MicrobiologyBytes

Wolbachia is a maternally transmitted intracellular bacterial symbiont of arthropods. The organism is mainly localized in the reproductive tissues of arthropods and it is responsible for the induction of a number of reproductive alterations including feminization, parthenogenesis, male-killing and cytoplasmic incompatibility. Apart from reproductive parasitism, Wolbachia also participates in mutualistic relationships with nematode hosts. The widespread distribution of Wolbachia as well as the manipulation of host’s reproductive system places this symbiont among the most promising targets for disease/pest control.

Wolbachia was first discovered in the gonads of the mosquito Culex pipientis in 1924. Since then, Wolbachia has been detected in many host tissues. Wolbachia has evolved several strategies to ensure vertical transmission through the manipulation of host reproductive system. These strategies include feminization, parthenogenesis, male killing and cytoplasmic incompatibility. All the above phenotypes, commonly referred to as ‘reproductive parasitism’, increase the frequency of infected females in the host population.

Recent research on Wolbachia has grown on many levels, providing interesting insights on various aspects of the microbe’s biology. Although data from fully sequenced genomes of different Wolbachia strains and from experimental studies of host-microbe interactions continue to arise, most of the molecular mechanisms employed by Wolbachia to manipulate the host cytoplasmic machinery and to ensure vertical transmission are yet to be discovered. Apart from the well-established role of Wolbachia in triggering reproductive alterations, a new fascinating aspect is emerging, related to the ecological benefits that the symbiont provides to the host. The mutualistic relationship of Wolbachia strains with disease vectors remains among the top research priorities with new insights having an impact on putative anti-filarial strategies. Intensive research in this field keeps underlining the biological, ecological, and evolutionary significance of Wolbachia. Unravelling the molecular mechanisms underlying the establishment of the symbiosis and the induction of the reproductive phenotypes will promote the development of novel and environment friendly biotechnological strategies using Wolbachia for the control of insect pests and disease vectors.

Wolbachia: more than just a bug in insects genitals. Curr Opin Microbiol. Dec 23 2009

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• MicrobiologyBytes: Wolbachia
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In October 2009 it was reported that 68 of 101 patients with chronic fatigue syndrome (CFS) in the USA were infected with a novel gamma retrovirus, xenotropic murine leukaemia virus-related virus (XMRV), a virus previously linked to prostate cancer. This finding, if confirmed, would have a profound effect on the understanding and treatment of an incapacitating disease affecting millions worldwide. Researchers have now investigated CFS sufferers in the UK to determine if they are carriers of XMRV.

186 UK CFS patients were screened for XMRV provirus and for the closely related murine leukaemia virus. XMRV or MLV sequences were not amplified from DNA originating from CFS patients in the UK. The study found no evidence that XMRV is associated with CFS in the UK. This may be a result of population differences between North America and Europe regarding the general prevalence of XMRV infection, and might also explain the fact that two US groups found XMRV in prostate cancer tissue, while two European studies did not. Alternative explanations are also possible.

Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome. PLoS ONE 5(1): e8519. doi:10.1371/journal.pone.0008519

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Human cytomegalovirus (HCMV) is an opportunistic human pathogen that establishes a lifelong latent infection that can periodically reactivate which, if unchecked by a robust immune response, can result in severe disease in immuno-compromised patients. Following primary infection of healthy individuals, human cytomegalovirus (HCMV) is met with a robust immune response resulting in an asymptomatic infection and subsequent establishment of latency. To date, HCMV remains one of the leading viral agents of disease in immuno-suppressed transplant patients and is a cause of severe morbidity in late stage AIDS sufferers and cancer patients.

The threat from HCMV is exacerbated by the dual threat of primary infection/re-infection, and virus reactivation within the host. Since many instances of virus disease result from HCMV reactivation, many studies have analysed the regulation of latency and reactivation using experimental models. An informed consensus supports the myeloid lineage as an important site of HCMV latency and carriage and that terminal myeloid differentiation is needed for HCMV reactivation. A recurrent theme in HCMV latency/reactivation, this differentiation-dependent permissiveness also applies to lytic infection. Latently infected cells are, by definition, unable to support the viral lytic transcription program – pivotal to this is failure of IE gene expression.

Reactivation of latent virus in myeloid progenitor cells is concomitant with cellular differentiation through regulation of the MIEP by chromatin remodelling. This study analyses the expression of the latent gene transcript UL81-82as (LUNA). LUNA is expressed in latently infected CD34+ cells and expression decreases as CD34+ cells differentiate to immature dendritic cells. Upon maturation (and HCMV reactivation) a second wave of transcription occurs consistent with expression during lytic infection also. Furthermore, it shows that the LUNA promoter is associated with acetylated histones during HCMV latency in experimentally and naturally infected CD34+ cells thus suggesting that latent gene promoters are, like the MIEP, regulated by post-translational modifications of their associated histone proteins.

Analysis of latent viral gene expression in natural and experimental latency models of human cytomegalovirus and its correlation with histone modifications at a latent promoter. J Gen Virol. Nov 11 2009

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In this article in Microbiology Today (pdf) Charles Penn questions if the animals we keep in our homes are at risk of infection from living with us, rather than the other way round. Whilst much research has been done into human zoonoses, only a few investigations have been carried out into the transmission of pathogens from people to pets. New molecular techniques may enable scientists to be better informed about this in the future:

The underlying assumption in the great majority of studies has been that the animal is the source of human infection, and if the same pathogen is found in both hosts the animal almost automatically gets the blame for passing it on to the human! But is this rational? Is it not possible that pet animals might equally be infected with pathogens emanating from ourselves, or acquired as a result of our uninformed practices in ‘caring’ for our pets? Taking a step back, several issues have to be explored before these questions can be answered. Are healthy dogs and cats routinely carriers and sources of the zoonotic pathogens we fear? Or do they get sick as we do when infected, and perhaps cease to carry or shed these organisms when they recover? Can these pathogens be transiently excreted by pets after exposure to food or environmental or other sources?

Read more

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