About the virus
The Zika virus belongs to Flaviviridae and the genus Flavivirus, and is thus related to the dengue, yellow fever, Japanese encephalitis, and West Nile viruses.
About the vector
The (Aedes aegypti) is a mosquito that can be recognized by white markings on its legs and a marking in the form of a lyre on the upper surface of the thorax. The mosquito originated in Africa but is now found in tropical and subtropical regions throughout the world.
The average wing length of female Aedes aegypti mosquitoes varies greatly (1.67–3.83 mm in a Peruvian habitat). It also transmits the yellow fever virus.
Transmission
Zika virus is primarily transmitted to humans through bites from Aedes mosquitos, which often live around buildings in urban areas and are usually active during daylight hours (peak biting activity occurs in early mornings and late afternoons).
Some evidence suggests Zika virus can also be transmitted to humans through blood transfusion, perinatal transmission and sexual transmission. However, these modes are very rare.
The incubation period is typically between 2 and 7 days.
The disease
Zika fever (also known as Zika virus disease) is an illness caused by the Zika virus. Most cases have no symptoms, but when present are usually mild and can resemble dengue fever. Symptoms generally last less than seven days. Symptoms may include fever, red eyes, joint pain, headache, and a maculopapular rash. It has not caused any reported deaths during the initial infection. Infection has been linked to Guillain–Barré syndrome (GBS). Diagnosis is by testing the blood, urine, or saliva for the presence of Zika virus RNA when the person is sick.
Prevention involves decreasing mosquito bites in areas where the disease occurs, and proper use of condoms. Efforts include the use of insect repellent, covering much of the body with clothing, mosquito nets, and getting rid of standing water where mosquitoes reproduce. There is no effective vaccine. Health officials recommend that women in areas affected by outbreaks consider putting off pregnancy due to the 2015–16 Zika outbreak and pregnant women not travel to areas where outbreaks were occurring. While there is no specific treatment, but paracetamol (acetaminophen) may help with the symptoms. Admission into the hospital is rarely necessary.
The Zika virus story
On 18 April 1947, a rhesus monkey that researchers identified as 766 had a fever of 39.7°C, about 2°C higher than normal. The monkey was used for a study hunting for yellow fever virus and was living in a cage on a platform built into the tree canopy in the 1.5-kilometer-long Zika Forest, which runs adjacent to an arm of Lake Victoria in Uganda. Three days later, the investigators took a blood sample from the monkey and injected it into the brains of some mice. The mice “showed signs of sickness” after 10 days, and the researchers harvested their brains, from which they isolated a “filterable transmissible agent.”
The following year, around January, the same researchers trapped mosquitoes from these canopy platforms and took them back to the lab, hoping to isolate yellow fever virus. Others had shown that one of these species they caught, Aedes africanus, shuttled the yellow fever virus, so the investigators put 86 of the insects in a refrigerator to “render them inactive” and then ground them up in a blood-saline solution, which they again injected into the brains of mice. The animals “appeared inactive” after 7 days, and tests showed they harboured the same transmissible agent that had sickened Rhesus 766. The researchers called their “hitherto unrecorded virus” Zika.
The Uganda Virus Research Institute in Entebbe, located 11 kilometers northeast of the Zika Forest, just after the end of World War II carried out the meticulous work that isolated the pathogen. The researchers included a Scottish virologist, George Dick of the National Institute for Medical Research in London, and two former members of the Rockefeller Foundation in New York City, Stuart Kitchen and Alexander Haddow. They waited until September 1952 to publish their findings, which appeared in back-to-back papers in the Transactions of the Royal Society of Tropical Medicine and Hygiene. In addition to experiments with more rhesus monkeys and mice, their exhaustive studies put the Zika virus into grivet and red tail monkeys, cotton rats, guinea pigs, and rabbits. The virus caused damage to neurons only in mice. Six of 99 humans they tested in four different Ugandan locales had antibodies to their new bug, but none showed evidence of disease. As one of the two papers drily concluded, “The absence of the recognition of a disease in humans caused by Zika virus does not necessarily mean that the disease is either rare or unimportant.”
The same journal would publish 10 of the 24 total Zika studies that appeared in the scientific literature over the next 30 years, including a 1954 paper that attempted to link the virus to an epidemic of jaundice in Nigeria. The data in this study by esteemed virologist Francis Macnamara were sketchy and the correlations weak save for the detail that 50 of 84 people tested had antibodies against the strange agent—the first clue that it was widespread. Mice also became ill when injected with Zika-antibody-positive serum taken from one 10-year-old girl who had a temperature of 38.2°C and a headache. But she did not have jaundice. Confused by the results, medical researcher William Bearcroft decided to take matters into his own hands—literally. As he reported in September 1956, a 34-year-old European male who had been living in Nigeria for 4.5 months—that would be Bearcroft himself—injected into his arm a suspension of Zika-infected mouse brain used in the 1954 study. Eighty-two hours later, Bearcroft had a headache and a slight temperature.Curious about the route of viral transmission, on the 5th day after the injection—by which time his symptoms had disappeared—Bearcroft put a batch of female A. aegypti mosquitoes on his left forearm, and 95 of them became engorged with his blood. He did this two more times over the next few days and then put some of the mosquitoes on baby mice and ground up others, injecting them into the rodents. Nothing happened. Bearcroft suggested that his symptoms resembled those seen in the 10-year-old girl. “Whilst no conclusions can be drawn from an experience limited to two cases, it should be noted that in those which represent the only proved examples of the human disease no evidence of jaundice appeared,” he wrote.
Nothing more appeared in the literature about Zika virus infections of humans until 1964 when David Simpson, a student of Zika co-discoverer George Dick, reported that those first two cases likely were not Zika but its close relative, Spondweni. Simpson, who was working in the same Entebbe lab that discovered the virus, claimed that he had evidence of the first actual human case: a 28-year-old European male—David Simpson—who had been in Uganda for 2.5 months when he became ill while working with Zika strains isolated from mosquitoes. Simpson’s symptoms were distinct from the others in one key way: he had a “diffuse pink maculopapular rash which covered the face, neck, trunk and upper arms” and that eventually spread to all four limbs, the palms of the hands, and the soles of the feet. It did not itch, he reported, but the rash lasted for 5 days. He described the disease as “mild,” and noted that there was no “crippling bone pain” as occurred with three other mosquito-borne viruses: dengue, chikungunya, and o'nyong-nyong.
When Simpson inoculated mice with his blood, they became sick and some died. He passed blood from these mice into the brains of other mice, harvested that “material” and tested antibodies against Zika and 11 related viruses—including Spondweni—to see which stuck. He had Zika, no question. “If this was a typical infection with Zika virus it is not surprising that under normal circumstances the virus is not isolated frequently from man,” he wrote.
Nearly a decade would pass before another report of a human Zika infection appeared and, once again, it was a lab worker, this time in Mozambique with Portugal’s Institute of Hygiene and Tropical Medicine. In the 1973 paper, published in the German journal Archiv für die gesamte Virusforschung (Archive for the Entire Virus Research), C.M.V. Martins described his symptoms as fever with some pain in joints, but no rash. He recovered completely after 1 week.
According to Martins and co-authors, scientists had by then isolated 312 “arboviruses”—meaning spread by arthropods like mosquitoes and ticks—82 of which caused human infections, yet all but 39 were rarely observed diseases. “Thus, the knowledge of the pathogenic potential of about half of the arboviruses capable of causing symptomatic disease in humans has been acquired mainly from the study of laboratory infection,” they concluded. In other words, you needed lab accidents to understand disease.
Loads of countries began reporting evidence of Zika antibodies in humans and wild monkeys in the 1970s and 80s, but documented cases of people with disease remained scarce, with scattered reports of human Zika virus infections trickling in from Nigeria and Indonesia. Then nothing until 2007, when physicians on Yap Island in the Federated Republic of Micronesia noticed an outbreak of a disease that resembled mild cases of dengue but was distinct, in part because people had a rash. A report of this outbreak in 2009 for the first time earned Zika a slot in a high-profile publication, The New England Journal of Medicine. As the authors noted, “No outbreaks and only 14 cases of human Zika virus disease have been previously documented.
The paper documented 49 confirmed and 59 probable Zika cases.
But household surveys of 557 people found Zika antibodies in 74% of the islanders. The researchers estimated that some 5000 people had been infected, and that 900 of them had illness “attributable to Zika.” No one was hospitalized, and no one died. No mosquitoes, surprisingly, were found with the virus.
Odd case reports soon followed. Two U.S. scientists diagnosed in Colorado were apparently infected in Senegal, and one of them infected his wife, presumably through sex, when he returned home; they only thought to test for Zika because of a chance meeting with a grandson of Alexander Haddow, one of the researchers who discovered the virus. A U.S. Navy research station in Cambodia detected a case in a 3-year-old boy. A 52-year-old woman in Australia was diagnosed after returning home from a holiday in Indonesia. Then in 2013, an outbreak walloped French Polynesia, with 333 confirmed cases and an estimated 19,000 suspected others. For the first time, the disease was associated with serious symptoms: mainly neurological disorders, including Guillain-Barré syndrome, which sometimes causes a temporary paralysis, and, in rare instances, is deadly. Two babies also were infected in utero or during delivery, but neither had lasting health problems.
Cases of traveller-associated Zika began to mount: A Norwegian who vacationed in Tahiti, a Canadian who went to Thailand, and Japanese tourists who visited Bora Bora, an Australian who explored the Cook Islands, and a German who returned from Malaysian Borneo.
The first published report of “autochthonous” cases in Brazil—meaning they were not imported—appeared in June 2015.
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