ZIKA VIRUS (45): WORLDWIDE, WHO, RESEARCH, COMMENT
A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases <http://www.isid.org>
In this update:
 WHO worldwide
 Zika virus infection and Guillain-Barre syndrome  Virus persistence in newborns  Vaginal infection, mouse model  Culex vectors NOT  Vector dissemination
 WHO worldwide
Date: 1 Sep 2016
Source: WHO situation report [edited]
– Overall, the global risk assessment has not changed.
– The geographic expansion of Zika virus, after having slowed in April through June 2016, has increased somewhat in July and August 2016.
This is likely due to increased activity of the mosquito vector in the northern hemisphere during the warmer summer months.
– While some countries such as those in South America are reporting downward trends in Zika transmission, other areas including those recently affected (for example, Saint Barthelemy in the Caribbean) and those affected earlier (for example, Puerto Rico) are experiencing upward trends. As most countries do not report absolute numbers of Zika cases, it is not possible to make generalizations about the global trend of the Zika outbreak.
– Although the African lineage preliminarily identified in Guinea-Bissau has not been associated with microcephaly and other neurologic complications, further surveillance is needed as there have been very few confirmed cases of the African lineage. At this point, it is still too early to dismiss this possible threat.
– 72 countries and territories (figure 1, table 1 [see URL above for figures and tables]) have reported evidence of mosquitoborne Zika virus transmission since 2007 (69 with reports from 2015):
– 55 with a 1st reported outbreak from 2015 onwards (figure 2, table 1).
– Four with having possible endemic transmission or evidence of local mosquitoborne Zika infections in 2016.
– 13 with evidence of local mosquitoborne Zika infections in or before 2015, but without documentation of cases in 2016, or with the outbreak terminated.
– Since February 2016, 11 countries have reported evidence of person-to-person transmission of Zika virus (table 2).
– 20 countries or territories have reported microcephaly and other CNS malformations potentially associated with Zika virus infection or suggestive of congenital infection (table 3). Four of the 20 countries reported microcephalic babies born from mothers in countries with no endemic Zika virus transmission but who reported recent travel history to Zika-affected countries.
– Outcomes of pregnancies with laboratory evidence of possible Zika virus in the United States of America:
– 16 total liveborn infants with birth defects
– Five total pregnancy losses with birth defects
– Outcomes of pregnancies with laboratory evidence of possible Zika virus in territories of the United States of America:
– One total liveborn infant with birth defects
– One total pregnancy loss with birth defects
– 18 countries and territories have reported an increased incidence of GBS and/or laboratory confirmation of a Zika virus infection among GBS cases (table 4).
– In Guinea-Bissau, the gene sequencing results of the four confirmed Zika cases sent in July 2016 have preliminarily confirmed that the cases are of the African lineage — that is, not the predominant global outbreak Asian lineage. The investigation of 5 reported cases of microcephaly is ongoing.
– The 2016 Summer Paralympic Games will be held in Rio de Janeiro, Brazil, from 7 to 18 Sep 2016. WHO, particularly through the Regional Office for the Americas, continues to provide technical support to the Ministry of Health to ensure the 2016 Summer Paralympic Games are as safe as possible for all athletes, volunteers, visitors and residents.
Table 1. Countries reporting mosquitoborne Zika virus transmission (data as of 31 Aug 2016):
Category 1: Countries with a 1st reported outbreak from 2015 onward:
– Africa: Cabo Verde; Guinea-Bissau
– Americas: Anguilla; Antigua and Barbuda; Argentina; Aruba; Bahamas; Barbados; Belize; Bolivia (Plurinational State of), Bonaire, Sint Eustatius and Saba – Netherlands*; Brazil; British Virgin Islands; Cayman Islands; Colombia; Costa Rica; Cuba; Curacao; Dominica; Dominican Republic; Ecuador; El Salvador; French Guiana; Grenada; Guadeloupe; Guatemala; Guyana; Haiti; Honduras; Jamaica; Martinique; Mexico; Nicaragua; Panama; Paraguay; Peru; Puerto Rico; Saint Barthelemy; Saint Lucia; Saint Martin; Saint Vincent and the Grenadines; Sint Maarten; Suriname; Trinidad and Tobago; Turks and Caicos; United States of America; United States Virgin Islands; Venezuela (Bolivarian Republic of)
– Pacific: American Samoa; Fiji; Marshall Islands; Micronesia (Federated States of); Samoa; Singapore; Tonga Category 2: Countries with possible endemic transmission or evidence of local mosquitoborne Zika infections in 2016:
– South East Asia: Indonesia, Thailand, Philippines, Viet Nam
Category 3: Countries with evidence of local mosquitoborne Zika infections in or before 2015, but without documentation of cases in 2016, or outbreak terminated:
– Africa: Gabon
– Western Pacific: Easter Island (Chile)
– South Asia and Indian Ocean: Bangladesh, Maldives
– Southeast Asia and Western Pacific: Cambodia; Cook Islands**; French Polynesia**; Lao People’s Democratic Republic; Malaysia; New Caledonia; Papua New Guinea; Solomon Islands; Vanuatu
*This includes confirmed Zika virus cases reported in Bonaire – Netherlands, Sint Eustatius and Saba – Netherlands.
**These countries and territories have not reported Zika virus cases in 2015 or 2016.
Categories are defined as follows:
Category 1: Countries with a 1st reported outbreak from 2015 onwards
– A laboratory confirmed, autochthonous, mosquitoborne case of Zika virus infection in an area where there is no evidence of circulation of the virus in the past (prior 2015), whether it is detected and reported by the country itself or by another state party diagnosing returning travellers, or
– A laboratory confirmed, autochthonous, mosquitoborne case of Zika virus infection in an area where transmission has been previously interrupted. The assumption is that the size of the susceptible population has built up to a sufficient level to allow transmission again; the size of the outbreak will be a function of the size of the susceptible population, or
– An increase of the incidence of laboratory confirmed, autochthonous, mosquitoborne Zika virus infection in areas where there is ongoing transmission, above 2 standard deviations of the baseline rate, or doubling the number of cases over a 4-week period. Clusters of febrile illnesses, in particular when epidemiologically-linked to a confirmed case, should be microbiologically investigated.
Category 2: Countries with possible endemic transmission or evidence of local mosquito-borne Zika infections in 2016 with the reporting period beginning in 2007
– Countries or territories that have reported an outbreak with consistent presence of laboratory confirmed, autochthonous, mosquitoborne cases of Zika virus infection 12 months after the outbreak, or
– Countries or territories where Zika virus has been circulating for several years with consistent presence of laboratory confirmed, autochthonous, mosquitoborne cases of Zika virus infection or evidence of local mosquito-borne Zika infections in 2016. Reports can be from the country or territory where infection occurred, or from a 3rd party where the case is 1st recorded according to the International Health Regulations (IHR 2005). Countries with evidence of infection prior to
2007 are listed in
Category 3: Countries with evidence of local mosquitoborne Zika infections in or before 2015, but without documentation of cases in 2016, or outbreak terminated with the reporting period beginning in
– Absence of confirmed cases over a 3-month period in a specific geographical area with climatic conditions suitable for year-round arbovirus transmission, or over a 12-month period in an area with seasonal vector activity.
Table 2. Countries reporting non mosquitoborne Zika virus transmission since February 2016 Countries with evidence of person-to-person transmission of Zika virus, other than mosquitoborne transmission:
Americas: Argentina, Canada, Chile, Peru, USA
Europe: France, Germany, Italy, Portugal, Spain Western Pacific: New Zealand
Table 3. Countries and territories reporting microcephaly and/or CNS malformation cases potentially associated with Zika virus infection
Country / No. cases microcephaly or CNS malformation suggestive or potentially associated with Zika virus infections:
Brazil / 1845
Cabo Verde / 9
Canada / 1
Costa Rica / 1
Colombia / 34
Dominican Republic / 3
El Salvador / 4
French Guiana / 3
French Polynesia / 8
Haiti / 1
Honduras / 1
Marshall Islands / 1
Martinique / 10
Panama / 5
Paraguay / 2
Puerto Rico / 1
Slovenia (ex Brazil) / 1
Spain (ex Colombia, Venezuela) / 2
Suriname / 1
USA (ex various) / 21
Table 4. Countries and territories reporting Guillain-Barre syndrome
(GBS) potentially associated with Zika virus infection
– Reported increase in incidence of GBS cases, with at least one GBS case with confirmed Zika virus infection:
Brazil, Colombia, Dominican Republic, El Salvador*, French Guiana, French Polynesia, Honduras, Jamaica, Martinique, Suriname**, Venezuela
– No increase in GBS incidence reported, but at least one GBS case with confirmed Zika virus infection:
Costa Rica, Grenada, Guadeloupe, Guatemala, Haiti, Panama, Puerto Rico
ProMED-mail rapporteur Mary Marshall
 Zika virus infection and Guillain-Barre syndrome
Date: Wed 31 Aug 2016
Source: N Engl J Med DOI: 10.1056/NEJMc1609015 [edited] <http://www.nejm.org/doi/full/10.1056/NEJMc1609015#t=article>
Thais dos Santos, Angel Rodriguez, Maria Almiron, Antonio Sanhueza, Pilar Ramon, et al. Zika Virus and the Guillain-Barre syndrome — case series from 7 countries. N Engl J Med DOI: 10.1056/NEJMc1609015
>From 1 Apr 2015, to 31 Mar 2016, a total of 164 237 confirmed and
suspected cases of ZIKV disease and 1474 cases of the Guillain-Barre syndrome were reported in Bahia, Brazil; Colombia; the Dominican Republic; El Salvador; Honduras; Suriname; and Venezuela. To examine the temporal association between ZIKV disease and the Guillain-Barre syndrome, graphical and time-series analyses were applied to these 2 independent data sets, which were collected through official International Health Regulations channels or from ministry of health websites. The data obtained from country reports contained no personally identifiable information and were collected as part of routine public health surveillance; therefore, the analysis was exempt from review by an ethics board. Differences between the observed and expected numbers of cases of the Guillain-Barre syndrome during the ZIKV transmission period, as well as differences in the incidence of the Guillain-Barre syndrome and ZIKV disease according to age and sex, were analyzed with the use of Poisson regression models.
The analysis suggests that changes in the reported incidence of ZIKV disease during 2015 and early 2016 were closely associated with changes in the incidence of the Guillain-Barre syndrome. During the weeks of ZIKV transmission, there were significant increases in the incidence of the Guillain-Barre syndrome, as compared with the pre-ZIKV baseline incidence, in Bahia State (an increase of 172 per cent), Colombia (211 per cent), the Dominican Republic (150 per cent), El Salvador (100 per cent), Honduras (144 per cent), Suriname (400 per cent), and Venezuela (877 per cent) In the 6 countries that also reported decreases in the incidence of ZIKV disease, the incidence of the Guillain-Barre syndrome also declined. When the 7 epidemics of ZIKV disease are aligned according to week of peak incidence, the total number of cases of ZIKV disease and the Guillain-Barre syndrome are closely coincident, although the period from acquiring infection to reporting disease is approximately 2 weeks longer for ZIKV than for the Guillain-Barre syndrome, a pattern that is especially visible in data from Colombia and Venezuela. Whether the 2-week difference can be explained in terms of incubation periods or reporting delays is not yet known. We explored the potential effect of dengue virus circulation on the incidence of the Guillain-Barre syndrome and found no link. In any event, we infer from these 2 series of cases, which were collected independently of each other, that ZIKV infection and the Guillain-Barre syndrome are strongly associated. Additional studies are needed to show that ZIKV infection is a cause of the Guillain-Barre syndrome.
Overall, females had a 75 per cent higher reported incidence rate of ZIKV disease than did males (rate ratio, 1.75; 95 per cent confidence interval [CI], 1.71 to 1.79); the rate was especially high among women
20 to 49 years of age. This difference was also observed in the Yap Island (Micronesia) epidemic and could be due to greater exposure to the intradomiciliary mosquito vector, to more severe symptoms among women in this age group, to active health care-seeking behavior by females, or to enhanced reporting by health workers, given the risk of infection during pregnancy. However, the greater apparent risk of ZIKV disease among women 20 to 49 years of age was not matched by a similarly higher incidence of the Guillain-Barre syndrome, which may indicate an age and sex bias in the reporting of ZIKV disease. The reported incidence of the Guillain-Barre syndrome was 28 percent higher among males than among females (rate ratio, 1.28; 95 per cent CI, 1.09 to 1.50) and consistently increased with age, findings that are in line with previous reports.
ProMED-mail rapporteur Mary Marshall
[This report adds additional indirect evidence that ZIKV infections can lead to GBS. – Mod.TY]
 Virus persistence in newborns
Date: Wed 24 Aug 2016
Source: N Engl J Med DOI: 10.1056/NEJMc1607583 [edited] <http://www.nejm.org/doi/full/10.1056/NEJMc1607583#t=article>
Danielle BL Oliveira, Flavia J Almeida, Edison L Durigon, et al.
Prolonged shedding of Zika virus associated with congenital infection.
N Engl J Med DOI: 10.1056/NEJMc1607583
We report a case of a newborn who had continued viremia with ZIKV for at least 67 days after birth.
On 2 Jan 2016, a male child was born with microcephaly in Sao Paulo, Brazil, at 40 weeks of gestation to a mother who had reported having symptoms associated with ZIKV infection during the 26th week of pregnancy. At birth, the weight was 3095 g, the length 48 cm, and the head circumference 32.5 cm. The neurologic abnormality was not detected during an initial physical examination.
An analysis of cerebrospinal fluid and ophthalmologic and otoacoustic evaluations were normal. Magnetic resonance imaging (MRI) showed a reduced brain parenchyma, notably in the frontal and parietal lobes, foci of calcification in the subcortical area, and compensatory dilatation of the infratentorial supraventricular system. At day 54, serum, saliva, and urine were tested for ZIKV on quantitative real-time polymerase-chain-reaction (qRT-PCR) assay. All 3 assays were positive for ZIKV RNA, with 1.4A–10^5 copies per milliliter in the serum, 4.1A–10^4 in the saliva, and 5.4A–10^3 in the urine.
RNA sequencing of a urine sample obtained from the infant showed a high degree of similarity with samples isolated in the Americas with
98.5 per cent bootstrap support.
ZIKV-specific IgM and IgG were positive as well. On day 67, ZIKV RNA in the serum continued to be detected on qRT-PCR, with 2.8A–10^4 copies per milliliter. On day 216, ZIKV RNA was no longer detected in the serum on qRT-PCR; the ZIKV-specific IgG titer was high (over 320) in comparison with the 1st and 2nd samples (average titer, under 99).
When the infant was examined on day 54, he had no obvious illness or evidence of any immunocompromising condition. However, by 6 months of age, he showed neuro-psychomotor developmental delay, with global hypertonia and spastic hemiplegia, with the right dominant side more severely affected.
[It will be interesting to know whether this case of long-term virus shedding is unusual in infants that are infected in utero. Results of studies in other Zika virus infected infants exposed during gestation will be of considerable interest. – Mod.TY]
 Vaginal infection, mouse model
Date: Thu 25 Aug 2016
Source: Cell Vol. 166, Issue 5, p1247-1256.e4 [edited] <http://www.cell.com/fulltext/S0092-8674(16)31053-4>
Laura J Yockey, Luis Varela, Tasfia Rakib, William Khoury-Hanold, Susan L Fink, Bernardo Stutz, et al. Vaginal exposure to Zika virus during pregnancy leads to fetal brain infection. Cell 2016; 166(5):
In this study, we demonstrate that vaginal ZIKV infection of female mice leads to productive replication of the virus within the vaginal mucosa even in WT animals. This was observed in both virgin female mice that were pretreated with Depo-Provera [medroxyprogesterone acetate. Mod.SH] and in pregnant dams. Direct comparison of ZIKV RNA in the spleen after intraperitoneal injection and in the vagina after intravaginal inoculation revealed that the vaginal mucosa supports robust viral replication compared to other organs. In pregnant WT mice, ZIKV replication in the vaginal tissue was followed by the infection of fetal brain and IUGR [intrauterine growth restriction], despite the absence of viremia. These results highlight the vaginal tract as a susceptible site for ZIKV replication, even in immunocompetent hosts. The consequences of vaginally-acquired ZIKV infection on the fetus appear to vary depending on the gestation stage at which the virus was introduced. Vaginal ZIKV exposure at early pregnancy (E4.5) resulted in IUGR of the fetus, while exposure at E8.5 resulted in normal fetal weight. Nevertheless, ZIKV-infected cells were found within the cerebellum and the cortex of the fetal brain after infection at both time points. Therefore, the female genital tract represents a productive site of viral replication. Our studies also indicate that ZIKV brain infection can occur in fetuses without causing gross growth defects or malformations. It will be important to further investigate how fetal brain infection with ZIKV impacts the postnatal brain development and the cognitive functions of the offspring.
Vaginal exposure of ZIKV in pregnant mice resulted in IUGR and fetal brain infection in the absence of viremia in WT mice. These data suggest a possible direct transmission route from the vaginal tract through the cervix to the intrauterine space. From there, the virus may enter the decidua and infect the placenta, thereby entering the fetus through the umbilical cord. Alternatively, the virus may spread from the decidua to invade the chorion and amnion and enter the amniotic cavity to directly infect the fetus. Because of the absence of viremia in infected WT dams, we hypothesize that the vaginal transmission of ZIKV might give the virus a direct access to the placenta or the fetus via an ascending route. Our studies also highlight that, even though WT mice are able to control ZIKV well compared to mice lacking IFNAR signaling, the virus still has a high predilection for the developing fetal brain. Consistent with a previous study (Wu et al., 2016), our study shows that infection of the fetal brain of WT C57BL/6 does occur when pregnant dams are infected with ZIKV.
Vaginal ZIKV exposure of dams deficient in IRF3 and IRF7 resulted in very high levels of viral replication in the vaginal tissue. In contrast to WT mice, some of these Irf3 mice also supported ZIKV replication in the placenta and fetal bodies. Further, IFNAR-deficient dams infected with ZIKV early during pregnancy led to fetal loss and later during pregnancy led to severe IUGR. Because both of these genotypes support viremia, ZIKV may infect the placenta through blood-placental transmission and bypass the placental barrier to infect the fetus. These results are consistent with the hematogenous transplacental route of infection described by Miner et al. (Miner et al, 2016), who showed viremia and IUGR following subcutaneous infection of IFNAR dams at E6.5 or E7.5.
How might our findings apply to humans? A recent study demonstrated that ZIKV NS5 protein antagonizes human STAT2 but not mouse STAT2 (Grant et al, 2016). Therefore, humans are naturally more susceptible to ZIKV infection than mice because infected cells can no longer respond to IFNs. Consequently, we speculate that ZIKV introduced into the human vagina is likely to replicate more robustly than in the vaginal cavity of WT mice. Our findings that ZIKV replicates in the vagina of mice is consistent with the report of sexual transmission from an infected female to her uninfected male partner. Currently, we do not know if sexual transmission of ZIKV poses a different risk of birth defects than mosquitoborne transmission in pregnant women.
However, our results from the mouse model would predict negative consequences on fetal development following vaginal ZIKV exposure of the mothers during early pregnancy. Finally, while mosquitoborne transmission is blamed for the increased incidence of microcephaly, it is possible that sexual transmission of ZIKV might account for some of the fetal diseases even within the _Aedes_ ZIKV endemic regions. Given the fact that human placental trophoblasts provide protective type III IFNs (Bayer et al, 2016), ascending infection from the vagina to the fetus in humans may provide the ZIKV direct access. Our findings in mice indicate that sexual transmission of ZIKV is harmful to the fetus and provide a model to study the impact of interventional and therapeutic treatment of vaginal ZIKV viral infection during pregnancy.
[This study provides additional information about vaginal infection with ZIKV. How similar the mouse model is to human susceptibility remains to be seen. Perhaps these findings will lead to vaginal mucosa sampling of women infected with ZIKV and to the search for additional cases of female to male sexual transmission in humans. – Mod.TY
See original paper for references cited above. – Mod.SH]
 Culex vectors NOT
Date: Thu 1 Sep 2016
Source: Euro Surveill. 2016;21(35):pii=30333 [edited] <http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=22573>
Amraoui F, Atyame-Nten C, Vega A, Loureno-de-Oliveira R, Vazeille M, Failloux AB. Culex mosquitoes are experimentally unable to transmit Zika virus. Euro Surveill. 2016;21(35):pii=30333
We report that 2 laboratory colonies of _Culex quinquefasciatus_ and _Culex pipiens_ mosquitoes were experimentally unable to transmit ZIKV either up to 21 days post an infectious blood meal or up to 14 days post intrathoracic inoculation. Infectious viral particles were detected in bodies, heads or saliva by a plaque forming unit assay on Vero cells. We therefore consider it unlikely that Culex mosquitoes are involved in the rapid spread of ZIKV.
Members of the _Cx. pipiens_ species complex are among the most widely distributed mosquitoes in the world and can act as disease vectors.
The species complex comprises several members including _Cx. pipiens_ and _Cx. quinquefasciatus_, which are the most abundant Culicinae mosquitoes in temperate and tropical regions, respectively. _Cx.
pipiens_ is the most ubiquitous mosquito species in temperate regions, occurring in rural and domestic environments and can be found in nature in two biological forms, _pipiens_ and _molestus_, which are morphologically indistinguishable. The Tabarka strain, used in this study, is a mix of both forms and has been shown to be a primary vector of West Nile virus (WNV) in the Mediterranean basin. _Cx.
quinquefasciatus_ is mainly associated with human habitats and can experimentally transmit WNV, making it an ideal vector for domestic/urban transmission of WNV in tropical regions. Our results show that laboratory colonies of _Cx. quinquefasciatus_ and _Cx.
pipiens_ were unable to transmit an Asian genotype of ZIKV. Using mosquito colonies for vector competence studies can be considered as a proxy for measuring the genetic ability of one species to transmit a given pathogen. In addition, the experimental ability to transmit a pathogen — vector competence — can vary according to specific combinations of virus and mosquito genotypes, which can be affected by environmental factors such as temperature. The mosquito midgut barrier is the site where the initial steps such as viral attachment, penetration and replication take place before the release of newly produced virions into the mosquito haemocoel. We have shown that bypassing this midgut barrier, by inoculating viral particles into the haemocoel, did not favour viral dissemination nor transmission. Thus, our results strongly suggest that the _Cx. quinquefasciatus_ and _Cx.
pipiens_ colonies were unable to transmit ZIKV, as has already been suggested for natural populations of _Cx. quinquefasciatus_ collected during an outbreak of ZIKV infection in Mexico and demonstrated for laboratory colonies of _Culex_ mosquitoes.
Both mosquito species can tolerate environments highly charged with organic matter and high levels of chemical pollutants including insecticides. Repeatedly confronted with insecticidal molecules, mosquito populations have developed resistance to insecticides, making vector control more difficult. As _Aedes_ and _Culex_ mosquitoes do not share the same breeding sites, control measures targeting each of them are basically different. On the basis of our results, we consider that vector control should continue to focus on larval and adult habitats specific to _Aedes_ mosquitoes, in order to efficiently control ZIKV vectors. While a vaccine is pending, surveillance and vector control should be reinforced against _Ae. aegypti_ and _Ae.
albopictus_, species that are able to transmit dengue virus, chikungunya virus and ZIKV.
ProMED-mail rapporteur Mary Marshall
[ZIKV was isolated from _Culex quinquefasciatus_ in Brazil earlier this year (2016), raising the question about their role as vectors of the virus. The above report takes that observation to the next step, addressing the susceptibility of this species to ZIKV infection and efficiency of transmission. Assuming that the mosquitoes used in the above experiments are representative of those species in nature, the finding of non-transmission is good news indeed. Had they proved to be efficient vectors, that would have expanded the geographic area for risk of ZIKV transmission substantially around the world. – Mod.TY]
 Vector dissemination
Date: Fri 2 Sep 2016
From: Robert Wolff <email@example.com> [edited]
As I work with insects and pathogens, I have been somewhat concerned about the pronouncements that _Aedes aegypti_ (and _A. albopictus_) females do not spread because of their limited flying. The following statement might be of interest to your subscribers and the public health establishment.
It has been reported that ZIKV-infected female mosquitos of the species _Aedes aegypti_ and _Ae. albopictus_ will not fly to new areas because they generally have very short ranges in which they fly (up to
200 meters for _A. aegypti_ and to 500 meters for _A. albopictus_).
This lack of wide flight dispersal after becoming an adult should limit the spread of locally acquired ZIKV. While this is true, there are 2 mechanisms by which ZIKV- (or other virus) infected females can spread the infection to areas beyond the 500 meters range. 1st, adult mosquitoes may take refuge in automobiles, trucks or other vehicles.
When they are driven to new areas, the infected mosquito may then be able to infect within the new area. Wind gusts are also able to blow the weak flying mosquitos beyond their normal flight range.
Of interest to local and nearby communities where infections are spreading is a simple recommendation that might provide a small decrease in the area of spread: Vehicles of all kinds should keep their windows rolled up and any doors closed when the vehicles are standing or parked. If the mosquitos do not enter the vehicle and find a resting place, there is a reduced likelihood that they will be transported to uninfected neighborhoods.
Robert J Wolff, PhD
Professor of Science and Health Science, Columbia Campus South University, Columbia
9 Science Ct, Columbia, SC 29203
[ProMED-mail thanks Dr Wolff for his comments and for providing information on transport mechanisms that may result in long-distance movement of viruses, including Zika virus, via infected mosquitoes. An additional mechanism is transport of infected mosquitoes, sometimes over very long distances, via commercial aircraft. It has been hypothesized that this is how West Nile virus arrived in New York, USA. – Mod.TY]
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Suspected Female-to-Male Sexual Transmission of Zika Virus — New York City, 2016
Early Release / July 15, 2016 / 65