Zika, which was discovered incidentally in Uganda in 1947 in the course of mosquito and primate surveillance, had until now remained an obscure virus confined to a narrow equatorial belt running across Africa and into Asia.. The virus circulated predominantly in wild primates and arboreal mosquitoes such as Aedes africanus and rarely caused recognized “spillover” infections in humans, even in highly enzootic areas.
Its current explosive pandemic reemergence is therefore truly remarkable. Decades ago, African researchers noted that aedes-transmitted Zika epizootics inexplicably tended to follow aedes-transmitted chikungunya epizootics and epidemics. An analogous pattern began in 2013, when chikungunya spread pandemically from west to east, and Zika later followed.
With the exception of West Nile virus, which is predominantly spread by culex-species mosquitoes, the arboviruses that recently reached the Western Hemisphere have been transmitted by aedes mosquitoes, especially the yellow fever vector mosquito A. aegypti. These viruses started to emerge millennia ago, when North African villagers began to store water in their dwellings. ArborealA. aegypti then adapted to deposit their eggs in domestic water-containing vessels and to feed on humans, which led to adaptation of arboreal viruses to infect humans. The yellow fever, dengue, and chikungunya viruses evolved entirely new maintenance cycles of human–A. aegypti–human transmission.
Through early epidemiologic surveillance and human challenge studies, Zika was characterized as a mild or inapparent denguelike disease with fever, muscle aches, eye pain, prostration, and maculopapular rash. In more than 60 years of observation, Zika has not been noted to cause hemorrhagic fever or death. There is in vitro evidence that Zika virus mediates antibody-dependent enhancement of infection, a phenomenon observed in dengue hemorrhagic fever; however, the clinical significance of that finding is uncertain
Its current explosive pandemic reemergence is therefore truly remarkable. Decades ago, African researchers noted that aedes-transmitted Zika epizootics inexplicably tended to follow aedes-transmitted chikungunya epizootics and epidemics. An analogous pattern began in 2013, when chikungunya spread pandemically from west to east, and Zika later followed.
With the exception of West Nile virus, which is predominantly spread by culex-species mosquitoes, the arboviruses that recently reached the Western Hemisphere have been transmitted by aedes mosquitoes, especially the yellow fever vector mosquito A. aegypti. These viruses started to emerge millennia ago, when North African villagers began to store water in their dwellings. ArborealA. aegypti then adapted to deposit their eggs in domestic water-containing vessels and to feed on humans, which led to adaptation of arboreal viruses to infect humans. The yellow fever, dengue, and chikungunya viruses evolved entirely new maintenance cycles of human–A. aegypti–human transmission.
Through early epidemiologic surveillance and human challenge studies, Zika was characterized as a mild or inapparent denguelike disease with fever, muscle aches, eye pain, prostration, and maculopapular rash. In more than 60 years of observation, Zika has not been noted to cause hemorrhagic fever or death. There is in vitro evidence that Zika virus mediates antibody-dependent enhancement of infection, a phenomenon observed in dengue hemorrhagic fever; however, the clinical significance of that finding is uncertain
Comentarios