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Zika virus disease is a mosquito-borne viral disease caused by Zika virus (ZIKV), a flavivirus from the Flaviviridae family and Spondweni serocomplex. The virus was first identified in 1947 in the Zika forest in Uganda in the rhesus macaque population [8]. There are two main lineages of ZIKV, the African lineage and the Asian lineage [9-11].
The main symptoms of ZIKV disease include:
low-grade fever (<38.5?C)
transient arthritis/arthralgia with possible joint swelling mainly in the smaller joints of the hands and feet
maculo-papular rash often spreading from the face to the body conjunctival hyperaemia or bilateral non-purulent conjunctivitis
general non-specific symptoms such as myalgia, asthenia and headaches.
The incubation period ranges from 3 to 12 days [12]. The disease symptoms are usually mild and last for 2 to 7 days. Infection may go unrecognised or be misdiagnosed as dengue, chikungunya or other viral infections giving fever and rash. Asymptomatic infections are common ?as described with flaviviral infections such as dengue and West Nile fever? and only one in four people infected with ZIKV are believed to develop symptoms [13,14].
Association with neurological complications such as Guillain-Barr? syndrome has been suspected during the French Polynesia outbreak and remains under investigation [12,15-17]. Most people recover fully without severe complications, and hospitalisation rates are low. To date, there have been no reported deaths associated with ZIKV infection.
Prenatal or perinatal complications of ZIKV infections have not been described in the literature. There is some evidence that perinatal transmission can occur, most probably transplacental or during the delivery of a viraemic mother [14,18,19]. ZIKV transfusion-derived transmission is theoretically possible as 3% of asymptomatic blood donors (42/1 505) were found positive for ZIKV by PCR during the ZIKV outbreak in French Polynesia, from November 2013 to February 2014 [13]. The presence of a viable virus was detected in semen more than two weeks after recovery from an illness consistent with ZIKV infection [20]. Possible cases of sexual transmission of ZIKV have been reported [20,21]. However, the three modes of transmission described above have been rarely reported to date.
Zika virus vectors
In East Africa, ZIKV is maintained in a sylvatic cycle with cyclic epizooty involving non-human primates and a wide variety of sylvatic and peri-domestic Aedes mosquitoes [22-25]. In Asia, Aedes aegypti is considered an important vector of ZIKV as the virus has been detected in wild-caught Aedes aegypti, and experimental infections show that this species is capable of transmitting ZIKV [26,27]. During the outbreak in Yap in Micronesia, Aedes hensilii has been suspected as a vector because of its abundance coinciding with the outbreak. ZIKV was not detected in Aedes hensilii captured during this outbreak [14], but it has been shown to be a potential vector of ZIKV based on evidence from experimental infections [28]. In Singapore, Aedes albopictus is also a potential vector of ZIKV, based on data from experimental infections [29]. Aedes albopictus has been found naturally infected in Gabon [30].
Zika virus epidemiology
Since its first isolation in 1947 in Uganda, serological, epidemiological and entomological studies reported the circulation of the ZIKV in tropical areas of western Africa (Nigeria, Sierra Leone, Ivory Coast, Cameroon and Senegal) and of central Africa (Gabon, Uganda and Central African Republic), in Asia (Pakistan, Indonesia, Philippines, Malaysia, Cambodia and Thailand) and in several islands of the pacific region since 2007 (Micronesia, Cook Islands, French Polynesia, New Caledonia, Guam, Samoa, Vanuatu and Solomon Islands).
Outbreaks of ZIKV infection on Yap Island (2007) and in French Polynesia (2013?2014), with further spread to New Caledonia, the Cook Islands and Easter Island, have shown the propensity of this arbovirus to spread outside its usual geographical range and to cause large outbreaks [31].
Between 7 October 2013 and 6 April 2014, 8 750 suspected cases of ZIKV infection were reported by the syndromic surveillance sentinel network of French Polynesia, with 383 confirmed cases and an estimated 32 000 cases having consulted a healthcare facility for the condition [32,33]. During the outbreak, 74 individuals presented with neurological symptoms or auto-immune syndrome following a disease episode with symptoms consistent with ZIKV infection in previous days [17,34-36]. Of these, 42 were confirmed as Guillain-Barr? syndrome, with 37 cases having presented with a previous viral syndrome. The causal link between ZIKV infection and Guillain-Barr? syndrome is still not established.
Since 2014, indigenous circulation of ZIKV has been detected in the Americas. In February 2014, the public health authorities of Chile confirmed the first case of autochthonous transmission of ZIKV infection on Easter Island and cases were reported until June 2014. Since February 2015, cases of rash illness were reported in north-eastern Brazil in the states of Bahia, Maranhao, Pernambuco, Rio Grande do Norte, Para?ba and Sergipe [37]. A total of 14 835 cases of acute exanthematous illness have been reported in 12 health districts of Salvador ? the third city of Brazil ? between 15 February 2015 and 25 June 2015 (overall attack rate 5.5 cases/10 000 inhabitants) [38]. Twenty-four case of Guillain-Barr? syndrome were hospitalised during this period. The outbreak peaked in May at the time of ZIKV confirmation in patients leaving nearby Salvador city. During the same period the number of dengue cases did not vary substantially and 58 suspected chikungunya were identified by the Salvador Epidemiologic Surveillance Office. The authors suggest ZIKV as an etiological factor of this exanthematous illness outbreak because of the low frequency of arthralgia usually seen in chikungunya disease and concomitant confirmed ZIKV infections in the area [38].
In May 2015, the public health authorities of Brazil confirmed autochthonous transmission of ZIKV in the states of Bahia and Rio Grande do Norte [39]. As of November 2015, 15 states had confirmed autochthonous virus transmission [40]. In Brazil, between January and July 2015, 121 cases of neurological manifestations and GuillainBarr? syndrome have been notified in several north-eastern states with history of previous rash illness [41]. Investigations were launched and are on-going regarding possible association with ZIKV infection [42]. Phylogenetic analysis on serum samples from patients hospitalised in March at Santa Helena Hospital in Cama?ari, Bahia, Brazil showed that ZIKV sequences identified belonged to the Asian lineage and showed 99% identity with a sequence from a ZIKV isolate from French Polynesia [43].
In September 2015, Colombian health authorities reported the detection of the first autochthonous cases of ZIKV infection in the state of Bol?var. As of week 45, 488 confirmed cases of ZIKV infections and 1 583 suspected cases have been reported, distributed in 26 of the 36 departments [44].
On 3 November 2015, the Cape Verde Ministry of Health reported that 17 out of 64 blood samples sent for confirmation at Pasteur Institute in Dakar were positive for ZIKV and there were approximately 1 000 suspected cases with symptoms consistent with ZIKV infection as of 1 November 2015 [45].
On 12 November 2015, health authorities in Suriname reported five confirmed cases of ZIKV [46].
In conclusion, there is limited but increasing knowledge about ZIKV infection in humans [47,48]. Uncertainties remain about disease complications, genetic susceptibility and levels of risk for pregnant women, newborns or patients presenting with specific co-morbidities. The expansion of the ZIKV infections to South America constitutes a significant development in the epidemiology of this emerging vector-borne disease.
The main symptoms of ZIKV disease include:
low-grade fever (<38.5?C)
transient arthritis/arthralgia with possible joint swelling mainly in the smaller joints of the hands and feet
maculo-papular rash often spreading from the face to the body conjunctival hyperaemia or bilateral non-purulent conjunctivitis
general non-specific symptoms such as myalgia, asthenia and headaches.
The incubation period ranges from 3 to 12 days [12]. The disease symptoms are usually mild and last for 2 to 7 days. Infection may go unrecognised or be misdiagnosed as dengue, chikungunya or other viral infections giving fever and rash. Asymptomatic infections are common ?as described with flaviviral infections such as dengue and West Nile fever? and only one in four people infected with ZIKV are believed to develop symptoms [13,14].
Association with neurological complications such as Guillain-Barr? syndrome has been suspected during the French Polynesia outbreak and remains under investigation [12,15-17]. Most people recover fully without severe complications, and hospitalisation rates are low. To date, there have been no reported deaths associated with ZIKV infection.
Prenatal or perinatal complications of ZIKV infections have not been described in the literature. There is some evidence that perinatal transmission can occur, most probably transplacental or during the delivery of a viraemic mother [14,18,19]. ZIKV transfusion-derived transmission is theoretically possible as 3% of asymptomatic blood donors (42/1 505) were found positive for ZIKV by PCR during the ZIKV outbreak in French Polynesia, from November 2013 to February 2014 [13]. The presence of a viable virus was detected in semen more than two weeks after recovery from an illness consistent with ZIKV infection [20]. Possible cases of sexual transmission of ZIKV have been reported [20,21]. However, the three modes of transmission described above have been rarely reported to date.
Zika virus vectors
In East Africa, ZIKV is maintained in a sylvatic cycle with cyclic epizooty involving non-human primates and a wide variety of sylvatic and peri-domestic Aedes mosquitoes [22-25]. In Asia, Aedes aegypti is considered an important vector of ZIKV as the virus has been detected in wild-caught Aedes aegypti, and experimental infections show that this species is capable of transmitting ZIKV [26,27]. During the outbreak in Yap in Micronesia, Aedes hensilii has been suspected as a vector because of its abundance coinciding with the outbreak. ZIKV was not detected in Aedes hensilii captured during this outbreak [14], but it has been shown to be a potential vector of ZIKV based on evidence from experimental infections [28]. In Singapore, Aedes albopictus is also a potential vector of ZIKV, based on data from experimental infections [29]. Aedes albopictus has been found naturally infected in Gabon [30].
Zika virus epidemiology
Since its first isolation in 1947 in Uganda, serological, epidemiological and entomological studies reported the circulation of the ZIKV in tropical areas of western Africa (Nigeria, Sierra Leone, Ivory Coast, Cameroon and Senegal) and of central Africa (Gabon, Uganda and Central African Republic), in Asia (Pakistan, Indonesia, Philippines, Malaysia, Cambodia and Thailand) and in several islands of the pacific region since 2007 (Micronesia, Cook Islands, French Polynesia, New Caledonia, Guam, Samoa, Vanuatu and Solomon Islands).
Outbreaks of ZIKV infection on Yap Island (2007) and in French Polynesia (2013?2014), with further spread to New Caledonia, the Cook Islands and Easter Island, have shown the propensity of this arbovirus to spread outside its usual geographical range and to cause large outbreaks [31].
Between 7 October 2013 and 6 April 2014, 8 750 suspected cases of ZIKV infection were reported by the syndromic surveillance sentinel network of French Polynesia, with 383 confirmed cases and an estimated 32 000 cases having consulted a healthcare facility for the condition [32,33]. During the outbreak, 74 individuals presented with neurological symptoms or auto-immune syndrome following a disease episode with symptoms consistent with ZIKV infection in previous days [17,34-36]. Of these, 42 were confirmed as Guillain-Barr? syndrome, with 37 cases having presented with a previous viral syndrome. The causal link between ZIKV infection and Guillain-Barr? syndrome is still not established.
Since 2014, indigenous circulation of ZIKV has been detected in the Americas. In February 2014, the public health authorities of Chile confirmed the first case of autochthonous transmission of ZIKV infection on Easter Island and cases were reported until June 2014. Since February 2015, cases of rash illness were reported in north-eastern Brazil in the states of Bahia, Maranhao, Pernambuco, Rio Grande do Norte, Para?ba and Sergipe [37]. A total of 14 835 cases of acute exanthematous illness have been reported in 12 health districts of Salvador ? the third city of Brazil ? between 15 February 2015 and 25 June 2015 (overall attack rate 5.5 cases/10 000 inhabitants) [38]. Twenty-four case of Guillain-Barr? syndrome were hospitalised during this period. The outbreak peaked in May at the time of ZIKV confirmation in patients leaving nearby Salvador city. During the same period the number of dengue cases did not vary substantially and 58 suspected chikungunya were identified by the Salvador Epidemiologic Surveillance Office. The authors suggest ZIKV as an etiological factor of this exanthematous illness outbreak because of the low frequency of arthralgia usually seen in chikungunya disease and concomitant confirmed ZIKV infections in the area [38].
In May 2015, the public health authorities of Brazil confirmed autochthonous transmission of ZIKV in the states of Bahia and Rio Grande do Norte [39]. As of November 2015, 15 states had confirmed autochthonous virus transmission [40]. In Brazil, between January and July 2015, 121 cases of neurological manifestations and GuillainBarr? syndrome have been notified in several north-eastern states with history of previous rash illness [41]. Investigations were launched and are on-going regarding possible association with ZIKV infection [42]. Phylogenetic analysis on serum samples from patients hospitalised in March at Santa Helena Hospital in Cama?ari, Bahia, Brazil showed that ZIKV sequences identified belonged to the Asian lineage and showed 99% identity with a sequence from a ZIKV isolate from French Polynesia [43].
In September 2015, Colombian health authorities reported the detection of the first autochthonous cases of ZIKV infection in the state of Bol?var. As of week 45, 488 confirmed cases of ZIKV infections and 1 583 suspected cases have been reported, distributed in 26 of the 36 departments [44].
On 3 November 2015, the Cape Verde Ministry of Health reported that 17 out of 64 blood samples sent for confirmation at Pasteur Institute in Dakar were positive for ZIKV and there were approximately 1 000 suspected cases with symptoms consistent with ZIKV infection as of 1 November 2015 [45].
On 12 November 2015, health authorities in Suriname reported five confirmed cases of ZIKV [46].
In conclusion, there is limited but increasing knowledge about ZIKV infection in humans [47,48]. Uncertainties remain about disease complications, genetic susceptibility and levels of risk for pregnant women, newborns or patients presenting with specific co-morbidities. The expansion of the ZIKV infections to South America constitutes a significant development in the epidemiology of this emerging vector-borne disease.
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