“In the 1990s, experts thought they were close to eliminating measles for good. But now the World Health Organization (WHO) has put back its target date for getting rid of the disease to 2015. But even that seems unlikely. The reason? A measles outbreak which is spreading across Europe, affecting France, Belgium, Germany and Romania – and now the UK…”
Read more: BBC News – Measles outbreak warning as cases rise in Europe and UK
Culicoides biting midges are widely distributed throughout the world and are vectors of internationally important livestock viruses, including bluetongue virus (BTV), African horse sickness virus (AHSV), Akabane virus and Epizootic haemorrhagic disease virus (EHDV). Bluetongue disease (BT) has gained considerable notoriety in recent years because of an unprecedented globalisation and climate change-mediated expansion of its range in Europe, resulting in BTV reaching areas with no historical record of the disease. The economic impact of outbreaks of BTV in these areas has been considerable as a result of both indirect costs (e.g. the restrictions placed on movement of infected ruminants) and direct losses from disease in both sheep and cattle. In addition, whilst vaccination campaigns across northern Europe eventually controlled outbreaks in this region, it took approximately eighteen months from the initial incursion in 2006 to the deployment of vaccine in the field. During this lag period, attempts to control the spread of BTV were limited to the restriction of animal movement and the application of methods to control Culicoides midges (primarily through the use of pour-on pyrethroid insecticides to vulnerable stocks).
BTV is an arbovirus and therefore depends almost entirely on the occurrence of farm-associated populations of competent Culicoides biting midges for transmission to its ruminant hosts. As a period of extrinsic replication is required within these vectors, control measures directed at adults have the potential to reduce the spread of midge-transmitted diseases through shortening or interrupting their lifespan. Indeed, epidemiological transmission models of vector-borne diseases show that the adult lifespan is the single most important factor affecting risk of transmission. At present, the majority of approaches to control populations of biting midges are based upon the application of insecticides (primarily synthetic pyrethroids) which in northern Europe are most commonly applied to livestock, although systematic testing of compounds to date has demonstrated equivocal results. Wide scale larvicidal or adulticidal use of these compounds against Culicoides has not been considered sustainable because of the paucity of knowledge surrounding larval habitats and adult resting places, combined with increasing restrictions within the EU on untargeted use of pyrethroid insecticides. An alternative insecticide, Ivermectin, is effective in killing Culicoides species when applied intradermally or subcutaneously and also toxic to midge larvae when excreted in faeces (a potential breeding site) but has also been shown to be harmful to beneficial insects such as dung beetles. Farmers are therefore caught between the need to control populations of biting midges and the diminishing number of chemical insecticides as they are withdrawn because of their perceived risk to humans and the environment.
Entomopathogenic Fungus as a Biological Control for an Important Vector of Livestock Disease: The Culicoides Biting Midge. 2011 PLoS ONE 6(1): e16108. doi:10.1371/journal.pone.0016108
The recent outbreak of bluetongue virus in northern Europe has led to an urgent need to identify control measures for the Culicoides (Diptera: Ceratopogonidae) biting midges that transmit it. Following successful use of the entomopathogenic fungus Metarhizium anisopliae against larval stages of biting midge Culicoides nubeculosus Meigen, we investigated the efficacy of this strain and other fungi (Beauveria bassiana, Isaria fumosorosea and Lecanicillium longisporum) as biocontrol agents against adult C. nubeculosus in laboratory and greenhouse studies.
Exposure of midges to ‘dry’ conidia of all fungal isolates caused significant reductions in survival compared to untreated controls. Metarhizium anisopliae strain V275 was the most virulent, causing a significantly decrease in midge survival compared to all other fungal strains tested. The LT50 value for strain V275 was 1.42 days compared to 2.21–3.22 days for the other isolates. The virulence of this strain was then further evaluated by exposing C. nubeculosus to varying doses (108–1011 conidia m−2) using different substrates (horse manure, damp peat, leaf litter) as a resting site. All exposed adults were found to be infected with the strain V275 four days after exposure. A further study exposed C. nubeculosus adults to ‘dry’ conidia and ‘wet’ conidia (conidia suspended in 0.03% aq. Tween 80) of strain V275 applied to damp peat and leaf litter in cages within a greenhouse. ‘Dry’ conidia were more effective than ‘wet’ conidia, causing 100% mortality after 5 days.
This is the first study to demonstrate that entomopathogenic fungi are potential biocontrol agents against adult Culicoides, through the application of ‘dry’ conidia on surfaces (e.g., manure, leaf litter, livestock) where the midges tend to rest. Subsequent conidial transmission between males and females may cause an increased level of fungi-induced mortality in midges thus reducing the incidence of disease.
“A new vaccine can protect macaques against the monkey equivalent of HIV and could provide a fresh approach to an HIV vaccine, a study suggests. US researchers say the vaccine offered protection to 13 of 24 rhesus macaques treated in the experiment. In 12 of the monkeys, the vaccine was still effective 12 months later.”
via BBC News – Monkey HIV vaccine ‘effective’, say researchers
MicrobiologyBytes: Encouraging news but – 50% protection against the same strain of virus after 12 months? Would you trust your life to this?
Original Source: Profound early control of highly pathogenic SIV by an effector memory T-cell vaccine. Nature 11 May 2011 doi:10.1038/nature10003 (subscription required)
Rift Valley fever (RVF), a mosquito-borne zoonotic disease among humans and ruminants, is caused by Rift Valley fever virus (RVFV) belonging to the family Bunyaviridae, genus Phlebovirus. RVF is endemic to sub-Saharan African countries and has caused major outbreaks in several countries including Kenya, Tanzania, Somalia, South Africa, Madagascar, Egypt, Sudan, Mauritania, Senegal, Saudi Arabia, and Yemen. Pregnant ruminants infected with RVFV typically are subject to high- rate abortions, fetal malformation, and subclinical-to-fatal febrile illness, while newborn lambs usually die by acute hepatitis. RVFV infection in humans primarily causes a self-limiting febrile illness; however, some patients develop hemorrhagic fever, neurological disorders, or blindness after the febrile period. In endemic area, floodwater Aedes mosquitoes serve as vectors, and the virus could be transmitted into offspring transovarially. Heavy rainfall or flooding of river banks due to construction of dams increases the number of permanent fresh water species of mosquitoes such as Culex pipens, which play a role in amplifying RVFV among mosquitoes, ruminants and humans. An outbreak of RVF in developed countries, e.g., the U.S. or Europe, could force a curtailing of livestock movement to prevent RVFV spread, causing massive economic loss, and a substantial degree of panic in our society, because the body fluids of infected animals contain infectious RVFV, and mosquitoes such as Culex spp. Aedes spp. or Anopheles spp. might further spread RVFV into other mosquitoes, humans and animals. Effective vaccines and antiviral drugs are necessary for the containment of outbreaks and treatment of RVF patients, respectively. However, neither safe and effective vaccines nor efficient treatment is available. A correct understanding of RVF pathogenesis is essential for the development of effective vaccines and antiviral drugs against RVF. This review describes clinical and pathological findings of RVF in humans and animals and discuss viral and host factors that affect RVF pathogenesis.
The Pathogenesis of Rift Valley Fever. Viruses 2011, 3(5), 493-519; doi:10.3390/v3050493
Rift Valley fever (RVF) is an emerging zoonotic disease distributed in sub-Saharan African countries and the Arabian Peninsula. The disease is caused by the Rift Valley fever virus (RVFV) of the family Bunyaviridae and the genus Phlebovirus. The virus is transmitted by mosquitoes, and virus replication in domestic ruminant results in high rates of mortality and abortion. RVFV infection in humans usually causes a self-limiting, acute and febrile illness; however, a small number of cases progress to neurological disorders, partial or complete blindness, hemorrhagic fever, or thrombosis. This review describes the pathology of RVF in human patients and several animal models, and summarizes the role of viral virulence factors and host factors that affect RVFV pathogenesis.
“It is mostly a well-told tale with lots of “wow” moments, but A Planet of Viruses was marred somewhat by a handful of inaccuracies. Among my quibbles is the claim that H5N1 bird flu started in 2006, when it first took hold in China in 1997 and exploded onto the world stage in 2004.
But what was notably absent in the book was the politics – what all of this means for us. This slim volume would have benefitted from more context, perhaps at the expense of some of the bio-factoids. For example, swine flu showed us that we can’t make pandemic vaccine fast enough – and that hand-washing is no substitute. West Nile virus revealed a dangerous lack of communication between doctors and veterinarians, while SARS showed what works. Many such compelling and important stories were given short shrift, or none at all.
In this book, wise scientists are portrayed as having everything firmly in hand, and all is well in the virus-riddled garden. The real situation, unfortunately, is more complex – and exciting – than that.” via CultureLab: Cool viruses from pox to pandemics
Bacterial microcompartments (BMCs) are organelles composed entirely of protein. They promote specific metabolic processes by encapsulating and colocalizing enzymes with their substrates and cofactors, by protecting vulnerable enzymes in a defined microenvironment, and by sequestering toxic or volatile intermediates. Prototypes of the BMCs are the carboxysomes of autotrophic bacteria. However, structures of similar polyhedral shape are being discovered in an ever-increasing number of heterotrophic bacteria, where they participate in the utilization of specialty carbon and energy sources. Comparative genomics reveals that the potential for this type of compartmentalization is widespread across bacterial phyla and suggests that genetic modules encoding BMCs are frequently laterally transferred among bacteria. The diverse functions of these BMCs suggest that they contribute to metabolic innovation in bacteria in a broad range of environments.
Bacterial microcompartments. Annu Rev Microbiol. 2010 64: 391-340
It is commonly accepted that the spread of most viruses occurs via the diffusion of ‘cell-free’ viral particles. In support of this, infectious viruses have been found in biological fluids and aerosols, and could be propagated in vitro using virus stocks produced from infected cell-culture supernatants. This mode of viral dissemination requires high numbers of stable viral particles released by the infected cell into the extracellular environment, such as the host bodily fluids. ‘Free’ viral particles were associated with a variety of components, such as lipids or proteins, which might reinforce virus envelop integrity and prevent envelope glycoprotein shedding. However, for other viruses, few viral particles are released, or they are poorly infectious when separated from infected cells. In such cases, virus propagation largely requires the presence of infected cells, suggesting that cell contacts mediate viral spread. This type of dissemination is mainly reported for enveloped viruses, such as some herpes viruses and some retroviruses, particularly deltaretroviruses such as the human T-cell leukemia virus type 1 (HTLV-1). Many aspects of this mode of virus dissemination are largely unknown, such as (i) the nature and the mechanism for forming cellular junctions that mediate cell–cell virus spread, and (ii) the nature of the infectious material transferred. Both of these factors depend on the virus and the type of infected cells.
Of note, the spread of two human retroviruses that infect leukocytes, HIV-1 and HTLV-1, occurs between mobile cells forming dynamic contacts with other cells. Both retroviruses cause severe chronic viral infections. Their transmission between individuals occurs through sexual contact and blood transfusion, and vertically from mother to child, including through breastfeeding. In addition to HTLV-1 dissemination through division of infected cells carrying viral genomes, transmission of HTLV-1 viral particles is known to occur mainly through cell contact in vitro and in vivo, with the exception of dendritic cells, which can be infected by cell-free viral particles. By contrast, HIV-1 spread can occur by both diffusion and direct cell–cell transfer. Nevertheless, compelling evidence indicates that direct spread through cell contact is the most efficient mode of HIV-1 dissemination in vitro, and might play a crucial role in vivo:
Can viruses form biofilms? Trends Microbiol. Mar 31 2011
The recent finding that the human T-cell leukemia virus type 1 (HTLV-1) encases itself in a carbohydrate-rich adhesive extracellular ‘cocoon’, which enables its efficient and protected transfer between cells, unveiled a new infectious entity and a novel mechanism of viral transmission. These HTLV-1 structures are observed at the surface of T cells from HTLV-1-infected patients and are reminiscent of bacterial biofilms. The virus controls the synthesis of the matrix, which surrounds the virions and attaches them to the T cell surface. We propose that, similar to bacterial biofilms, viral biofilms could represent ‘viral communities’ with enhanced infectious capacity and improved spread compared with ‘free’ viral particles, and might constitute a key reservoir for chronic infections.
The role of RNA localization in controlling gene expression and RNA stability in eukaryotes has been well established, but until recently there were no bacterial RNAs known to localize to specific subcellular sites. Studies in Caulobacter crescentus and Escherichia coli have now demonstrated that both regulatory RNAs and mRNAs can be concentrated at fixed positions in bacterial cells. tmRNA, a regulatory RNA involved in trans-translation, is localized to a helical structure in C. crescentus, and some mRNAs are localized to discrete spots in C. crescentus and E. coli. Given that bacteria also localize proteins, plasmids, and regions of the chromosome, the localization of RNA may not be particularly surprising. Nonetheless, the possibility that RNA activity and abundance can be controlled by subcellular localization represents a new paradigm for regulation of RNA, and suggests that many new discoveries of bacterial RNA localization lie ahead. Why are RNAs localized, and how is RNA localization achieved? Our understanding is far from complete because these questions are just beginning to be addressed, yet it is now reasonable to review what is known about the mechanisms and physiological rationales for localization of RNAs in bacteria, and to speculate about what additional pathways remain to be discovered.
RNA localization in bacteria. Curr Opin Microbiol. 2011 14(2):155-159
Bacteria localize proteins and DNA regions to specific subcellular sites, and several recent publications show that RNAs are localized within the cell as well. Localization of tmRNA and some mRNAs indicates that RNAs can be sequestered at specific sites by RNA binding proteins, or can be trapped at the location where they are transcribed. Although the functions of RNA localization are not yet completely understood, it appears that one function of RNA localization is to regulate RNA abundance by controlling access to nucleases. New techniques for visualizing RNAs will likely lead to increased examination of spatial control of RNAs and the role this control plays in the regulation of gene expression and bacterial physiology.
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