Legionella pneumophila S1P-lyase targets host sphingolipid metabolism and restrains autophagy.

Autophagy is an essential component of innate immunity, enabling the detection and elimination of intracellular pathogens. Legionella pneumophila, an intracellular pathogen that can cause a severe pneumonia in humans, is able to modulate autophagy through the action of effector proteins that are translocated into the host cell by the pathogen's Dot/Icm type IV secretion system. Many of these effectors share structural and sequence similarity with eukaryotic proteins.

Molecular mimicry: an important virulence strategy employed by Legionella pneumophila to subvert host functions.

It is 32 years since Legionella pneumophila was identified and recognized as a human pathogen, causing the severe form of pneumonia termed Legionnaires' disease, or legionellosis. This bacterium is found in freshwater reservoirs where it replicates in aquatic protozoa and can invade man-made water distribution systems. Although the disease can be treated by antibiotherapy and prevented through surveillance and control measures, reported cases of Legionnaires' disease continue to rise across Europe and outbreaks of major public health significance still occur.

Functional diversity of HIV-1 envelope proteins expressed by contemporaneous plasma viruses.

Background: Numerous studies have shown that viral quasi-species with genetically diverse envelope proteins (Env) replicate simultaneously in patients infected with the human immunodeficiency virus type 1 (HIV-1). Less information is available concerning the extent that envelope sequence diversity translates into a diversity of phenotypic properties, including infectivity and resistance to entry inhibitors.

Methods: To study these questions, we isolated genetically distinct contemporaneous clonal viral populations from the plasma of 5 HIV-1 infected individuals (n = 70), and evaluated the infectivity of recombinant viruses expressing Env proteins from the clonal viruses in several target cells.

Contribution of recombination to the evolution of human immunodeficiency viruses expressing resistance to antiretroviral treatment.

Viral recombination has been postulated to play two roles in the development of human immunodeficiency virus (HIV) resistance to antiretroviral drugs. First, recombination has the capacity to associate resistance mutations expressed by distinct viruses, thereby contributing to the development of viruses with improved drug resistance. In addition, recombination could preserve diversity in regions outside those subject to strong selective pressure.

Extensive recombination among human immunodeficiency virus type 1 quasispecies makes an important contribution to viral diversity in individual patients.

Although recombination during human immunodeficiency virus type 1 (HIV-1) replication in vitro and in vivo has been documented, little information is available concerning the extent that recombination contributes to the diversity of HIV-1 quasispecies in the course of infection in individual patents. To investigate the impact of recombination on viral diversity, we developed a technique that permits the isolation of contemporaneous clonal viral populations resulting from single infectious events by plasma-derived viruses, thereby permitting the assessment of recombination throughout the viral genomes, including widely separated loci, from individual patients. A comparison of the genomic sequences of clonal viruses from six patients, including patients failing treatment with antiretroviral therapy, demonstrated strong evidence for extensive recombination.