Effects of the trematode Maritrema novaezealandensis on the behaviour of its amphipod host: adaptive or not?

There are many recorded cases of parasites that are capable of altering the behaviour of their host to enhance their transmission efficiency. However, not all of these cases are necessarily the results of the parasites actively manipulating host behaviour; they may rather be the 'by-products' of pathology caused by the parasite's presence. This study investigates the effect of the microphallid trematode Maritrema novaezealandensis on the behaviour of one of its crustacean intermediate hosts, the amphipod Paracalliope novizealandiae. Uninfected amphipods were experimentally infected by exposure to M. novaezealandensis cercariae. The activity level and vertical position of experimentally infected amphipods were compared with uninfected amphipods at 2 weeks and 6 weeks post-infection, i.e. both before and after the parasite achieved infectivity to its definitive host. Infected amphipods were found to exhibit significantly lower levels of activity and to occur significantly lower in the water column than uninfected controls during both periods. Based on the timing of the change in behaviour exhibited by infected amphipods, the results suggest that the altered behaviour exhibited by P. novizealandiae infected with M. novaezealandensis is most likely due to pathology caused by the parasite rather than a case of active, and adaptive, behavioural manipulation.     

Assembly of vaccinia virus revisited: de novo membrane synthesis or acquisition from the host?

In 1968 it was proposed that the first membrane structures that assemble in vaccinia virus-infected cells, the crescents, are formed by a unique viral mechanism in which a single membrane bilayer is synthesized de novo. 25 years later it was suggested that the vaccinia membranes are derived from an organelle that is part of the host cell's secretory pathway, the intermediate compartment (IC), and that the viral crescents are made of two tightly apposed membranes rather than a single bilayer. Several independent studies have subsequently shown that membrane proteins of the intracellular mature virus (IMV) insert co-translationally into endoplasmic reticulum (ER) membranes, and are targeted to and retained in the IC, the compartment from which the virus acquires its membranes. Furthermore, a recent study on the entry of both the IMV and extracellular enveloped virus (EEV) suggests that these viruses do not enter by a simple fusion mechanism, consistent with the idea that both are surrounded by more than one lipid bilayer.     

Discovery of the first virus, the tobacco mosaic virus: 1892 or 1898?

Two scientists contributed to the discovery of the first virus, Tobacco mosaic virus. Ivanoski reported in 1892 that extracts from infected leaves were still infectious after filtration through a Chamberland filter-candle. Bacteria are retained by such filters, a new world was discovered: filterable pathogens. However, Ivanovski probably did not grasp the full meaning of his discovery. Beijerinck, in 1898, was the first to call 'virus', the incitant of the tobacco mosaic. He showed that the incitant was able to migrate in an agar gel, therefore being an infectious soluble agent, or a 'contagium vivum fluidum' and definitively not a 'contagium fixum' as would be a bacteria. Ivanovski and Beijerinck brought unequal but decisive and complementary contributions to the discovery of viruses. Since then, discoveries made on Tobacco mosaic virus have stood out as milestones of virology history.     

Who is the puppet master? Replication of a parasitic wasp-associated virus correlates with host behaviour manipulation

Many parasites modify their host behaviour to improve their own transmission and survival, but the proximate mechanisms remain poorly understood. An original model consists of the parasitoid Dinocampus coccinellae and its coccinellid host, Coleomegilla maculata; during the behaviour manipulation, the parasitoid is not in contact with its host anymore. We report herein the discovery and characterization of a new RNA virus of the parasitoid (D. coccinellae paralysis virus, DcPV). Using a combination of RT-qPCR and transmission electron microscopy, we demonstrate that DcPV is stored in the oviduct of parasitoid females, replicates in parasitoid larvae and is transmitted to the host during larval development. Next, DcPV replication in the host''s nervous tissue induces a severe neuropathy and antiviral immune response that correlate with the paralytic symptoms characterizing the behaviour manipulation. Remarkably, virus clearance correlates with recovery of normal coccinellid behaviour. These results provide evidence that changes in ladybeetle behaviour most likely result from DcPV replication in the cerebral ganglia rather than by manipulation by the parasitoid. This offers stimulating prospects for research on parasitic manipulation by suggesting for the first time that behaviour manipulation could be symbiont-mediated.     

Molecular Probes: What Is the Range of Their Interaction with the Environment?

We performed pressure-tuning hole-burning experiments on a modified cytochrome c protein in a glycerol/buffer glass. The shift and the broadening of the holes were investigated for various frequencies within the inhomogeneous band. On the basis of a simple model, we were able to estimate the interaction range between chromophore and protein. It is ~4.5 Å. The parameters that enter the model are the compressibility, the static mean-square displacement, the inhomogeneous width, and the average spectral shift per pressure. From this result and from our experiments on pressure-induced denaturing, we conclude that water molecules have to be brought very close to the chromophore during the denaturation process.     

Interaction of proteins of the adenylate cyclase complex: Area-limited mobility or movement along the whole membrane? Analysis with the application of the percolation theory

Extraction of the fluid lipid fraction from rat reticulocyte plasma membranes by phospholipase/BSA treatment leads to a reduction in the percentage of -adrenoreceptors complexed with the regulatory N-proteins and to a decrease of adenylate cyclase stimulation with a -agonist. Analysis of the data obtained on the basis of the percolation theory suggests that proteins of the adenylate cyclase complex move along the whole membrane.     

Interaction of the ΦHSIC Virus with Its Host: Lysogeny or Pseudolysogeny?

The marine phage ΦHSIC has been previously reported to enter into a lysogenic relationship with its host, HSIC, identified as Listonella pelagia. This phage produces a variety of plaques on its host, including turbid and haloed plaques, from which lysogens were previously isolated. These lysogens were unstable during long-term storage at −80^° C and were lost. When HSIC was reinfected with phage ΦHSIC, pseudolysogen-like interactions between the phage and its host were observed. The cells (termed HSIC-2 or HSIC-2e) produced high viral titers (10¹¹ ml⁻¹) in the absence of inoculating phage and yet reached culture densities of nearly 10⁹ ml⁻¹. Prophages were not induced by mitomycin C or the polyaromatic hydrocarbon naphthalene in cells harboring such infections. However, such cells were homoimmune to superinfection. Colonies hybridized strongly with a gene probe from a 100-bp fragment of the ΦHSIC genome, while the host did not. Analysis of chromosomal DNA preparations suggested the presence of a chromosomally integrated prophage. Phage adsorption experiments suggested that HSIC-2 was adsorption impaired. Because of the chromosomal prophage integration and homoimmunity, we interpret these results to indicate that ΦHSIC establishes a lysogenic relationship with its host that involves an extremely high level of spontaneous induction. This could be caused by a weak repressor of phage production. Additionally, poor phage adsorption of HSIC-2 compared to the wild type probably helped maintain this pseudolysogen-like relationship. In many ways, pseudolysogenic phage-host interactions may provide a paradigm for phage-host interactions in the marine environment.     

Survival of the feces: Does a nematode lungworm adaptively manipulate the behavior of its cane toad host?

Parasites can enhance their fitness by modifying the behavior of their hosts in ways that increase rates of production and transmission of parasite larvae. We used an antihelminthic drug to experimentally alter infections of lungworms (Rhabdias pseudosphaerocephala) in cane toads (Rhinella marina). We then compared subsequent behaviors of dewormed toads versus toads that retained infections. Both in the laboratory and in the field, the presence of parasites induced hosts to select higher body temperatures (thereby increasing rates of lungworm egg production), to defecate in moister sites, and to produce feces with higher moisture content (thereby enhancing survival of larvae shed in feces). Because those behavioral modifications enhance rather than decrease parasite fitness, they are likely to have arisen as adaptive manipulations of host behavior rather than as host adaptations to combat infection or as nonadaptive consequences of infection on host physiology. However, the mechanisms by which lungworms alter cane toad thermal preference and defecation are not known. Although many examples of host manipulation by parasites involve intermediate hosts facilitating their own demise, our findings indicate that manipulation of definitive hosts can be as subtle as when and where to defecate.     

Occult infection with hepatitis C virus: friend or foe?

Hepatitis C virus (HCV) infection is a global pandemic associated with a growing disease burden due to cirrhosis and the consequent morbidity and mortality. Transmission is largely via blood-to-blood contact. Following primary infection, a minority of individuals clear the infection predominantly via cellular immune mechanisms, whereas the majority become chronically infected. Recent data suggest that a third outcome may also be possible, termed 'occult' infection in which subjects who are known, or suspected to have previously been infected with HCV, no longer have viral RNA in their serum at levels detectable by sensitive commercial assays, but do have virus detected by ultra-sensitive techniques. Occult infection has also been detected in peripheral blood mononuclear cells, which may indicate an extra-hepatic reservoir of the virus. Although the clinical significance of occult infection remains unknown, most authors have raised concerns of recrudescent infection. Here we critically review the published literature, suggest further avenues of investigation and propose that occult infection may be beneficial to the host by maintaining immunological memory to protect against reinfection.     

Characterization of the Sulfolobus host–SSV2 virus interaction

The Sulfolobus spindle virus, SSV2, encodes a tyrosine integrase which furthers provirus formation in host chromosomes. Consistently with the prediction made during sequence analysis, integration was found to occur in the downstream half of the tRNA^Gly (CCC) gene. In this paper we report the findings of a comparative study of SSV2 physiology in the natural host, Sulfolobus islandicus REY15/4, versus the foreign host, Sulfolobus solfataricus, and provide evidence of differently regulated SSV2 life cycles in the two hosts. In fact, whereas a significant induction of SSV2 replication takes place during the growth of the natural host REY15/4, the cellular content of SSV2 DNA remains fairly low throughout the incubation of the foreign host. The accumulation of episomal DNA in the former case cannot be traced to decreased packaging activity because of a simultaneous increase in the virus titre in the medium. In addition, the interaction between SSV2 and its natural host is characterized by the concurrence of host growth inhibition and the induction of viral DNA replication. When this virus–host interaction was investigated using S. islandicus REY15A, a strain which is closely related to the natural host, it was found that the SSV2 replication process was induced in the same way as in the natural host REY15/4.     

Exploiting host compensatory responses: the 'must' of manipulation?

Parasite-induced alterations of the host phenotype have been reported in many systems. These changes are traditionally categorized into three kinds of phenomena: secondary outcomes of infection with no adaptive value, host adaptations that reduce the detrimental consequences of infection and parasitic adaptations that facilitate transmission. However, this categorization is a simple view, and host modifications should be considered as co-evolved traits, rather than a total takeover. Here, we present a novel scenario of manipulation, which has considerable potential to resolve issues that are specific to the evolution of behavioural alterations induced by parasites. It is proposed that certain parasites affect fitness-related traits in their hosts to trigger host compensatory responses because these responses can meet the transmission objectives of parasites.     

Campylobacter jejuni host tissue tropism: a consequence of its low-carb lifestyle?

Mechanisms underlying virulence properties of Campylobacter jejuni have historically been difficult to identify. In this issue of Cell Host & Microbe, Hofreuter et al. (2008) show that C. jejuni's ability to metabolize glutamine, glutathione, and asparagine affects its ability to colonize specific host tissues. These findings reflect the emerging theme of bacterial physiology directly impacting pathogenesis.