripheral blood mononuclear cells occurs in patients infected with genotype 1 but not genotype 3 hepatitis C virus. Next generation sequencing sheds light on the natural history of hepatitis C infection in patients that fail treatment.
Modulation of triglyceride and cholesterol ester synthesis impairs assembly of infectious hepatitis C virus.
Genetic complementation of hepatitis C virus nonstructural protein functions associated with replication exhibits requirements that differ from those for virion assembly. Determining the cellular diversity of hepatitis C virus quasispecies by single-cell viral sequencing. Non cell autonomous upregulation of CDKN2 transcription linked to progression of chronic hepatitis C disease. Bidirectional lipid droplet velocities are controlled by differential binding strengths of HCV Core DII protein.
Fluorescence lifetime imaging of alterations to cellular metabolism by domain 2 of the Hepatitis C virus core protein. Increasing rate of cleavage at boundary between non-structural proteins 4B and 5A inhibits replication of Hepatitis C virus. Structural analysis of Hepatitis C virus core-E1 signal peptide and requirements for cleavage of the genotype 3a signal sequence by signal peptide peptidase.
Intravascular transfer contributes to postprandial increase in numbers of very-low-density hepatitis C virus particles. Comparison of U2OS and Huh-7 cells for identifying host factors that affect hepatitis C virus RNA replication.

Requirement of cellular DDX3 for hepatitis C virus replication is unrelated to its interaction with the viral core protein.
Apolipoprotein E interacts with hepatitis C virus nonstructural protein 5A and determines assembly of infectious particles. Functional characterization of core genes from patients with acute hepatitis C virus infection.
The hepatitis c virus ns4b protein can trans-complement viral rna replication and modulates production of infectious virus. Initiation of hepatitis C virus infection requires the dynamic microtubule network: role of the viral nucleocapsid protein. Transcriptional slippage prompts recoding in alternate reading frames in the hepatitis C virus (HCV) core sequence from strain HCV-1. Hepatitis C virus core protein induces lipid droplet redistribution in a microtubule- and dynein-dependent manner.
Visualization of double-stranded RNA in cells supporting hepatitis C virus RNA replication. Maturation of hepatitis C virus core protein by signal peptide peptidase is required for virus production.
The lipid droplet binding domain of hepatitis C virus core protein is a major determinant for efficient virus assembly.
Disrupting the association of hepatitis C virus core protein with lipid droplets correlates with a loss in production of infectious virus. Mobility analysis of an NS5A-GFP fusion protein in cells actively replicating hepatitis C virus subgenomic RNA.
Efficient cleavage by signal peptide peptidase requires residues within the signal peptide between the core and E1 proteins of hepatitis C virus strain J1. Signal peptide peptidase cleavage of GB virus B core protein is required for productive infection in vivo. Development and characterization of a transient-replication assay for the genotype 2a hepatitis C virus subgenomic replicon.
A PPAR response element regulates transcription of the gene for human adipose differentiation-related protein. Characterisation of the differences between hepatitis C virus genotype 3 and 1 glycoproteins.
Live cell analysis and targeting of the lipid droplet-binding adipocyte differentiation-related protein.
Herpes simplex virus tegument protein VP22 contains overlapping domains for cytoplasmic localization, microtubule interaction, and chromatin binding.
Intramembrane proteolysis promotes trafficking of hepatitis C virus core protein to lipid droplets. The transmembrane domain of the hepatitis C virus E2 glycoprotein is required for correct folding of the E1 glycoprotein and native complex formation. Sequence motifs required for lipid droplet association and protein stability are unique to the hepatitis C virus core protein. Properties of the hepatitis C virus core protein: a structural protein that modulates cellular processes.
Covalent interactions are not required to permit or stabilize the non-covalent association of hepatitis C virus glycoproteins E1 and E2.

The abundance of the herpes simplex virus type 1 UL37 tegument protein in virus particles is closely controlled.
Overexpression of the herpes simplex virus type 1 tegument protein VP22 increases its incorporation into virus particles. Characterization of a herpes simplex virus type 1 deletion variant (1703) which under-produces Vmw63 during immediate early conditions of infection.
Herpes simplex virus IE63 acts at the posttranscriptional level to stimulate viral mRNA 3' processing. Characterization of enveloped tegument structures (L particles) produced by alphaherpesviruses: integrity of the tegument does not depend on the presence of capsid or envelope. Assembly of enveloped tegument structures (L particles) can occur independently of virion maturation in herpes simplex virus type 1-infected cells. The large subunit of herpes simplex virus type 1 ribonucleotide reductase: expression in Escherichia coli and purification. Purification and characterization of the herpes simplex virus type 1 ribonucleotide reductase small subunit following expression in Escherichia coli. Insertion of DNA sequences at a unique restriction enzyme site engineered for vector purposes into the genome of herpes simplex virus type 1. A modular system for the assay of transcription regulatory signals: the sequence TAATGARAT is required for herpes simplex virus immediate early gene activation. The consensus sequence YGTGTTYY located downstream from the AATAAA signal is required for efficient formation of mRNA 3a€? termini. Organization of the Herpes Simplex virus Type 1 transcription unit encoding two early proteins with molecular weights of 140000 and 40000. DNA sequence homology between two co-linear loci on the HSV genome which have different transforming abilities. It is estimated that between 140-185 million people, are infected with the virus worldwide. It has been divided into 7 genotypes based on diversity at the nucleotide sequence level but there also many sub-types of each genotype. Typically, HCV will establish a chronic infection that does not clear without intervention, leading to progressive liver disease and increased risk of hepatocellular cancer. Even within an infected person, the virus is highly variable and exists as quasispecies, which is a population of diverse but closely-related variants.
It is now recognised that HCV infection is one of the leading causes of serious liver disease in many countries and is a growing burden on healthcare services. The extent of variability will depend on many factors; the amount of circulating virus, the genetics of the infected host and other external factors. Previously, treatment consisted of a long course of interferon and ribavirin which was often poorly tolerated due to side effects, and had a low overall success rate. Although there are now new drugs available (called direct-acting antivirals; DAAs) that often do not require the use of interferon and give much higher cure rates even with reduced length of treatment, resistance to these drugs has been demonstrated which may limit their use in the future.

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