Global & Disaster Medicine

Archive for the ‘Zika virus’ Category

edes aegypti mosquitoes that carry Zika can also transmit dengue and chikungunya in the same bite.

Nature

Rückert, C. et al. Impact of simultaneous exposure to arboviruses on infection and transmission by Aedes aegypti mosquitoes. Nat. Commun. 8, 15412 doi: 10.1038/ncomms15412 (2017).

“…..Thus, we here expose Ae. aegypti mosquitoes to chikungunya, dengue-2 or Zika viruses, both individually and as double and triple infections. Our results show that these mosquitoes can be infected with and can transmit all combinations of these viruses simultaneously. Importantly, infection, dissemination and transmission rates in mosquitoes are only mildly affected by coinfection…..”


A novel retinal sign that appears to be specific to Ebola survivors.

Citation:  Steptoe PJ, Scott JT, Baxter JM, Parkes CK, Dwivedi R, Czanner G, et al. Novel retinal lesion in Ebola survivors, Sierra Leone, 2016. Emerg Infect Dis. 2017 Jul [date cited]. https://dx.doi.org/10.3201/eid2307.161608

Abstract:  We conducted a case–control study in Freetown, Sierra Leone, to investigate ocular signs in Ebola virus disease (EVD) survivors. A total of 82 EVD survivors with ocular symptoms and 105 controls from asymptomatic civilian and military personnel and symptomatic eye clinic attendees underwent ophthalmic examination, including widefield retinal imaging. Snellen visual acuity was <6/7.5 in 75.6% (97.5% CI 63%–85.7%) of EVD survivors and 75.5% (97.5% CI 59.1%–87.9%) of controls. Unilateral white cataracts were present in 7.4% (97.5% CI 2.4%–16.7%) of EVD survivors and no controls. Aqueous humor from 2 EVD survivors with cataract but no anterior chamber inflammation were PCR-negative for Zaire Ebola virus, permitting cataract surgery. A novel retinal lesion following the anatomic distribution of the optic nerve axons occurred in 14.6% (97.5% CI 7.1%–25.6%) of EVD survivors and no controls, suggesting neuronal transmission as a route of ocular entry.

 

Volume 23, Number 7—July 2017

Research

Novel Retinal Lesion in Ebola Survivors, Sierra Leone, 2016

Paul J. SteptoeComments to Author , Janet T. Scott, Julia M. Baxter, Craig K. Parkes, Rahul Dwivedi, Gabriela Czanner, Matthew J. Vandy, Fayiah Momorie, Alimamy D. Fornah, Patrick Komba, Jade Richards, Foday Sahr, Nicholas A.V. Beare, and Malcolm G. Semple
Author affiliations: University of Liverpool, Liverpool, UK (P.J. Steptoe, J.T. Scott, G. Czanner, N.A.V. Beare, M.G. Semple); Royal Liverpool Hospital, Liverpool (P.J. Steptoe, J.M. Baxter, C.K. Parkes, R. Dwivedi, N.A.V. Beare); National Institute for Health Research Health Protection Research Unit in Emerging and Zoonotic Infections, Liverpool (J.T. Scott, M.G. Semple); Connaught Hospital, Freetown, Sierra Leone (M.J. Vandy); 34th Regiment Military Hospital, Freetown (F. Momorie, A.D. Fornah, P. Komba, F. Sahr); Public Health England Laboratory, Makeni, Sierra Leone (J. Richards)

Main Article

Figure 2

Composite scanning laser ophthalmoscope retinal images showing type 6 Ebola peripapillary or peripheral lesions, observed following the anatomic distribution of the ganglion cell axon (retinal nerve fiber layer), in a case–control study of ocular signs in Ebola virus disease survivors, Sierra Leone, 2016. A) Example 1, right eye. B) Illustration of the ganglion cell axon anatomic distribution. Courtesy of W.L.M. Alward. C) Example 2, right eye. Asterisks indicate curvilinear lesions distinct fro

Figure 2. Composite scanning laser ophthalmoscope retinal images showing type 6 Ebola peripapillary or peripheral lesions, observed following the anatomic distribution of the ganglion cell axon (retinal nerve fiber layer), in a case–control study of ocular signs in Ebola virus disease survivors, Sierra Leone, 2016. A) Example 1, right eye. B) Illustration of the ganglion cell axon anatomic distribution. Courtesy of W.L.M. Alward. C) Example 2, right eye. Asterisks indicate curvilinear lesions distinct from the retinal vasculature. White arrowhead indicates retinal nerve fiber wedge defect.

Figure 3

Characteristic features of lesions observed in a case–control study of ocular signs in Ebola virus disease survivors, Sierra Leone, 2016. A) Composite scanning laser ophthalmoscope retinal image, left eye. Arrow indicates direction of the optical coherence tomography scan. B) Optical coherence tomography. White, long, dashed line indicates cross-sectional plane; white arrowhead indicates Ebola lesion limited to the retinal layers with an intact retinal pigment epithelium. Magnified 1.5× from ori

Figure 3. Characteristic features of lesions observed in a case–control study of ocular signs in Ebola virus disease survivors, Sierra Leone, 2016. A) Composite scanning laser ophthalmoscope retinal image, left eye. Arrow indicates direction of the optical coherence tomography scan. B) Optical coherence tomography. White, long, dashed line indicates cross-sectional plane; white arrowhead indicates Ebola lesion limited to the retinal layers with an intact retinal pigment epithelium. Magnified 1.5× from original image (panel A). C) Examples of straight-edged, sharp angulated lesions (magnified from panel A). D) Example of tangential section through the human fovea with illustrative highlighting of a triangular photoreceptor matrix corresponding to Ebola lesional shape. Courtesy of Ahnelt et al. (17).


Brazil has declared an end to a national emergency over the Zika virus after the number of cases dropped 95% between January and April, compared to the same period a year ago.

BBC


A novel virus-like particle (VLP) Zika vaccine elicited high titers of virus-neutralizing antibodies in mice.

PLOS

“…..Here we describe a novel strategy to assemble Zika virus-like particles (VLPs) by co-expressing the structural (CprME) and non-structural (NS2B/NS3) proteins, and demonstrate their effectiveness as vaccines. VLPs are produced in a suspension culture of mammalian cells and self-assembled into particles closely resembling Zika viruses as shown by electron microscopy studies. We tested various VLP vaccines and compared them to analogous compositions of an inactivated Zika virus (In-ZIKV) used as a reference. VLP immunizations elicited high titers of antibodies, as did the In-ZIKV controls. However, in mice the VLP vaccine stimulated significantly higher virus neutralizing antibody titers than comparable formulations of the In-ZIKV vaccine. The serum neutralizing activity elicited by the VLP vaccine was enhanced using a higher VLP dose and with the addition of an adjuvant, reaching neutralizing titers greater than those detected in the serum of a patient who recovered from a Zika infection in Brazil in 2015. Discrepancies in neutralization levels between the VLP vaccine and the In-ZIKV suggest that chemical inactivation has deleterious effects on neutralizing epitopes within the E protein. This along with the inability of a VLP vaccine to cause infection makes it a preferable candidate for vaccine development….”


Zika virus IgM can persist beyond 12 weeks in a subset of infected people.

CDC

Distributed via the CDC Health Alert Network
May 05, 2017 1130 ET (11:30 AM ET)
CDCHAN-00402

Prolonged IgM Antibody Response in People Infected with Zika Virus: Implications for Interpreting Serologic Testing Results for Pregnant Women

Summary
In July 2016, CDC issued Interim Guidance for Health Care Providers Caring for Pregnant Women with Possible Zika Virus Exposure – United States, July 2016 (https://www.cdc.gov/mmwr/volumes/65/wr/mm6529e1.htm) that includes Zika virus immunoglobulin M (IgM) testing of pregnant women. However, some flavivirus infections can result in prolonged IgM responses (>12 weeks) that make it difficult to determine the timing of infection, especially in testing of asymptomatic people. Emerging epidemiologic and laboratory data indicate that Zika virus IgM can persist beyond 12 weeks in a subset of infected people. Therefore, detection of IgM may not always indicate a recent infection. Although IgM persistence could affect IgM test interpretation for all infected people, it would have the greatest effect on clinical management of pregnant women with a history of living in or traveling to areas with Zika virus transmission. Pregnant women who test positive for IgM antibody may have been infected with Zika virus and developed an IgM response before conception.

For asymptomatic pregnant women with a history of living in or traveling to areas with Zika virus transmission, Zika virus nucleic acid test (NAT) testing at least once per trimester is recommended, in addition to IgM testing as previously recommended. If positive, this may provide a more definitive diagnosis of recent Zika infection. However, a negative NAT does not rule out recent infection because viral ribonucleic acid (RNA) declines over time. Other diagnostic methods, such as NAT testing of amniocentesis specimens or serial ultrasounds, may provide additional information to help determine whether the IgM test results suggest a recent infection. Providers should counsel women on the limitations of all tests. In addition, providers may wish to consider IgM testing as part of pre-conception counseling to establish baseline IgM results before pregnancy; however, preconception negative IgM results might have limited value for women at ongoing risk of Zika infection. NAT testing should be performed for any pregnant woman who becomes symptomatic or who has a sexual partner who tests positive for Zika virus infection.

Recommendations
For asymptomatic pregnant women with possible Zika virus exposure before conception, (particularly women who lived in or traveled to areas with posted CDC Zika Travel Notices https://wwwnc.cdc.gov/travel/page/zika-information), CDC recommends that healthcare providers take these steps:

  1. Screen pregnant women for risk of Zika exposure and symptoms of Zika. Promptly test pregnant women with NAT if they become symptomatic during their pregnancy or if a sexual partner tests positive for Zika virus infection.
  2. Conduct NAT testing at least once per trimester, unless a previous test has been positive.*
  3. Consider NAT testing of amniocentesis specimens if amniocentesis is performed for other reasons.
  4. Counsel pregnant women each trimester on the limitations of IgM and NAT testing. For more information about Zika virus testing, see: https://www.cdc.gov/zika/pdfs/living_in.pdf. For more information about counseling before testing, see: https://www.cdc.gov/zika/pdfs/pretestingcounselingscript_livingin.pdf.
  5. Consider IgM testing to determine baseline Zika virus IgM levels as part of preconception counseling.§ For more information about preconception counseling, see:  https://www.cdc.gov/zika/pdfs/preconception-counseling.pdf

Recommendations for testing symptomatic pregnant women, remain unchanged (https://www.cdc.gov/mmwr/volumes/65/wr/mm6529e1.htm). However, if a symptomatic pregnant woman is IgM positive and NAT negative, and lived in or traveled to an area with a posted CDC Zika Travel Notice (https://wwwnc.cdc.gov/travel/page/zika-information), healthcare providers should recognize that the positive IgM result does not necessarily indicate recent infection.

CDC will update clinical management (https://www.cdc.gov/mmwr/volumes/65/wr/mm6529e1.htm) and laboratory testing (https://www.cdc.gov/zika/laboratories/lab-guidance.html) recommendations as new information becomes available.

Background
Some flavivirus infections have been reported to result in prolonged IgM responses that make it difficult to differentiate recent from prior infections in areas with ongoing transmission. For dengue virus, IgM was determined to persist for 6 months (179 days [95% confidence interval, 155 to 215 days]) for primary infections and 4.6 months (139 days [95% confidence interval, 119 to 167 days]) after infection with another flavivirus1. IgM antibodies against West Nile virus, another flavivirus related to Zika virus, have been detected in asymptomatic, infected blood donors for at least three months after they donated blood, and almost half of tested patients with West Nile virus infection had serum IgM antibodies >1 year after infection2,3.

Recent findings suggest that Zika virus infection may also result in IgM persistence that may make it difficult to differentiate prior from recent infections. A recent study in Puerto Rico of symptomatic patients with NAT-confirmed Zika virus infection detected Zika virus IgM in 100% (28/28) of participants at 8 to 15 days after symptom onset, and 87% (52/60) at greater than 60 days after symptom onset4. Unpublished data on the symptomatic patients from this ongoing study show a median time to first negative Zika virus IgM as 4 months (122 days [range 8-210 days]). More data are needed to accurately estimate the proportion of persons who are likely to have Zika IgM persist beyond 12 weeks after infection.

IgM test results can also be difficult to interpret because of cross-reactivity with other flaviviruses, particularly dengue virus, when a person has been previously infected or vaccinated with a related flavivirus. During 2016, Puerto Rico had limited dengue virus transmission and, therefore, people who tested positive for Zika IgM antibody could be assumed to have had recent Zika virus infection. However, if dengue virus transmission were to increase, guidance for interpretation of Zika virus IgM testing results may need to be reconsidered.

NAT testing may be useful in testing pregnant women as an indicator of current infection and increased risk to the fetus. In the same study from Puerto Rico discussed above, viral RNA was detected in 36% (10/28) of participants at 8‒15 days after symptom onset, 21% (27/129) at 16‒30 days after symptom onset, and 4% (3/79) more than 60 days after symptom onset4. A limited number of studies have demonstrated detection of viral nucleic acid in some pregnant women for even longer periods after symptom onset. For example, three of the five pregnant women included in the study from Puerto Rico had detectable RNA at 46 days and one still had detectable RNA at 80 days after symptom onset4. In another case series, some pregnant women had Zika virus RNA detectable up to 107 days after symptom onset5.

For More Information
Update: Interim Guidance for Health Care Providers Caring for Pregnant Women with Possible Zika Virus Exposure – United States, July 2016. MMWR Morb Mortal Wkly Rep. 2016 Jul 25;65(29):739-44. https://www.cdc.gov/mmwr/volumes/65/wr/mm6529e1.htm

Guidance for U.S. Laboratories Testing for Zika Virus Infection. https://www.cdc.gov/zika/laboratories/lab-guidance.html

Update: Interim Guidance for Preconception Counseling and Prevention of Sexual Transmission of Zika Virus for Persons with Possible Zika Virus Exposure – United States, September 2016. MMWR Morb Mortal Wkly Rep. 2016 Oct 7;65(39):1077-1081. https://www.cdc.gov/mmwr/volumes/65/wr/mm6539e1.htm?s_cid=mm6539e1_w

References

  1. Prince HE, Matud JL.  Estimation of dengue virus IgM persistence using regression analysis. Clin Vaccine Immunol 2011;18: 2183-5.
  2. Roehrig JT, Nash D, Maldin B, et al. Persistence of virus-reactive serum immunoglobulin M antibody in confirmed West Nile virus encephalitis cases. Emerg Infect Dis 2003;9:376-9. http:// dx.doi.org/10.3201/ eid0903.020531
  3. Busch MP, Kleinman SH, Tobler LH, et al. Virus and antibody dynamics in acute West Nile virus infection. J Infect Dis 2008;198:984-93. http:// dx.doi.org/10.1086/591467
  4. Paz-Baily G, Rosenberg ES, Doyle K, et al. Persistence of Zika virus in body fluids— Preliminary report. N Engl J Rep 2017. DOI: 10.1056/NEJMoa1613108
  5. Suy A, Sulleiro E, Rodó C, et al. Prolonged Zika virus viremia during pregnancy. N Engl J Med. 2016;375:2611-2613.
  6. Reynolds MR, Jones AM, Petersen EE, et al. Vital signs: Update on Zika virus–associated birth defects and evaluation of all U.S. infants with congenital Zika virus exposure — U.S. Zika pregnancy registry, 2016. MMWR Morb Mortal Wkly Rep 2017;66:366-373.

Footnotes
* Birth defects have been reported in a higher proportion of fetuses or infants whose mothers were infected during the first trimester of pregnancy than in later trimesters. In pregnancies with symptom onset or exposure during the first trimester that were limited to those with laboratory-confirmed Zika virus infection, 15% of completed pregnancies had reported birth defects of the type seen with congenital Zika infection6.
† Consideration of amniocentesis should be individualized, because data about its usefulness in diagnosing congenital Zika virus infection are limited. The presence of Zika virus RNA in the amniotic fluid might indicate fetal infection; however, a negative result does not exclude congenital Zika virus infection
§ Preconceptional IgM testing is recommended to establish a baseline IgM level before pregnancy.  However, given the limitations of interpreting IgM testing, the results of these tests should not be used to guide decisions about pregnancy timing for women living in areas with ongoing risk of transmission.


Echocardiography evaluation of a group of Brazilian babies with Zika-related birth defects found three times the expected rate of congenital heart disease (CHD), but only one infant had symptoms and most had minor septal defects that weren’t hemodynamically significant.

Cavalcanti DD, Alves LV, Furtado GJ, Santos CC, Feitosa FG, Ribeiro MC, et al. (2017) Echocardiographic findings in infants with presumed congenital Zika syndrome: Retrospective case series study. PLoS ONE 12(4): e0175065. https://doi.org/10.1371/journal.pone.0175065

 


Phase 2 Zika vaccine trial begins in U.S., Central and South America

NIH

Friday, March 31, 2017

Study will evaluate NIH’s experimental DNA vaccine.

Vaccinations have begun in a multi-site Phase 2/2b clinical trial testing an experimental DNA vaccine designed to protect against disease caused by Zika infection. The vaccine was developed by government scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH). NIAID is leading the trial, which aims to enroll at least 2,490 healthy participants in areas of confirmed or potential active mosquito-transmitted Zika infection, including the continental United States and Puerto Rico, Brazil, Peru, Costa Rica, Panama and Mexico. The two-part trial, called VRC 705, further evaluates the vaccine’s safety and ability to stimulate an immune response in participants, and assesses the optimal dose for administration. It also will attempt to determine if the vaccine can effectively prevent disease caused by Zika infection.

Most people with Zika infection have either no or only mild symptoms, such as fever, rash, joint pain and conjunctivitis (red eyes). However, when Zika infection occurs during pregnancy, the pregnant woman can pass the virus to her fetus, which can result in a range of fetal defects known collectively as congenital Zika syndrome. Currently there is no licensed vaccine to prevent disease caused by Zika infection, which is mainly transmitted via the bite of infected Aedes aegypti mosquitoes but also can be transmitted sexually.

“We are pleased to have advanced rapidly one of NIAID’s experimental Zika vaccines into this next stage of testing in volunteers. We expect this study will yield valuable insight into the vaccine’s safety and ability to prevent disease caused by Zika infection,” said NIAID Director Anthony S. Fauci, M.D. “A safe and effective Zika vaccine is urgently needed to prevent the often-devastating birth defects that can result from Zika virus infection during pregnancy. Evidence also is accumulating that Zika can cause a variety of health problems in adults as well. This trial marks a significant milestone in our efforts to develop countermeasures for a pandemic in progress.”

Scientists at NIAID’s Vaccine Research Center (VRC) developed the NIAID Zika virus investigational DNA vaccine. It entered early-stage human testing in 2016 following extensive testing in animal models. Initial findings indicate the vaccine is safe and able to induce a neutralizing antibody response against Zika virus. The Phase 2/2b trial aims to gain more safety and immune response data and determine if this immune response protects against disease caused by natural Zika infection.

The Zika vaccine platform is based on a strategy VRC scientists used previously to develop a West Nile virus vaccine candidate. The Zika vaccine candidate being tested in this study contains a small circular piece of DNA called a plasmid into which scientists have inserted genes that encode two proteins found on the surface of the Zika virus. Once injected into muscle, the encoded proteins assemble into particles that mimic Zika virus and trigger the body’s immune system to respond. The vaccine does not contain infectious material, so it cannot cause Zika infection.

The trial is being led by protocol co-chairs Julie E. Ledgerwood, D.O., chief of VRC’s Clinical Trials Program, and Grace L. Chen, M.D., deputy chief of the same program.

The trial consists of two studies: part A and part B. Part A will build on ongoing Phase 1 trials to further evaluate the vaccine’s safety and ability to stimulate an immune response, specifically in populations where Zika could be endemic. It will also help determine the optimal dose and injection sites for administration. Part A will enroll 90 healthy men and non-pregnant women ages 18-35 years at three sites in Houston, Miami and San Juan, Puerto Rico. All participants will receive the investigational vaccine intramuscularly at three separate clinic visits each four weeks apart. Participants will be randomly assigned to receive either a standard dose or a high dose of the investigational vaccine at all three visits, and will be followed for about 32 weeks total.

Part B of the trial will enroll at least 2,400 healthy men and non-pregnant women ages 15-35 years. This part of the trial aims to determine if the vaccine can effectively protect against Zika-related disease when someone is naturally exposed to the virus. Sites will include the three locations from part A (Houston, Miami and San Juan) as well as two additional sites in San Juan, two sites in Costa Rica, and one site each in Peru, Brazil, Panama and Mexico. Additional sites might be added in the future. Participants will be randomly assigned to receive either the investigational vaccine or a placebo at three separate clinic visits each four weeks apart. The trial is double-blind, meaning neither the study investigators nor the participants will know who receives the investigational vaccine.

Part B participants will be followed for nearly two years, during which time they will undergo assessments for adverse events and symptoms of Zika infection. Trial participants in both parts will be counseled on how to protect against Zika infection. Investigators will compare the rates of confirmed cases of Zika in the placebo group and the vaccinated group to determine if the investigational vaccine protects against disease caused by Zika infection.

Each site will have a principal investigator responsible for ensuring daily review of safety data as they become available. A protocol safety review team that includes the protocol chairs and other medical officers at NIAID will review safety data reports weekly. The NIAID Intramural Data and Safety Monitoring Board will also review cumulative study data at least twice per year. The study is currently expected to be completed by 2019.

For more information about the trial, visit Questions and Answers: VRC 705: Phase 2/2b Trial Testing the NIAID Zika Virus Investigational DNA Vaccine.

NIAID conducts and supports research — at NIH, throughout the United States, and worldwide — to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH…Turning Discovery Into Health®

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CDC: ZikaV in the USA (current situational maps)

Map of the United States showing Travel-associated and Locally acquired cases of the Zika virus. The locations and number of cases can be found in the table below.

 

CDC


Brazil: Like malaria or yellow fever, Zika is a continuing threat rather than an urgent pandemic.

NY Times

“….And doctors and researchers are just starting to grasp the medical consequences of Zika. Besides the alarmingly small heads characteristic of microcephaly, many babies have a long list of varied symptoms, leading experts to rename their condition “congenital Zika syndrome.” They can have seizures, breathing problems, trouble swallowing, weakness and stiffness in muscles and joints preventing them from even lifting their heads, clubbed feet, vision and hearing problems, and ferocious irritability.

Some have passed their first birthdays, but have neurological development closer to that of 3-month-old infants, doctors say. Some microcephaly cases appear so dire that experts liken them to a previously rare variant called “fetal brain disruption sequence.” And new issues keep cropping up, including hydrocephalus,…..”

 


A new Zika virus classification scheme

WHO, the United States Centers for Disease Control and Prevention and the European Centre for Disease Prevention and Control have developed a new Zika virus classification scheme. The classification serves to categorize the presence of and potential for vector-borne ZIKV transmission and to inform public health recommendations. Based on the defined criteria and expert review, some countries, territories and subnational areas were reclassified and some were classified for the first time.

Category 1: Area with new introduction or re-introduction with ongoing transmission

  • A laboratory-confirmed autochthonous, vector-borne case of ZIKV infection in a country /territory/subnational area where there is no evidence of virus circulation before 2015, whether it is detected and reported by the country /territory/subnational area where infection occurred, or by another country by diagnosis of a returning traveller; or
  • A laboratory-confirmed autochthonous, vector-borne case of ZIKV infection in a country/territory/subnational area where transmission has been previously interrupted, whether it is detected and reported by the country where infection occurred, or by another country by diagnosis of a returning traveller.

Category 2: Area either with evidence of virus circulation before 2015 or area with ongoing transmission that is no longer in the new or re-introduction phase, but where there is no evidence of interruption

This category takes into account those countries with known historical laboratory evidence of ZIKV circulation prior to 2015, based on the literature as well as all ZIKV surveillance data whether detected and reported by the country where infection occurred or by another country reporting a confirmed case in a returning traveller. Countries in this category may have seasonal variations in transmission. These countries may also experience outbreaks of ZIKV disease.

Laboratory criteria to ascertain the presence of ZIKV in past studies are:

  • Detection of the virus in humans, mosquitoes or animals; and/or
  • Serologic confirmation of ZIKV infection with tests conducted after 1980, and considered as confirmed infection on expert review based on testing for all appropriate cross-reactive flaviviruses and utilization of comprehensive testing methodologies. Because of testing and interpretation limitations with serological data antedating 1980, they were not used for classification purposes.

Category 3: Area with interrupted transmission and with potential for future transmission

The minimum timeline for determining transition to an interrupted state is 12 months after the last confirmed case, and no cases identified in travellers. For countries with a high capacity for diagnostic testing, consistent timely reporting of diagnostic results, a comprehensive arboviral surveillance system and/or a temperate climate or island setting, the interruption of vector-borne transmission is defined as the absence of ZIKV infection 3 months after the last confirmed case. Countries where interruption is epidemiologically likely to have occurred should provide surveillance data to WHO to support the assessment by expert review.

Category 4: Area with established competent vector but no known documented past or current transmission

All countries/territories/subnational areas where the main competent vector (A. aegypti) is established, but which have not had a documented, autochthonous, vector-borne case of ZIKV infection. This category also includes a subgroup of countries/ territories /subnational areas where ZIKV transmission may occur because of a shared border with a neighbouring Category 2 country, by belonging to the same ecological zone and having evidence of dengue virus transmission. In this subgroup, a first laboratory-confirmed, autochthonous vector-borne case of ZIKV infection may not necessarily indicate new introduction (Category 1), but rather previously unknown and undetected transmission (Category 2), and these countries/territories/subnational areas will be reclassified accordingly.


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