Posts Tagged ‘insect’

Advances and insights into Rift Valley fever

Wednesday, July 14th, 2010

Africa This article reviews recent research on Rift Valley fever virus (RVFV) infection, encompassing four main areas: epidemiology and outbreak prediction, viral pathogenesis, human diagnostics and therapeutics, and vaccine and therapeutic candidates. RVFV continues to extend its range in Africa and the Middle East. Better definition of RVFV-related clinical syndromes and human risk factors for severe disease, combined with early-warning systems based on remote-sensing, simplified rapid diagnostics, and tele-epidemiology, hold promise for earlier deployment of effective outbreak control measures. Advances in understanding of viral replication pathways and host cell-related pathogenesis suggest means for antiviral therapeutics and for more effective vaccination strategies based on genetically engineered virus strains or subunit vaccines. RVFV is a significant health and economic burden in many areas of Africa, and remains a serious threat to other parts of the world. Development of more effective methods for RVFV outbreak prevention and control remains a global health priority.

Advances in Rift Valley fever research: insights for disease prevention. Curr Opin Infect Dis. Jul 6 2010 doi: 10.1097/QCO.0b013e32833c3da6

The dengue vector Aedes aegypti

Thursday, March 11th, 2010

Dengue transmission Aedes aegypti is the urban vector of dengue viruses worldwide. While climate influences the geographical distribution of this mosquito species, other factors also determine the suitability of the physical environment for this mosquito. Importantly, the close association of Ae. aegypti with humans and the domestic environment allows this species to persist in regions that may otherwise be unsuitable based on climatic factors alone. This review highlights the need to incorporate the impact of the urban environment in attempts to model the potential distribution of Ae. aegypti and briefly discuss the potential for future technology to aid management and control of this widespread vector species.

The dengue vector Aedes aegypti: What comes next. Microbes Infect. Jan 20 2010. doi:10.1016/j.micinf.2009.12.011

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One virus particle can be enough to cause infection

Monday, May 18th, 2009

Virus particles In the vast majority of systems, it is unknown how many individual pathogens are required to cause infection of a host organism. Estimates of this number are necessary to predict the likelihood that hosts are infected by multiple genotypes, and so predict the magnitude of genetic drift, the evolution of new pathogen genotypes and the interactions between pathogens and their hosts – all features which are highly relevant in the face of an influenza pandemic. These interactions include competition, complementation and recombination. There is experimental evidence that the number of virions causing an infection can be small, as shown by the data from two experimental approaches. First, genetic drift can be very strong when low virus doses are used, suggesting that only a small number of virions caused the infection. Second, results of dose–response experiments suggest that the number of virions causing infection is in some instances very small. Although the data suggest that the number may be small, there has been no absolute proof that one virus particle is enough be enough to cause infection of a host. Recent research with insect viruses has now shown that one virus particle is enough to cause infection and subsequent disease.

Virus populations are usually composed of collections of variants. In order to investigate whether virus particles (virions) can cause an infection independently from each other, and therefore individually, the researchers set up an experiment with two marked virus variants. The results showed that exposure to a low dose of virus particles resulted in a small number host infections, around 20%. The majority of these hosts turned out to be infected by a single virus genotype. In contrast, exposure to a high dose of virus resulted in virtually all the hosts becoming infected. Here most of the hosts were infected by both types of virus and only 14% were infected by only one of the variants.

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Based on the assumption that every virus particle operates independently from all other virus particles, the researchers set up a probability model to predict how many virus particles have caused an infection and how many different virus genotypes are present in infected hosts. The results of the infection experiments show that virus particles can indeed act independently, and that a single virus particle can be enough to cause an infection.

In infection caused by few virus particles (as may occur frequently in natural situations), the number of virus particles determines the degree of virus diversity that will be present within the host. This is an important finding because the interactions between virus variants, such as competition and exchanging genetic information, determine the progression of disease and the evolution of the virus. This is highly significant in the case of the new H1N1 influenza strain which has just entered the human population. Although each of the eight gene segments in the new virus has been seen in pigs in the past 10 years, this virus has only been in humans for a few months, and is quite unstable. Although less pathogenic than H5N1 influenza, which now seems to be endemic in countries like China, Indonesia, Vietnam and Egypt, recombination resulting in a virus which combines the high transmissibility of H1N1 with the killing power of the H5N1 becomes more likely as both viruses circulate in human populations.

Hold on tight, it might be a bumpy ride.

An experimental test of the independent action hypothesis in virus–insect pathosystems. 2009 Proc. R. Soc. B 276: 2233-2242
The independent action hypothesis (IAH) states that each pathogen individual has a non-zero probability of causing host death and that pathogen individuals act independently. IAH has not been rigorously tested. In this paper, we (i) develop a probabilistic framework for testing IAH and (ii) demonstrate that, in two out of the six virus–insect pathosystems tested, IAH is supported by the data. We first show that IAH inextricably links host survivorship to the number of infecting pathogen individuals, and develop a model to predict the frequency of single- and dual-genotype infections when a host is challenged with a mixture of two genotypes. Model predictions were tested using genetically marked, near-identical baculovirus genotypes, and insect larvae from three host species differing in susceptibility. Observations in early-instar larvae of two susceptible host species support IAH, but observations in late-instar larvae of susceptible host species and larvae of a less susceptible host species were not in agreement with IAH. Hence the model is experimentally supported only in pathosystems in which the host is highly susceptible. We provide, to our knowledge, the first qualitative experimental evidence that, in such pathosystems, the action of a single virion is sufficient to cause disease.

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Tough Choices – DDT or Malaria?

Monday, October 8th, 2007

DDTThe organochlorine compound DDT (Dichloro-Diphenyl-Trichloroethane) was first synthesized in 1874, but its insecticidal properties were not discovered until 1939 by the Swiss scientist Paul Muller, who was awarded the 1948 Nobel Prize in Physiology and Medicine for his efforts. DDT kills by opening sodium ion channels in insect neurons, causing the neuron to fire spontaneously. This leads to spasms and eventual death. Insects with mutations in their sodium channel gene or with up-regulation of genes expressing cytochrome P450 may become resistant to DDT and similar insecticides.

In the early years of World War II DDT was used with great effect to combat mosquitoes spreading malaria, typhus, and other insect-borne human diseases among both military and civilian populations. After the war, DDT was made available as an agricultural insecticide, and its production and use skyrocketed.

In 1955 the World Health Organization began a program to eradicate malaria worldwide, relying largely on DDT. Though this effort was initially highly successful (reducing mortality rates from 192 per 100,000 to a low of 7 per 100,000), resistance soon emerged in many insect populations as a consequence of the widespread agricultural use of DDT. In the 1960s, the environmental impacts of indiscriminate spraying of DDT became known. As a persistent organic pollutant, DDT accumulated in the food chain and had severe effects on fish, amphibians, birds, and rather less well known impacts on mammals, including humans. DDT can still be found in the fat reserves of polar bears, penguins, and possibly you, thousands of miles away from where it was ever sprayed. In 1987 the US EPA classified DDT as a probable human carcinogen. DDT is also known to be an endocrine disruptor and to cause developmental problems in infants.

In the 1970s and 1980s, agricultural use of DDT was banned in most developed countries, in 1970 in Scandinavia, 1972 in the USA, but not until 1984 in the UK. The Stockholm Convention which came into effect in 2004 outlawed several persistent organic pollutants, and restricted the use of DDT to the control of insect vectors of human diseases. After these bans, the populations of many severely threatened species, such as the American bald eagle, rebounded.

In September 2006, the World Health Organization announced that DDT will be used as one of the three main tools against malaria, and recommended indoor spraying in epidemic areas and places with high malaria transmission. USAID now funds the use of DDT overseas. DDT sprayed inside a home provides protection from mosquitoes for up to six months. New studies show that despite mosquito resistance to DDT, it also acts as a powerful insect repellent.

Malaria afflicts between 300 million and 500 million people each year. The World Health Organization estimates that around 1 million people die of malaria and malaria-related illness every year, with 90% of these deaths in Africa, mostly in children under the age of five. To put that in perspective, that is equivalent to the death toll of around ten of the nuclear bombs dropped on Hiroshima during World War II. Malaria also weakens the economies of poor countries. People who become infected cannot work or die. Infected children can suffer brain damage. The World Bank estimates that malaria costs Africa more than US$100 billion annually and this cost is growing by 1.3 per cent each year. In 2004, when Uganda publicly contemplated reintroducing DDT to fight malaria, the European Union made threats that the country’s US$32 billion agriculture exports could be at risk if tough new measures were not taken to ensure DDT residues did not find their way into food crops.

As a result of the WHO program, the number of African countries spraying DDT inside houses has exploded. Eritrea, Madagascar, Ethiopia, Swaziland, Senegal, Ghana, Angola, South Africa, Mauritius, Mozambique, Zimbabwe, Namibia, Zambia and Burkina Faso are all using the chemical. Uganda, where more than 100,000 people died from malaria in 2006, began spraying it this year in a pilot project, and Tanzania and Malawi may follow. But Rwanda, Burundi and Kenya (a major producer of pyrethrum, the main alternative to DDT) are so far refusing to adopt the use of the chemical. In 1995, South Africa stopped spraying DDT to control malaria, citing international pressures, but as soon as the ban started, the incidence of malaria rose.

DDT is cheap. Safer pyrethrum-based insecticides are 20 times more costly, often too expensive for developing countries. The price of controlling malaria in Africa has been estimated at US$1 billion per year, but foreign aid targeting the disease has never topped US$200 million.

So my question to you is this: imagine you are the president of the world, but with a limited budget. What would you do?

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