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There have always been economic migrants – people who swap regions, countries, even continents, to find better wages to pay for a better life. One out of every ten people on the planet either sends or receives money from abroad. And unlike all other forms of financial aid that travel into developing countries, remittances go directly to poor people. Worldwide it’s estimated that amounts to a staggering two hundred billion dollars a year. What impact can it have in the fight against poverty? To find out more, Life has travelled to the United States and El Salvador to uncover this hidden economy.

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Don Terry, of the Inter-American Development Bank, explains: ‘Remittances have been around for generations upon generations. But they are accelerating. People move north by the millions and money moves south by the billions’¦ It turns out that remittances to Latin America are more than all of the foreign direct investment and all the official development assistance, all the foreign aid combined.’

Because of the huge sums involved, the way this money is sent from A to B is being revolutionised. Not surprisingly, the banking community is starting to show an interest. As a result, the days of smuggling dollars home may soon be over together with the expense of using transfer agents.

More than 1 million come from El Salvador, a country hard hit by tragedy in the last 25 years. First a bitter 12-year civil war, which ended in 1992, claimed the lives of 75,000. Then came a series of natural disasters. Hurricane Mitch in 1998 followed by a number of earthquakes in 2001. Each has contributed to the country’s poverty’¦ and sent tens of thousands in search of work abroad. As a consequence, remittances leapt from less than a billion dollars in 1994 to $2.5 billion dollars in 2004 – roughly 17.1 per cent of GDP. Today the exodus of workers still continues, and the government has created a special ministerial office for them.

The journey north is often difficult and dangerous, and their troubles are not over when they get there, as Margarita Escobar, Deputy Minister for Salvadorans Abroad explains: “If they manage to achieve this, they have other problems, such as wage levels, labour rights, social security coverage, all the problems of being undocumented that affects migrants to their core.”

In rural areas like Tronalagua, up to a third of the people depend on money from abroad. Julio and Anna Cortez are among them. Each month they get $200 dollars from their elder children in Washington. It’s made a world of difference to Julio and Anna and their remaining children.

Julio Cortez explains how remittances have changed their lives: ‘Here’s the kitchen. Over there you have the utensils’¦. The telephone to call my children. Here is the living room and this is the refrigerator. Here on the entertainment centre, is the television. All of this with remittances.’

Almost four thousand miles away, suburban Washington, USA, some of Anna and Julio’s older children live and work. They arrived here illegally. First Elmer 1998, Hector in 1999 and finally Dalila in 2001. But they are lucky. They may have arrived illegally but they have since been granted temporary protected status – TPS – a kind of amnesty. It was introduced by the US government in 1990 to help people who can’t return home because of conflict or natural disasters. So far it’s been granted to nearly 350,000 Latin Americans. But the permit is temporary. If Dalila and her brothers can return to El Salvador, they would not be allowed back into the United States.

Dalila has heard on the news that those with temporary permits might be given residency but they didn’t say when. She might prefer to live in El Salvador, but there is still a shortage of jobs and there’s a big gap between rich and poor. In 1999 the richest fifth of the population received 45 per cent of the wealth – the poorest fifth just 5.6 per cent.

Margarita Escobar worries about the social effects of migration: “Another effect of migration is the disintegration of the nuclear family. This has had an enormous social impact.”

Increasingly, migrant groups in the US have formed what they call hometown associations, which raise extra cash to send home for community projects. In 2004, they sent back more than $2 million dollars to El Salvador.

Francesco Castro of the United Salvadoran Communities explains: ‘We’ve been building churches, a Red Cross building. We’ve been driving ambulances from here. The last project we had was a reforestation project because that’s very critical in my country right now. We raise money constantly.’

Some communities get enough money so they don’t need to rely on the government to fund local projects. Don Terry, of the Inter-American Development Bank, says:

‘The governments themselves in these developing countries absolutely need to be doing a much better job than they have been doing over the past 25 years. I think it is important to underscore that remittances are not a substitute for sound economic policies at home and remittances are certainly not a substitute for foreign assistance.’

But the El Salvador government is already working with international development organizations’¦ hoping to encourage those who receive remittances to use the money more productively. With assistance from the International Fund for Agricultural Development (IFAD), Julio and Anna have invested some money back into their farm. They used to grow maize and beans, but just for their own consumption. Now they grow fruit trees and rear more animals, all which earn them a profit of $200 dollars a month.

Having opportunities to invest their remittances has helped pull the Cortez family further from poverty. But what about the rest of the community’¦is there a way to spread the benefits? One answer may be to change how remittances are sent. The old methods were well known and dangerous. ‘Mules’ or money smugglers would regularly carry thousands of dollars across the borders – and still do. Money transfer agents are a much more secure route.

Now with the scent of serious money, some banks are getting involved. And that could lead to a reduction in costs, as well as a change in how remittances are transferred.

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Katie Klingensmith, of the US Treasury Department, points out: ‘In the US we have seen banks increasingly become interested in this market. It’s partly because they understand that many immigrants in this country stay and become bank customers. Remittances are often called a loss leader. They might be offering five, ten dollar, free remittance service. It’s not free for a bank to offer a remittance service but they use it as a way to get immigrants in through the door.’

To poor people who receive remittances, banking can give them a new financial possibilities. For example, they could get credit to start a business. Anna and Julio Cortez do manage toA make some savings – between $10 and $20 dollars a month. If they – and people like them – put those savings into a banks and credit unions rather than under their mattress, it’s estimated it would add another 250 million dollars to the country’s economy.

Rosemary Vargas-Lundius of IFAD adds: ‘By encouraging financial institutions to enter into the business of remittances, even families that aren’t receiving remittances benefit because they will have a financial institution nearby that can provide them with services which they didn’t have access to before.’

Aiding the flow of money to poor rural areas may be the most important effect in the current transformation of the remittance market. But as remittances increase, and with better ways of harnessing that wealth, perhaps one day the real opportunities will be found in El Salvador. Until then, the exodus of workers is bound to continue.

RELATED LINKS:

The Inter-American Development Bank website has pages on Migrant remittances as a development tool. See also Women’s World Banking: Microfinance and Remittances, and the World Bank’s pages on International Migration and Remittances.

The World Bank has also just published a new report on International Migration, Remittances and the Brain Drain. For the website of Inter-American Dialogue, Manuel Orozco’s organisation, go here.

On El Salvador, read World Hunger Notes article on remittances and poverty in El Salvador, and the TravelDocs page on El Salvador’s economy.

The International Fund for Agricultural Development (IFAD) has published a paper on Remittances and Rural Development, and a Factsheet on Remittances.

Websites on the attractions of El Savador include El Salvador Tourism, Lonely Planet, and El Salvador in Images, including pictures of the Chinameca Volcano.

Cache Valley orthobunyavirus (CVV) is a member of the order Bunyavirales, genus Orthobunyavirus, and serogroup Bunyamwera, which was first isolated in 1956 from Culiseta inornata mosquitos collected in Utah's Cache Valley.^[1] CVV is an enveloped arbovirus, nominally 80–120 nm in diameter, whose genome is composed of three single-stranded, negative-sense RNA segments.^[1][2] The large segment of related bunyaviruses is approximately 6800 bases in length and encodes a probable viral polymerase.^[1] The middle CVV segment has a 4463-nucleotide sequence and the smallest segment encodes for the nucleocapsid, and a second non-structural protein.^[1] CVV has been known to cause outbreaks of spontaneous abortion and congenital malformations in ruminants such as sheep and cattle. CVV rarely infects humans, but when they are infected it has caused encephalitis and multiorgan failure.^[3]

Virology[edit]

Genome[edit]

The Cache Valley virus genome is split into three parts.^[4] The three parts are called the small, medium, and large segments, based on the number of bases. The large segment encodes the L protein, which is the RNA dependent RNA polymerase. The small segment utilizes an open reading frame with alternative initiation sites to encode two proteins. Depending on the initiation site, it can either code for the protein that makes up the nucleocapsid, N, or a non-structural protein, NSs.^[5] The medium segment encodes 2 type 1 integral transmembrane glycoproteins, Gn and Gc, as well as a non-structural protein Nsm. The Gc and Gn proteins start as one precursor protein and are then cleaved cotranslationally. They are modified by N-linked glycosylation.^[6]

Replication cycle[edit]

The attachment, entry, replication, and release of CVV specifically have not been studied. However, there is information of the replication cycle for the genus orthobunyavirus, which CVV is a part of. A heterodimer of integral transmembrane proteins Gn and Gc form spikes on the surface of the virus particle. They are involved in virus attachment and cell fusion.^[7] Once inside the cell, the viral membrane fuses with the endosomal membrane, and the virus genome is released. Transcription involves an RNA dependent RNA polymerase, and it occurs in the cytoplasm of the cell. Transcription of the tripartite genome is terminated by a strong hairpin loop sequence at the end of each segment. Once the virus has replicated enough, it is encapsidated.^[8] Assembly and budding of the newly synthesized virions occurs at the membranes of the Golgi apparatus.^[9]

Host interactions[edit]

In terms of CVV alone, very little is known about the regulation of host-processes and interactions with host cells. However, CVVs Bunyamwera serogroup's two non-structural proteins play an important role in infection. Bunyamwera virus (BUNV) codes for two non-structural proteins: NSm on the medium RNA segment and NSs on the smallest RNA segment.^[10] Bunyamwera virus NSs protein is a nonessential gene that contributes to viral pathogenesis. It has been shown that in mammalian cells, NSs induces shut-off of host protein synthesis, which leads to cell death.^[10] It also counteracts the host cell antiviral response and seems to be the main virulence factor,^[11] acting at the level of transcription by inhibiting RNA polymerase II–mediated transcription.^[12] In mosquito cells neither host cell transcription nor translation are inhibited,^[13] and although so far no function for the orthobunyavirus NSs protein has been found in mosquito cells,^[14] it seems the differential behavior of NSs could be one of the factors responsible for different outcomes of infection in mammalian and mosquito cell lines.^[10]

Human cases[edit]

Prior to 1956 there were no known cases of acute infections of Cache Valley virus (CVV) in humans. However antibodies against CVV have been reported.^[15] One study found neutralizing antibody to CVV in 12% of 356 persons surveyed in Maryland and Virginia in the 1960s. These results and other such serosurveys are based on nonrandom sampling and therefore often difficult to interpret.^[16]

CVV disease is a neuroinvasive illness.^[16] Of the three confirmed human cases of CVV disease two resulted in non-fatal meningitis, only the first case caused fatal encephalitis and multiorgan failure.

The first case was a 28-year-old man from North Carolina in 1995. It is likely he was infected with the virus via mosquitos during a deer-hunting trip. The patient's first symptoms were muscle pain, fever, chills and a headache. He began vomiting the day after the first symptoms appeared. Six days after the onset of the illness more severe symptoms appeared including confusion, tachycardia (elevated heart rate), a rash, bilateral conjunctivitis and meningismus. The next day the patient became hypotensive and delirious. Later respiratory failure, seizures and necrosis of the fingers and toes occurred. One leg was amputated because of extensive muscle and cutaneous necrosis. Seven months after the onset of the illness the patient died of pulmonary complications. The causative agent was identified as a virus in the family Bunyaviridae by electron microscopy. This was then identified genetically as CVV. Viremia was recorded seven days after the onset of fever; this is a longer period of viremia than what is normally observed in cases of Bunyaviridae infections.^[15]

The second human case of CVV was a 41-year-old man from Wisconsin in October 2003. He developed an acute illness with severe nausea, vomiting, fatigue and headache. He was diagnosed with acute aseptic meningitis. After three days the patient was released from the hospital; he reported feeling fully recovered four months later, though he experienced headaches more frequently than usual. The causative agent was observed with electron microscopy as being virions morphologically similar to bunyaviruses. Nucleotide sequencing identified the virus as CVV.^[16]

The third human case of CVV was a 63-year-old woman in New York, in September 2011. When she was admitted to the hospital her symptoms were fever, headache, neck stiffness and photophobia. A week before she had noticed a lesion on her arm, as this began to fade a rash developed and spread. She then developed a fever and symptoms of meningitis. The patient was discharged, but returned the next day with nausea and vomiting. She was diagnosed with aseptic meningitis. She was discharged four days later. Two months after this she reported ongoing difficulties in word finding and headaches. CVV was identified as the causative agent by PCR, sequence analysis confirmed this identification.^[4]

It is likely that CVV disease is underreported. Very few human cases have been reported despite its wide geographic distribution and the large number of mosquito species that transmit it.^[4] The rarity of CVV disease diagnosis is partly due to the fact that laboratories rarely test for CVV. Therefore, the true incidence of CVV disease and its full clinical range are still unknown.^[16] Given the widespread distribution of CVV and other viruses in the same serogroup in the United States it is possible some unexplained cases of severe multiorgan failure, congenital anomalies and human viral encephalitis may be due to CVV or similar viruses. More research of such cases is needed.^[15]

Other animals[edit]

Cache Valley virus is the most common Orthobunyavirus in North America,^[17] and while isolated in 1956, was only linked to disease in Texas in 1987 during a large occurrence of aborted and malformed lambs in a sheep flock.^[18] The virus does not only infect sheep, however, as In 2002 a survey conducted in 22 states showed 28% of cattle expressed specific antibodies to CVV.^[19] Cache Valley virus has also been identified as a cause of fetal abnormalities in goats.^[20] Other serological surveys have also shown antibodies to CVV in domestic and wild ruminants, along with horses. Of wild ruminants, deer have a very high seroprevalence. With viraemia lasting 1 to 3 days, they are easily able to spread the virus to vectors including Culicoides midges and Aedes, Anopheles, Coquillettidia and Culiseta group mosquitoes. Therefore, deer tend to act as amplifying hosts to the virus.^[17]

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Symptoms in sheep[edit]

While the virus is able to replicate in adult animals, besides a slight febrile response in some cases, there are no known symptoms of infection.^[17][21] There is a quick period of viraemia before seroconversion and the infection is cleared quickly by the animal's immune system.^[21] However, if the animal is pregnant and not protected by antibodies from a previous infection, Cache Valley virus can be very lethal to a developing fetus.^[21]

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The symptoms the fetus develops from CVV infection are largely age dependent. At less than 28 days of gestation, the embryo usually dies and is reabsorbed by the mother.^[22] Between 28 and 45 days of gestation, infection leads to malformations in the developing fetus and occasionally leads to abortions. Early in this window, between 28 and 36 days, the virus leads to both central nervous system and musculoskeletal defects, while after 36 days of gestation infection only leads to musculoskeletal deformities.^[17] Death of the fetus usually occurs between 27 and 35 days gestation, when the central nervous system tissues are most susceptible.^[17] After 45–50 days of gestation CVV infection is not expected to cause harmful effects.^[22] After 76 days the fetus has a functioning immune system and antibodies to the virus are produced.^[17]

Autopsies of infected fetuses show severe lesions in the brain and spinal column, ranging from microscopic in size to whole sections of the brain missing.^[17][21] In one laboratory case, the cerebral hemispheres were nothing more than fluid-filled sacs that were easily ruptured.^[23] The most common musculoskeletal deformations include arthrogryposis and greatly reduced muscle mass, with the most severe cases having torticollis, scoliosis, and kyphosis.^[23] While most affected lambs are stillborn, those that do survive are usually so weak they die within minutes of birth.^[24] During the time that they are alive, these lamb are reported to act abnormal, such as acting weak, drowsy, or walking unsteadily.^[25]

Pathology[edit]

When ewes were experimentally infected with Akabane virus, a teratogenic virus of the genus Orthobunyavirus closely related to Cache Valley virus, the virus was shown to replicate in the trophoblastic cells of the placenta. When the virus crossed the placenta and infected the developing fetus, it showed a tropism for the immature fetal cells of the central nervous system and skeletal muscle.^[21] Hydranencephaly has also been identified in goat kids with presumptive in utero infection with Cache Valley virus.^[26]

History[edit]

Cache Valley virus was first isolated from mosquitoes in Utah in 1956.^[27] It derives its name from Cache Valley, an agricultural valley located in northern Utah and southeast Idaho. It is endemic to North America, specifically Canada, Mexico, and the United States.^[21] The first confirmed human case happened on November 2, 1995. In Texas in 1987, CVV was described as a possible causative agent of disease in sheep.^[18] The white-tailed deer population has been identified as a potential natural reservoir.^[4]

Prevention[edit]

Currently, there is no vaccine or known treatment available for CVV.^[28] The most effective method of protecting ruminants from CVV is to minimize their exposure to mosquito-infested areas during and shortly after breeding season.^[28] Concerning the safety of humans, it is advised that necessary precautions be taken, such as, putting on mosquito repellent or layers of clothing, when being exposed to mosquito-infested areas.

References[edit]

1. ^ ^abcdGrimstad, P. (2001). Cache Valley virus. Encyclopedia of Arthropod-transmitted Infections of Man and Domesticated Animals: 101-104.
2. ^Sims, R., Dr. (2009, December 30). Can Cache Valley virus trash your manufacturing? [Web log post]. http://rmcpharmanews.blogspot.com/2009/12/can-cache-valley-virus-trash-your.html.
3. ^Cache Valley virus. (2012). http://medical-dictionary.thefreedictionary.com/Cache Valley virus.
4. ^ ^abcdNguyen, N. L., Zhao, G., Hull, R., Shelly, M. A., Wong, S. J., Wu, G., … Menegus, M. A. (2013) Cache Valley Virus in a Patient Diagnosed with Aseptic Meningitis. Journal of Clinical Microbiology, 51(6), 1966–1969. doi:10.1128/JCM.00252-13
5. ^Obijeski, J., & Murphy, F. (1977, May 31). Bunyaviridae: Recent Biochemical Developments [Electronic version]. Journal of General Virology, 37, 1–14.
6. ^Shi, X., Kohl, A., Li, P., & Elliott, R. M. (2007, September). Role of the Cytoplasmic Tail Domains of Bunyamwera Orthobunyavirus Glycoproteins Gn and Gc in Virus Assembly and Morphogenesis. Journal of Virology, 81(18), 10151–10160. Retrieved from http://jvi.asm.org/content/81/18/10151.full /
7. ^Shi X, Goli J, Clark G, Brauburger K, Elliott RM (October 2009). 'Functional analysis of the Bunyamwera orthobunyavirus Gc glycoprotein'. J Gen Virol. 90 (10): 2483–2492. doi:10.1099/vir.0.013540-0. PMC2885756. PMID19570952.
8. ^Orthobunyavirus (n.d.). In Viral Zone. Retrieved from http://viralzone.expasy.org/all_by_species/250.html
9. ^Shi, X., van Mierlo, J. T., French, A., & Elliott, R. M. (2010, June 23). Visualizing the Replication Cycle of Bunyamwera Orthobunyavirus Expressing Fluorescent Protein-Tagged Gc Glycoprotein. Journal of Virology, 84(17), 8460–8469. Retrieved from http://jvi.asm.org/content/84/17/8460.full
10. ^ ^abcSzemiel A, Failloux AB, Elliott R. (2012). Role of Bunyamwera Orthobunyavirus NSs Protein in Infection of Mosquito Cells. PLoS Negl Trop Dis 6(9): e1823.
11. ^Kohl A, Clayton RF, Weber F, Bridgen A, Randall RE, et al. (2003) Bunyamwera virus nonstructural protein NSs counteracts interferon regulatory factor 3-mediated induction of early cell death. J Virol 77: 7999–8008.
12. ^Thomas D, Blakqori G, Wagner V, Banholzer M, Kessler N, et al. (2004) Inhibition of RNA polymerase II phosphorylation by a viral interferon antagonist. J Biol Chem 279: 31471–31477.
13. ^Hart TJ, Kohl A, Elliott RM (2009) Role of the NSs Protein in the Zoonotic Capacity of Orthobunyaviruses. Zoonoses Public Health 56: 285–296.
14. ^Blakqori G, Delhaye S, Habjan M, Blair C, Sanchez-Vargas I, et al. (2007) La Crosse bunyavirus nonstructural protein NSs serves to suppress the type I interferon system of mammalian hosts. J Virol 81: 4991–4999.
15. ^ ^abcSexton, D., Rollin, P., Breitschwerdt, E., Myers, S., Dumais, M., Bowen, M., & Goldsmith, C, et al. 1997, February 20). Life-Threatening Cache Valley Virus Infection [Electronic version]. The New England Journal of Medicine, 547–550. doi:10.1056/NEJM199702203360804
16. ^ ^abcdCampbell, G., Mataczynski, J., Reisdorf, E., Powell, J., Martin, D., Lambert, A., & Haupt, T, et al. (2006, May). Second Human Case of Cache Valley Virus Disease [Electronic version]. Emerging Infectious Diseases, 12(5)
17. ^ ^abcdefgBUNYAVIRAL DISEASES OF ANIMALS (excluding Rift Valley fever and Crimean—Congo haemorrhagic fever)*. (2012). In Manual of diagnostic tests and vaccines for terrestrial animals: (mammals, birds and bees) (7th ed., Vol. 2nd, pp. 2–4). Paris: Office international des épizooties.
18. ^ ^abChung, S., Livingston, C., Edwards, J., Crandell, R., Shope, R., Shelton, M., & Collisson, E. (1990). Evidence that cache valley virus induces congenital malformations in sheep. Veterinary Microbiology, 297–307.
19. ^Sahu, S., Pedersen, D., Ridpath, H., Ostlund, E., Schmitt, B., & Alstad, D. (2002). Serologic survey of cattle in the northeastern and north central United States, Virginia, Alaska, and Hawaii for antibodies to Cache Valley and antigenically related viruses (Bunyamwera serogroup virus). The American Journal of Tropical Medicine and Hygiene, 67, 119–122.
20. ^https://vetrecordcasereports.bmj.com/content/7/1/e000725
21. ^ ^abcdefZeller, H., & Bouloy, M. (2000). Infections by viruses of the families Bunyaviridae and Filoviridae. Scientific and Technical Review of the Office International des Epizooties, 19(1), 79–91. Retrieved from http://www.oie.int/doc/ged/d9289.pdf
22. ^ ^abSchoenian, S. (n.d.). Sheep 201: Sheep diseases A–Z. Retrieved December 5, 2014, from http://www.sheep101.info/201/diseasesa-z.html
23. ^ ^abEdwards, J., Livingston, C., Chung, S., & Collisson, E. (1989). Ovine Arthrogryposis and Central Nervous System Malformations Associated with in utero Cache Valley Virus Infection: Spontaneous Disease. Veterinary Pathology, 26, 33–39.
24. ^Redden, R., & Dyer, N. (2011, January 13). Cache Valley Virus May Have Affected N.D. Sheep (E. Crawford, Ed.). Retrieved December 6, 2014, from http://www.ag.ndsu.edu/news/newsreleases/2011/jan-10-2011/cache-valley-virus-may-have-affected-n-d-sheep
25. ^'Mosquito-spread virus affecting lamb crop Pipestone County Star'. Pipestone County Star. 16 February 2011.
26. ^https://vetrecordcasereports.bmj.com/content/7/1/e000725
27. ^Goldsmith, C., Ksiazek, T., Rollin, P., Corner, J., Nicholson, W., Peret, T., & Erdman, D, et al. (2013). Cell Culture and Electron Microscopy for Identifying Viruses in Diseases of Unknown Cause [Electronic version]. Medscape Multispecialty, 19(6)
28. ^ ^abHannaway N. (2014). Cache Valley Virus showing up in Ohio sheep. Ohio’s Country Journal: 1.