Neurovirulence of the West Nile Virus
Sunit K. Singh, Daniel Růžek in Neuroviral Infections, 2013
The virus was first isolated from a febrile female patient in the West Nile region of Uganda in 1937 (Smithburn et al. 1940), and is associated with periodic epidemics of febrile illness throughout Africa, Southwest Asia, and Eastern Europe (Murgue et al. 2002). Historically, WNV was found to cycle between Culicine mosquitoes and native birds. Birds served as the natural amplifying host, and humans were accidental secondary hosts. Symptoms of infection included dengue-like illness such as fever, malaise, lymphadenopathy, and rash. Most infections were self-limiting and resolved without much sequelae (Goldblum et al. 1954). In the 1990s however, fatal cases of encephalitis became a significant feature of WNV epidemics in Romania, Russia, and Israel. Approximately 60% of hospitalized patients had West Nile neuroinvasive disease (WNND) with a 4% to 7% mortality rate (Klein et al. 2005).
Yellow Fever
James H. S. Gear in CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
The world-wide distribution of yellow fever was mapped out in 1929 and later.23 Thousands of serum specimens from North and South America, Africa, Asia, the East Indies, and Australasia were tested in virus neutralization tests in intracerebrally inoculated white mice. Yellow fever antibodies were shown to be widespread in South America and Africa, with immunes also in Central America and certain of the West Indies. This sampling and testing fortunately was accomplished before the yellow fever vaccines had been developed. Prior vaccination can complicate the issue. The information gained was of particular value in confirming that yellow fever had never, within the lifetimes of people sampled, invaded the countries of Asia and Australasia. Aedes aegypti is prevalent in many of these countries, and dengue epidemics are frequent in many of them. (Dengue is also transmitted by Aedes aegypti.) Yellow fever introduction remains a possibility, and for these countries, a valid (sic) yellow fever immunization certificate is required of people entering Asia and/or Australasia from regions known to be endemic for yellow fever (i.e., Africa and South America).
The Diseases – Malaria, Filariasis and Dengue
Jacques Derek Charlwood in The Ecology of Malaria Vectors, 2019
The ability of the eggs to survive in this way has also helped in the spread of the mosquitoes from their original Southeast Asian (albopictus) and African (aegypti) origins. Because of human-aided transport in general, especially of such things as used car tyres, the mosquitoes now occur anywhere the temperature is sufficiently warm in the summer to sustain them (Figure 12.13). They pose an increased threat as global warming continues. In addition to the mosquito, dengue has also spread from a relatively confined area to become a global pandemic. In the Americas it was controlled as part of the campaign against yellow fever in the 1930s such that, by the 1970s, it had been removed from large areas. Control measures were discontinued (‘Where is the problem? There are no mosquitoes anymore’), and there was a subsequent resurgence of mosquitoes along with a resurgent dengue epidemic. There was a time, not so long ago, when going to Brazil was an open invitation to get dengue.
Dengue Maculopathy Associated with Choroidopathy and Pseudohypopyon: A Case Series
Published in Ocular Immunology and Inflammation, 2018
Christina W. K. Ng, P. Y. Tai, Shelina Oli Mohamed
Dengue is a mosquito-borne viral disease. Dengue virus is a Flaviviridae of four serotypes (DEN-1, DEN-2, DEN-3, and DEN-4) transmitted by infected female mosquitoes Aedes aegypti and Aedes albopictus. The mosquitoes also transmit yellow fever, chikungunya, and Zika infection. Dengue is found in tropical and subtropical climates worldwide, mostly in urban and semi-urban areas. It has rapidly spread in recent years and is now endemic in more than 100 countries in regions of the Americas, South-East Asia, Western Pacific, Africa, and the Eastern Mediterranean.1 The first three regions are the most seriously affected. A recent multinational study estimated there to be 390 million dengue infections per year, of which 96 million manifest clinically.2 In Malaysia, since the year 2000, the incidence of dengue infection increased from 32 cases per 100 000 population to 361 cases per 100 000 population in 2014.3
Beyond thrombocytopaenia, haemorrhage and shock: the expanded dengue syndrome
Published in Pathogens and Global Health, 2018
Senaka Rajapakse, Milanka Wattegama, Praveen Weeratunga, P. Chathurani Sigera, Sumadhya Deepika Fernando
Dengue is caused by a flavivirus transmitted by Aedes mosquitoes. It is prevalent in tropical and subtropical countries, and is currently endemic in South East Asia and the Asia-Pacific Regions. Almost 4 billion people are at risk, and 50–100 million people are infected with dengue each year [1,2]. There are four serotypes of dengue virus, DEN 1–4. Dengue infection has varied presentations, ranging from undifferentiated fever to life threatening haemorrhagic fever (DHF), characterised by plasma leakage and shock syndrome (DSS). Dengue must be considered as a probable diagnosis in patients who live in or recently travelled to a dengue endemic area, presenting with fever and at least two of the following: nausea, vomiting, rash, aches and pains, positive tourniquet test, leukopaenia, or any of a set of defined warning signs (abdominal pain or tenderness, persistent vomiting, clinical fluid accumulation, mucosal bleeding, lethargy, restlessness, hepatomegaly, increase in haematocrit with rapid decrease in platelet count). The latter warning signs may herald the onset of severe dengue, characterised by severe plasma leakage resulting in shock and other manifestations of third space fluid accumulation, and severe bleeding [3].
Vaccination against SARS-CoV-2 and disease enhancement – knowns and unknowns
Published in Expert Review of Vaccines, 2020
Raphaël M. Zellweger, T. Anh Wartel, Florian Marks, Manki Song, Jerome H. Kim
More recently, a live-attenuated tetravalent dengue vaccine proved to be protective in individuals who were seropositive for dengue prior to vaccination, but increased the risk of hospitalization and severe disease in individuals who were seronegative [20]. This was widely attributed to antibody-dependent enhancement (ADE) of infection, a phenomenon in which sub-neutralizing levels of antibodies increase Fc-receptor-mediated viral entry, resulting in higher viral burden and exacerbated disease. ADE of dengue is not only a concern after vaccination. Epidemiological data have long suggested that ADE is relevant in the context of natural immunity and infection as well [21]. Indeed, ADE is often used to explain why severe dengue disease is more frequent in individuals with a history of exposure to a heterologous dengue serotype, or in infants (around 6–9 months of age) born to dengue-immune mothers [21,22]. Hence, it is important to note that while vaccination against RSV and dengue both exemplified the possibility of vaccine-induced increased pathology upon infection, the mechanisms postulated for disease exacerbation were distinct.
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