Profound amplification of pathogenic murine polytropic retrovirus release from coinfected cells.

Previous studies indicate that mice infected with mixtures of mouse retroviruses (murine leukemia viruses [MuLVs]) exhibit dramatically altered pathology compared to mice infected with individual viruses of the mixture. Coinoculation of the ecotropic virus Friend MuLV (F-MuLV) with Fr98, a polytropic MuLV, induced a rapidly fatal neurological disease that was not observed in infections with either virus alone. The polytropic virus load in coinoculated mice was markedly enhanced, while the ecotropic F-MuLV load was unchanged.

Higher efficacy of nevirapine than efavirenz to achieve HIV-1 plasma viral load below 1 copy/ml.

Objectives: To compare the level of HIV-1 residual viremia, defined by a viral load below 50 copies/ml in patients receiving a tenofovir/emtricitabine and nevirapine (NVP) or efavirenz (EFV)-containing regimen.

Design: One hundred and sixty-five HIV-1-infected patients were retrospectively included since they achieved virological suppression (viral load <50 copies/ml) for at least 6 months with a tenofovir/emtricitabine and non-nucleoside reverse transcriptase inhibitor-containing regimen (NVP, n = 75 and EFV, n = 90).

Methods: Residual plasma viremia was measured using an ultrasensitive assay with a limit of quantification of 1 copy/ml.

Better health-related quality of life after switching from a virologically effective regimen to a regimen containing efavirenz or nevirapine.

Switching antiretroviral therapy has been shown as safe and effective, but its impact on health-related quality of life (HRQL) was rarely measured. Our objective was to assess changes in HRQL after switching to an non-nucleoside reverse transcriptase inhibitors (NNRTI) containing regimen among NNRTI-naive HIV-infected patients with viral load (VL) <500 copies/mL. In this prospective observational study, the Hospital Anxiety and Depression, Symptoms checklist, specific World Health Organization Quality of Life (WHOQoL) and generic SF-12v2 HRQL questionnaires were used to assess anxiety, depression, symptoms, and HRQL at baseline and months 1 (M1), 6 (M6), and 12 (M12).

In vivo interactions of ecotropic and polytropic murine leukemia viruses in mixed retrovirus infections.

Mixed retrovirus infections are the rule rather than the exception in mice and other species, including humans. Interactions of retroviruses in mixed infections and their effects on disease induction are poorly understood. Upon infection of mice, ecotropic retroviruses recombine with endogenous proviruses to generate polytropic viruses that utilize different cellular receptors.

Precise identification of endogenous proviruses of NFS/N mice participating in recombination with moloney ecotropic murine leukemia virus (MuLV) to generate polytropic MuLVs.

Polytropic murine leukemia viruses (MuLVs) are generated by recombination of ecotropic MuLVs with env genes of a family of endogenous proviruses in mice, resulting in viruses with an expanded host range and greater virulence. Inbred mouse strains contain numerous endogenous proviruses that are potential donors of the env gene sequences of polytropic MuLVs; however, the precise identification of those proviruses that participate in recombination has been elusive. Three different structural groups of proviruses in NFS/N mice have been described and different ecotropic MuLVs preferentially recombine with different groups of proviruses.

Antigenic subclasses of polytropic murine leukemia virus (MLV) isolates reflect three distinct groups of endogenous polytropic MLV-related sequences in NFS/N mice.

Polytropic murine leukemia viruses (MLVs) are generated by recombination of ecotropic MLVs with members of a family of endogenous proviruses in mice. Previous studies have indicated that polytropic MLV isolates comprise two mutually exclusive antigenic subclasses, each of which is reactive with one of two monoclonal antibodies termed MAb 516 and Hy 7. A major determinant of the epitopes distinguishing the subclasses mapped to a single amino acid difference in the SU protein.