User:Graham Beards/viruses/Zoonoses and emerging viruses

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On November 16, 2002, a 45-year-old man living in Foshan City, in the Guandong Province of China became severely ill with pneumonia. A short time later, four of his close relatives had caught his disease. Within three months the disease had spread throughout Guangzhou (the Province capital) and by February 2003, 305 cases, including five deaths were reported. Later that month infections occurred in Hong Kong, Vietnam, Singapore and Toronto. In March, the World Health Organisation received reports of a further 150 cases. Within weeks the disease spread to 8,096 people in 29 countries. A new disease – now known as SARS – had emerged.[1]

SARS (severe acute respiratory syndrome) is caused by a new type of coronavirus.[2] Other coronviruses were known to cause mild infections in humans, [3] so the virulence and rapid spread of this novel virus strain caused alarm among health professionals as well public fear.[4] But the fears of a major pandemic were not realised, and by July 2003, after causing around 8,000 cases and 800 deaths, it was all over.[5] The exact origin of the SARS virus is not known, but evidence suggests that it came from bats.[6] When viruses jump to other species the diseases caused in humans are called zoonoses or zoonotic infections.[7]

Influenza virus from animals can cross the species barrier by antigenic shift

Zoonoses[edit]

The most infamous and probably the most feared zoonotic infection is rabies. A disease transmitted from animals (usually dogs) to humans by bites. But many others occur. Influenza pandemics often begin as a zoonosis, and this is why they are called swine 'flu, or avian 'flu.[8] HIV began as a zoonotic infection from chimps, the deadly Ebola and Marburg viruses are transmitted to humans by monkeys,[9] and Lassa fever by rats (Mastomys natalensis).[10] Zoonotic infections can be severe because humans often have no natural resistance to the infection and it is only when viruses become well-adapted to new host that their virulence decreases. Some zoonotic infections are often "dead ends", in that after the initial outbreak the rate of subsequent infections subsides because the viruses are not efficient at spreading from person to person.[11]

West Nile virus maintains itself in nature by cycling between mosquitoes and birds. Other species such as humans and horses are incidental infections, as they are not the mosquitoes' preferred blood meal source. The virus does not amplify within these species and they are known as dead-end hosts.

West Nile virus, a flavivirus, was first identified in 1937 when it was found in the blood of a febrile woman. The virus, which is carried by mosquitoes and birds, caused outbreaks of infection in North Africa and the Middle East in the 1950s and by the 1960s horses in Europe fell victim. The largest outbreak in humans occurred in 1974 in Cape Province, South Africa and 10,000 people became ill.[12] An increasing frequency of epidemics and enzootics (in horses) began in 1996, around the Mediterranean basin and by the summer of 1999 the virus reached New York. Since then, the virus has spread throughout the United States.[13] In the US, mosquitoes carry the highest amounts of virus in late summer, and the rate of the disease increases in late August to early September. When the weather becomes colder, the mosquitoes die and the risk of disease decreases. In Europe, many outbreaks have occurred and in 2000 a surveillance programme began in the UK to monitor the incidence of the virus in humans, dead birds, mosquitoes and horses.[14] The mosquito (Culex modestus) that can carry the virus breeds on the marshes of north Kent. This species was not previously thought to be present in the United Kingdom but it is widespread in southern Europe, where it acts as the principle bridge vector of West Nile Virus.[15]

Emerging viruses[edit]

Marburg virus

Several highly lethal viral pathogens are members of the Filoviridae. Filoviruses are filament-like viruses that cause viral hemorrhagic fever, and include the Ebola and Marburg viruses. The Marburg virus attracted widespread press attention in April 2005 for an outbreak in Angola. Beginning in October 2004 and continuing into 2005, the outbreak was the world's worst epidemic of any kind of viral haemorrhagic fever.[16]

In 1997 an outbreak of respiratory disease occurred in Malaysian farmers and their pigs. Later more than 265 cases of encephalitis of which 105 were fatal, were recorded.[17] A new paramyxovirus was discovered in one of the victim's brains, which was named Nipah virus, after the village where he had lived. The infection was caused by a virus from fruit bats, after their colony had been disrupted by deforestation. The bats had moved to trees nearer the pig farm and the pigs caught the virus from their droppings.[18] Nipah virus was the inspiration for the MEV-1 virus in the film Contagion.[19]

A recurring theme is the invasion by humans of animal habitats and the transmission of novel viruses to densely populated urban centres. As the world gets smaller and its population continues to grow, the emergence of exotic viruses will continue,[20] – in September 2012, a Qatari man became critically ill with a previously unknown virus related to SARS.[21]

Public health implications[edit]

As was seen during the 2009 swine flu pandemic, rapidly emerging viral zoonoses, can be highly disruptive. Public health interventions might have little success and speculative reporting in the media can fuel unwarranted fears. Medical laboratories often see a huge demand for tests, which they do not have the resources to satisfy. And often the tests do not work,[22] or do not exist.[23] As seen in AIDS, the control of epidemics is strengthened when the affected populations are made aware of the nature of the virus, its route of transmission and behavioural risk factors.[24] Vaccines are rarely available or effective in the early stages of pandemics. Priority should be given to reasonably accurate estimates of morbidity and mortality rates and not assume the worst case scenario. In 2009, the world was convinced that history was about to repeat itself and an influenza epidemic on the scale of the one in 1918 was on the horizon. In the UK there were around 90 deaths during the first wave of the epidemic, and around 240 in the second.[25] In both waves most infections were asymptomatic, but the severity of illness was not part of the WHO pandemic definition. In contrast, the 1918 mortality rate was more than 100 times higher.[26]

  1. ^ Mahy (b) p.458–459
  2. ^ Mahy (b) p. 459
  3. ^ Weiss, S. R.; Leibowitz, J. L. (2011). "Coronavirus Pathogenesis". Advances in Virus Research Volume 81. Advances in Virus Research. Vol. 81. pp. 85–164. doi:10.1016/B978-0-12-385885-6.00009-2. ISBN 9780123858856. PMID 22094080.
  4. ^ Crawford (2011) p. 34
  5. ^ Crawford (2011) p. 37
  6. ^ MacLachlan p. 409
  7. ^ Levins p. 419
  8. ^ Kuiken, T.; Fouchier, R.; Rimmelzwaan, G.; Brand, J.; Riel, D.; Osterhaus, A. (2012). "Pigs, Poultry, and Pandemic Influenza: How Zoonotic Pathogens Threaten Human Health". Hot Topics in Infection and Immunity in Children VIII. Advances in Experimental Medicine and Biology. Vol. 719. pp. 59–66. doi:10.1007/978-1-4614-0204-6_6. ISBN 978-1-4614-0203-9. PMID 22125035.
  9. ^ Mahy (b) p. 382
  10. ^ Monath, T. P. (1975). "Lassa fever: Review of epidemiology and epizootiology". Bulletin of the World Health Organization. 52 (4–6): 577–592. PMC 2366662. PMID 782738.
  11. ^ Baum, S. G. (2008). "Zoonoses-with friends like this, who needs enemies?". Transactions of the American Clinical and Climatological Association. 119: 39–51, discussion 51–2. PMC 2394705. PMID 18596867.
  12. ^ Mahy (b) p. 504–505
  13. ^ Mahy (b) p. 504–505
  14. ^ Morgan, D. (2006). "Control of arbovirus infections by a coordinated response: West Nile Virus in England and Wales". FEMS Immunology & Medical Microbiology. 48 (3): 305–312. doi:10.1111/j.1574-695X.2006.00159.x. PMID 17054715.
  15. ^ Golding, N.; Nunn, M. A.; Medlock, J. M.; Purse, B. V.; Vaux, A. G.; Schäfer, S. M. (2012). "West Nile virus vector Culex modestus established in southern England". Parasites & Vectors. 5: 32. doi:10.1186/1756-3305-5-32. PMC 3295653. PMID 22316288.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  16. ^ Towner JS, Khristova ML, Sealy TK, et al.. Marburgvirus genomics and association with a large hemorrhagic fever outbreak in Angola. J. Virol.. 2006;80(13):6497–516. doi:10.1128/JVI.00069-06. PMID 16775337.
  17. ^ Crawford (2011) p.44–45
  18. ^ Chua KB, Chua BH, Wang CW (2002). "Anthropogenic deforestation, El Niño and the emergence of Nipah virus in Malaysia". Malays J Pathol. 24 (1): 15–21. PMID 16329551.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  19. ^ Uh-oh: Scientists say film 'Contagion' is for real
  20. ^ Crawford (2011) p. 48.
  21. ^ Meikle, James (Monday 24 September 2012). "Sars-like virus detected". The Guardian. Retrieved September 29, 2012. {{cite web}}: Check date values in: |date= (help)
  22. ^ Fleming, D. M.; Durnall, H. (2012). "Ten lessons for the next influenza pandemic—an English perspective : A personal reflection based on community surveillance data". Human Vaccines & Immunotherapeutics. 8 (1): 138–145. doi:10.4161/hv.8.1.18808. PMID 22251996.
  23. ^ Santos-Preciado, J.; Franco-Paredes, C.; Hernandez-Flores, I.; Tellez, I.; Del Rio, C.; Tapia-Conyer, R. (2009). "What Have We Learned from the Novel Influenza A (H1N1) Pandemic in 2009 for Strengthening Pandemic Influenza Preparedness?". Archives of Medical Research. 40 (8): 673–676. doi:10.1016/j.arcmed.2009.10.011. PMID 20304255.
  24. ^ Levin's p.281
  25. ^ Presanis, A. M.; Pebody, R. G.; Paterson, B. J.; Tom, B. D. M.; Birrell, P. J.; Charlett, A.; Lipsitch, M.; Angelis, D. D. (2011). "Changes in severity of 2009 pandemic A/H1N1 influenza in England: A Bayesian evidence synthesis". BMJ. 343: d5408. doi:10.1136/bmj.d5408. PMC 3168935. PMID 21903689.
  26. ^ Shanks, G. D.; Brundage, J. F. (2012). "Pathogenic Responses among Young Adults during the 1918 Influenza Pandemic". Emerging Infectious Diseases. 18 (2): 201–207. doi:10.3201/eid1802.102042. PMC 3310443. PMID 22306191.
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