Hepatitis B virus resistance substitutions: long-term analysis by next-generation sequencing.

HBV phylogenetics and resistance-associated mutations (RAMs) were surveyed by next-generation sequencing of 21 longitudinal samples from seven patients entering antiviral therapy. The virus populations were dominated by a few abundant lineages that coexisted with substantial numbers of low-frequency variants. A few low-frequency RAMs were observed before treatment, but new ones emerged, and their frequencies increased during therapy.

Evolution of hepatitis C virus in HIV coinfected patients under antiretroviral therapy.

Five patients (P) were followed-up for an average of 7.73years after highly active antiretroviral therapy (HAART) initiation. Patients' immune and virological status were determined by periodical CD4+T-cell counts and HIV and HCV viral load.

Virus evolution during chronic hepatitis B virus infection as revealed by ultradeep sequencing data.

Despite chronic hepatitis B virus (HBV) infection (CHB) being a leading cause of liver cirrhosis and cancer, HBV evolution during CHB is not fully understood. Recent studies have indicated that virus diversity progressively increases along the course of CHB and that some virus mutations correlate with severe liver conditions such as chronic hepatitis, cirrhosis and hepatocellular carcinoma. Using ultradeep sequencing (UDS) data from an intrafamilial case, we detected such mutations at low frequencies among three immunotolerant patients and at high frequencies in an inactive carrier.

Previous failure of interferon-based therapy does not alter the frequency of HCV NS3 protease or NS5B polymerase inhibitor resistance-associated variants: longitudinal analysis in HCV/HIV co-infected patients.

Since 2011, treatment of chronic hepatitis C virus (HCV) includes direct-acting antivirals (DAAs) in addition to pegylated interferon-α (peg-IFN) and ribavirin (RBV). IFN-based treatment induces strong cytotoxic T-lymphocyte activity directed to the protease- and polymerase-derived epitopes. This enhanced immunological pressure could favour the emergence of viral epitope variants able to evade immune surveillance and, when resistance-associated variants (RAVs) are implicated, could also be co-selected as a hitchhiking effect.

Inter and intra-host variability of hepatitis C virus genotype 1a hypervariable envelope coding domains followed for a 4-11 year of human immunodeficiency virus coinfection and highly active antiretroviral therapy.

The evolution of hepatitis C virus (HCV) quasispecies in patients with HIV-1 coinfection is not fully understood. The HCV-1a quasispecies heterogeneity was analyzed at inter and intra-host levels along 7.6 years in 21 coinfected patients that showed different virological and immunological responses to highly active antiretroviral therapy (HAART).

HIV-1 tropism dynamics and phylogenetic analysis from longitudinal ultra-deep sequencing data of CCR5- and CXCR4-using variants.

Objective: Coreceptor switch from CCR5 to CXCR4 is associated with HIV disease progression. The molecular and evolutionary mechanisms underlying the CCR5 to CXCR4 switch are the focus of intense recent research. We studied the HIV-1 tropism dynamics in relation to coreceptor usage, the nature of quasispecies from ultra deep sequencing (UDPS) data and their phylogenetic relationships.

Increased in vitro glial fibrillary acidic protein expression, telomerase activity, and telomere length after productive human immunodeficiency virus-1 infection in murine astrocytes.

Although HIV-associated neurocognitive disorders (HAND) result from injury and loss of neurons, productive infection routinely takes place in cells of macrophage lineage. In such a complex context, astrocytosis induced by local chemokines/cytokines is one of the hallmarks of HIV neuropathology. Whether this sustained astrocyte activation is able to alter telomere-aging process is unknown.