niman

Anthony Fauci notes that a non-human primate model replicates the persistence of Zika in pregnant females.

Chart of the Week: Why Congress Needs to Act on the Zika VirusAPRIL 6, 2016 AT 3:02 PM ET BY TANYA SOMANADERTWITTER FACEBOOK EMAIL Summary: Here's a map that estimates where the mosquitos that carry the Zika virus could potentially reach in the U.S.For months now, Americans who have been traveling or reading news reports have heard about the risk posed by the Zika virus, particularly those posed to pregnant women. In early January, President Obama convened his top advisors to formulate a proactive response to this epidemic -- including working closely with state and local elected officials, non-profits, health experts, and disease experts -- to contain and prevent the spread of the virus. In February, he asked Congress to support these efforts by providing $1.9 billion in emergency funding to combat Zika by supporting mosquito control, disease detection and testing, vaccine development, and support for maternal women's health. And since the President made that request, we've learned more concerning facts about this disease: Sexual transmission of the virus is more common than initially believedThe impact on fetal brain development is likely starker and more serious than first understoodIn the U.S., the geographical range of the particular mosquito that transmits Zika far exceeds our initial estimationThe Center for Disease Control has laid out an estimated range of the mosquitos that carry this disease in the United States this year. And while this map is not meant to represent risk for spread of the Zika virus, it shows where people may come into contact with the kinds of mosquitos that could be carrying this disease. We find ourselves in a rare moment where we have advance warning on a disease, and the likely birth defects that are associated with it, will be arriving in the U.S. Governors, state and local leaders are already working with us to get ahead of this threat. However, Congress continues to do nothing about the emergency funding. Because we cannot continue to fund a robust response to this disease without adequate resources, particularly for our partners in state and local government who will bear much of this burden, we are re-programming nearly $600 million of existing funds to address Ebola to help support our Zika response. This is not nearly enough to protect us from the significant threat posed by Zika. It’s a temporary fix, and not a long-term solution. As our Director of Management and Budget Shaun Donovan said this morning: As it gets warmer, the reach of these mosquitos will increase, and the need for a robust response will be more and more urgent. We have the opportunity to do get ahead of this epidemic, but Congress needs to do its part. Tanya SomanaderDirector of Digital Rapid Response for the Office of Digital StrategyFollow @blog44https://www.whitehouse.gov/blog/2016/04/06/chart-week-why-congress-needs-act-zika-virus

Taking Every Step Necessary, As Quickly As Possible, to Protect the American People from ZikaAPRIL 6, 2016 AT 11:00 AM ET BY SHAUN DONOVANTWITTER FACEBOOK EMAIL Summary: Nearly two months have passed since we submitted a request for emergency supplemental funding to combat the Zika virus. Congress has yet to act.The Administration is committed to taking every step necessary, as quickly as possible, to protect the American people from the Zika virus. That’s why we submitted to Congress a request for emergency supplemental funding in February to fortify our efforts to combat and stay ahead of the disease. But Congress has yet to act. Nearly two months have passed and the situation continues to grow more critical. Since we submitted the supplemental request to Congress, we have learned that sexual transmission of the virus is more common than believed; that the potential impact on fetal brain development is starker and more serious than first understood; and that within the United States the geographical range of the Aedis aegypti mosquito far exceeds our initial estimation. The Zika virus is spreading in Puerto Rico, the U.S. Virgin Islands, American Samoa, and abroad -- and there will likely be local mosquito-borne transmission in the continental United States in the upcoming spring and summer months. The World Health Organization (WHO) has stated there is a strong scientific consensus that the Zika virus is a cause of microcephaly and other poor pregnancy outcomes, Guillain-Barré Syndrome, and other neurological disorders. There is a confirmed case of a baby born with Zika-related microcephaly in Hawaii and there are additional microcephaly cases under investigation. As of last week, 33 countries and territories in the Americas reported active Zika transmission. We continue to call on Congress to take immediate action to provide the full requested amount for the emergency supplemental, but in the absence of Congressional action, we must scale up Zika preparedness and response activities now. Faced with this urgent need, we have identified $589 million – including $510 million of existing Ebola resources within the Department of Health and Human Services and Department of State/USAID – that can quickly be redirected and spent on immediate, time-critical activities such as mosquito control, lab capacity, development of diagnostics and vaccines, supporting affected expectant mothers and babies, tracking and mapping the spread and effects of Zika infections in humans, and other prevention and response efforts in the continental United States, Puerto Rico, other U.S. Territories, and abroad, especially within the Americas. We have always said that we were open to using a portion of the existing Ebola balances for Zika, but that this alone would not provide a sufficient enough response to the significant threat posed by Zika. This remains true. As such, the redirected funds are not enough to support a comprehensive Zika response and can only temporarily address what is needed until Congress acts on the Administration's emergency supplemental request. Emergency supplemental funding continues to be urgently needed to support the full range of activities needed to prevent, detect, and respond to further transmission of the Zika virus, including: Fortifying domestic and international public health systems; Accelerating vaccine research and development to provide a long-term strategy to limit the Zika virus;Enabling the development of better diagnostic tests, including tests that can be implemented in resource poor settings, and expanded laboratory capacity in both public health laboratories and in the private sector in the United States and abroad, particularly to meet the demand for Zika testing that we anticipate will dramatically increase; Conducting mosquito surveillance and deploying mosquito control tools, such as outdoor and indoor residual spraying, source reduction and larviciding, and widespread space spraying. In particular, as the rainy season gets underway in Central America and the Caribbean, these mosquito control efforts will be important internationally as well as domestically;Educating health care providers, pregnant women, and their partners;Supporting ongoing research efforts to improve our understanding of the Zika virus and its adverse health outcomes;Developing pathogen-reduction technology to help ensure the safety of the blood supply;Improving health services and support for low-income pregnant women; andEnhancing the ability of Zika-affected countries to better combat mosquitoes, control transmission, and support affected populations.Without the full amount of requested emergency supplemental funding, many activities that need to start now would have to be delayed, or curtailed or stopped, within months. For example, without supplemental funding, testing and manufacturing of vaccine candidates beyond the earliest stages of clinical trials would not be possible. In addition, lack of supplemental funding would prevent us from developing platform technologies for vaccine candidates for this Zika response and from accelerating the response to emerging infectious diseases in the future. Absent supplemental funding, we will need to delay contracting with manufacturers for the development of faster and more accurate diagnostic tests, which are needed to ensure that those who think they have been exposed to Zika can get tested. In particular, there is a critical need for point-of-care diagnostics that are faster and do not require laboratory capacity. Similarly, starting mosquito surveillance and control activities now, prior to the summer months which are peak season for mosquitoes, and prior to the start of the rainy season in Central America and the Caribbean, is prudent. Lack of funds could result in having to halt these efforts within months, which would increase the risk of more Americans contracting the Zika virus. Without supplemental funding, CDC would not be able to fully fund planned state grants for public health emergency preparedness, which would impede the ability for states to fully implement risk-based Zika preparedness and response plans. The full supplemental request is also needed to replenish the amounts that we are now spending from our Ebola accounts to fund Zika-related activities. The threat of Ebola remains front and center, as evidenced by the recent cases in Guinea and Liberia, and there is still critical work that is ongoing to make sure that we follow through on our Ebola response. There are currently 12 cases across Guinea and Liberia with nearly 1000 contacts under observation. Given the high-risk exposure of many of these contacts, we expect the case numbers to go up in the coming days. Replenishing the Ebola accounts will ensure we have sufficient contingency funds to address unanticipated needs related to both Zika and Ebola. As we have seen with both Ebola and Zika, there are still many unknowns about the science and scale of the outbreak and how it will impact mothers, babies, and health systems domestically and abroad. We urge Congress to act quickly on the emergency request for Zika to ensure we have funds to stay ahead of this disease, as well as Ebola, and do everything we can to protect the American people. Shaun DonovanDirector of the Office of Management and BudgetFollow @ShaunOMB https://www.whitehouse.gov/blog/2016/04/06/taking-every-step-necessary-quickly-possible-protect-american-people-zika

Map Update https://www.google.com/maps/d/u/0/edit?hl=en&hl=en&authuser=0&authuser=0&mid=zv94AJqgUct4.kT4qLMXp3SLU

Washoe County reports first confirmed Zika case Symptoms consistent with Zika virus developed after returning from travel to El Salvador. Media ReleaseFor Immediate Releasewww.washoecounty.us/health Contact: Phil [email protected] or 775.772.1659 RENO, NV - A female adult with recent travel history to a Zika-affected country is the first confirmed Zika case in Washoe County according to health officials. The woman developed symptoms consistent with Zika virus after returning from travel to El Salvador. Those symptoms included joint pain, body ache, fever, conjunctivitis, chills, abdominal pain, headache and rash. Her symptoms resolved within a week. The woman is one of twelve individuals in Washoe County who have been tested in recent weeks. No other positive results have been received to date. "We will continue to monitor the lab tests we have submitted to the Centers for Disease Control and Prevention," said Washoe County District Health Officer Kevin Dick. "We know that the general public is concerned about the rise in the number of Zika cases, so this serves as a reminder that people going to Zika-affected countries, particularly those that are pregnant or intending to become pregnant, should take precautions to avoid being bitten by mosquitoes while traveling." Zika virus can be spread from a pregnant woman to her fetus and has been linked to a serious birth defect of the brain called microcephaly in babies of mothers who had Zika virus while pregnant. Zika virus is spread to people primarily through the bite of an infected Aedes species mosquito (Ae. aegyptiand Ae. albopictus). To date, Zika has not been spread by mosquitoes in the continental United States. However, lab tests have confirmed Zika virus in travelers returning to the United States from areas with Zika. Zika virus can also be spread during sex by a man infected with Zika to his partners. Some non-travelers in the United States have become infected with Zika through sex with a traveler. According to local health officials, the mosquitoes known to carry Zika virus are not indigenous to our area. While the mosquito may find its way to northern Nevada, it is not known whether the insect can survive in our climate. The best way to prevent diseases spread by mosquitoes is to protect yourself and your family from mosquito bites. Wear long-sleeved shirts and long pants.Stay in places with air conditioning and window and door screens to keep mosquitoes outside.Treat your clothing and gear with DEET or permethrin or buy pre-treated items.Use Environmental Protection Agency (EPA)-registered insect repellents. https://www.epa.gov/insect-repellents Sleep under a mosquito bed net if air conditioned or screened rooms are not available or if sleeping outdoors.To learn more, please visit CDC's Zika virus page at http://www.cdc.gov/zika/index.html.

A female adult with recent travel history to a Zika-affected country is the first confirmed Zika case in Washoe County according to health officials. The woman developed symptoms consistent with Zika virus after returning from travel to El Salvador. Those symptoms included joint pain, body ache, fever, conjunctivitis, chills, abdominal pain, headache and rash. Her symptoms resolved within a week. The woman is one of twelve individuals in Washoe County who have been tested in recent weeks. No other positive results have been received to date. https://www.washoecounty.us/outreach/2016/03/2016-04-11-zika-positive-1.php

Map Update https://www.google.com/maps/d/u/0/edit?hl=en&hl=en&authuser=0&authuser=0&mid=zv94AJqgUct4.kT4qLMXp3SLU

April 11, 2016 DEPARTMENT OF HEALTH DAILY ZIKA UPDATE: ONE NEW TRAVEL-RELATED CASE IN LEE COUNTY Contact:Communications [email protected](850) 245-4111 Tallahassee, Fla.—In an effort to keep Florida residents and visitors safe and aware about the status of the Zika virus, the Florida Department of Health will issue a Zika virus update each week day at 2 p.m. Updates will include a CDC-confirmed Zika case count by county and information to better keep Floridians prepared. There is one new travel-related case in Lee County today.Of the cases confirmed in Florida, six cases are still exhibiting symptoms. According to the CDC, symptoms associated with the Zika virus last between seven to 10 days. Based on CDC guidance, several pregnant women who have traveled to countries with local-transmission of Zika have received antibody testing, and of those, five have tested positive for the Zika virus. The CDC recommends that a pregnant woman with a history of Zika virus and her provider should consider additional ultrasounds. It is recommended that women who are pregnant or thinking of becoming pregnant postpone travel to Zika affected areas. County Number of Cases (all travel related) Alachua 4 Brevard 2 Broward 13 Clay 1 Collier 1 Hillsborough 3 Lee 4 Miami-Dade 33 Orange 5 Osceola 4 Palm Beach 4 Polk 3 Santa Rosa 1 Seminole 1 St. Johns 1 Cases involving pregnant women* 5 Total 85 *Counties of pregnant women will not be shared. On Feb. 12, Governor Scott directed the State Surgeon General to activate a Zika Virus Information Hotline for current Florida residents and visitors, as well as anyone planning on traveling to Florida in the near future. The hotline, managed by the Department of Health, has assisted 1,333 callers since it launched. The number for the Zika Virus Information Hotline is 1-855-622-6735. All cases are travel-associated. There have been no locally-acquired cases of Zika in Florida. For more information on the Zika virus, click here. The department urges Floridians to drain standing water weekly, no matter how seemingly small. A couple drops of water in a bottle cap can be a breeding location for mosquitoes. Residents and visitors also need to use repellents when enjoying the Florida outdoors. More Information on DOH action on Zika: On Feb. 3, Governor Scott directed the State Surgeon General to issue a Declaration of Public Health Emergency for the counties of residents with travel-associated cases of Zika.The Declaration currently includes the 15 affected counties – Alachua, Brevard, Broward, Clay, Collier, Hillsborough, Lee, Miami-Dade, Orange, Osceola, Palm Beach, Polk, Santa Rosa, Seminole and St. Johns – and will be updated as needed. DOH encourages Florida residents and visitors to protect themselves from all mosquito-borne illnesses by draining standing water; covering their skin with repellent and clothing; and covering windows with screens.DOH has a robust mosquito-borne illness surveillance system and is working with the CDC, the Florida Department of Agriculture and Consumer Services and local county mosquito control boards to ensure that the proper precautions are being taken to protect Florida residents and visitors.On April 6, Governor Rick Scott and Interim State Surgeon General Dr. Celeste Philip hosted a conference call with Florida Mosquito Control Districts to discuss ongoing preparations to fight the possible spread of the Zika virus in Florida. There were 74 attendees on the call.Florida currently has the capacity to test 6,821 people for active Zika virus and 1,603 for Zika antibodies.Federal Guidance on Zika: According to the CDC, Zika illness is generally mild with a rash, fever and joint pain. CDC researchers are examining a possible link between the virus and harm to unborn babies exposed during pregnancy.The FDA released guidance regarding donor screening, deferral and product management to reduce the risk of transfusion-transmission of Zika virus. Additional information is available on the FDA website here.The CDC has put out guidance related to the sexual transmission of the Zika virus. This includes the CDC recommendation that if you have traveled to a country with local transmission of Zika you should abstain from unprotected sex.For more information on Zika virus, click here. About the Florida Department of Health The department, nationally accredited by the Public Health Accreditation Board, works to protect, promote and improve the health of all people in Florida through integrated state, county and community efforts. Follow us on Twitter at @HealthyFla and on Facebook. For more information about the Florida Department of Health, please visit www.FloridaHealth.gov. http://www.floridahealth.gov/newsroom/2016/04/041116-zika-update.html

County Number of Cases (all travel related) Alachua 4 Brevard 2 Broward 13 Clay 1 Collier 1 Hillsborough 3 Lee 4 Miami-Dade 33 Orange 5 Osceola 4 Palm Beach 4 Polk 3 Santa Rosa 1 Seminole 1 St. Johns 1 Cases involving pregnant women* 5 Total 85

Pennsylvania Blood Tests Submitted for Zika Testing as of April 11, 2016 Information updated Mondays at 2 p.m.CDC Confirmed Cases: 12Pending Test Results: 115

Allegheny County Residents Approved for Zika Testing: 61 CDC Confirmed Cases: 1(as of April 11)

Zika Virus – April 11, 2016. Texas has had 28 confirmed cases of Zika virus disease. Of those, 27 were in travelers who were infected abroad and diagnosed after they returned home; one of those travelers was a pregnant woman. One case involved a Dallas County resident who had sexual contact with someone who acquired the Zika infection while traveling abroad. Case counts by county: Bexar – 3Dallas – 5Fort Bend – 2Grayson – 1Harris – 11Tarrant – 3Travis – 2Wise – 1

Aedes aegypti mosquitoes Paulo Whitaker / Reuters SHARE Two studies published this week show that the Zika virus seems to prefer brain cells — and that it can cause many different types of damage to those cells. One of the studies shows that Zika — but not its close cousin, the dengue virus — destroys developing nerve cells. Another describes the cases of two Zika patients who developed nerve damage similar to that caused by multiple sclerosis. Confocal microscopy of human neural stem cell culture infected with Zika virus (red). Cell nuclei are shown in blue. Credit: Erick Loiola, PhD and Rodrigo Madeiro, PhD - IDOR / ScienceBoth add to the growing body of evidence that Zika virus, once virtually ignored as a rather harmless infection, is causing severe and sometimes deadly birth defects and other types of damage to victims of all ages. And because it's spreading so fast among so many people, it's adding up to thousands of victims. Patricia Garcez of the Federal University of Rio de Janeiro in Brazil and colleagues used human induced pluripotent stem (iPS) cells — lab-created stem cells — which they coaxed into become immature brain cells. Zika virus infected and killed them, they report in the journal Science. When they directed these iPS cells to become little batches of brain cells, the virus slowed their growth and development by 40 percent. But when Garcez's team tried the same thing with dengue virus, they did not see the same effects. The virus, which is very closely related to Zika, infected the nerve and brain cells but did not kill them. "THOUGH OUR STUDY IS SMALL, IT MAY PROVIDE EVIDENCE THAT IN THIS CASE THE VIRUS HAS DIFFERENT EFFECTS ON THE BRAIN THAN THOSE IDENTIFIED IN CURRENT STUDIES."This helps explain why Zika's effects were so unexpected. Viruses such as rubella and those in the herpes family are well known to cause birth defects and sometimes severe neurological effects in adults and children. But not so-called flaviviruses such as Zika and its cousin dengue. Zika was once believed to cause little more than a rash and some achiness - and even then only in a small percentage of people infected. Now it's known it can have serious effects on developing fetuses and adults as well. A second study shows more startling neurological effects. Dr. Maria Lucia Brito Ferreira of Restoration Hospital in Recife, Brazil and colleagues described the cases of two Zika patients who developed a condition called acute disseminated encephalomyelitis. It's an inflammation of the brain and spinal cord that damages the protective fatty myelin layer that covers nerve cells. That's similar to what multiple sclerosis does, but it's usually temporary - although the recovery can take months. Four more patients developed Guillain-Barre syndrome, a paralyzing condition hat's also caused by nerve damage, Ferreira's team said in remarks released ahead of an annual meeting of the American Academy of Neurology. "Though our study is small, it may provide evidence that in this case the virus has different effects on the brain than those identified in current studies," said Ferreira. When they left the hospital, five of the six people still had problems with movement and coordination and one had memory problems. "This doesn't mean that all people infected with Zika will experience these brain problems. Of those who have nervous system problems, most do not have brain symptoms," said Ferreira. "However, our study may shed light on possible lingering effects the virus may be associated with in the brain." Zika's spreading in both Latin America and the South Pacific. The mosquito-borne virus is blamed for thousands of birth defects, notably one called microcephaly, marked by an underdeveloped brain and head. The World Health Organization and the Centers for Disease Control and Prevention both warn travelers going to Zika-affected regions to do what they can to avoid mosquito bites. They're telling pregnant women to stay away completely if they can. Both also warn travelers who may bring Zika back home to avoid infecting loved ones sexually and to watch out not to get bitten by mosquitoes at home. The CDC predicts small, localized outbreaks in the U.S. as warmer weather fuels the breeding of the mosquitoes that spread Zika. http://www.nbcnews.com/health/health-news/there-s-more-evidence-zika-goes-straight-brain-n554041

HEALTH APR 11 2016, 11:00 AM ETThere's More Evidence Zika Goes Straight to the Brainby MAGGIE FOX Aedes aegypti mosquitoes Paulo Whitaker / Reuters SHARE Two studies published this week show that the Zika virus seems to prefer brain cells — and that it can cause many different types of damage to those cells. One of the studies shows that Zika — but not its close cousin, the dengue virus — destroys developing nerve cells. Another describes the cases of two Zika patients who developed nerve damage similar to that caused by multiple sclerosis. Confocal microscopy of human neural stem cell culture infected with Zika virus (red). Cell nuclei are shown in blue. Credit: Erick Loiola, PhD and Rodrigo Madeiro, PhD - IDOR / ScienceBoth add to the growing body of evidence that Zika virus, once virtually ignored as a rather harmless infection, is causing severe and sometimes deadly birth defects and other types of damage to victims of all ages. And because it's spreading so fast among so many people, it's adding up to thousands of victims. Patricia Garcez of the Federal University of Rio de Janeiro in Brazil and colleagues used human induced pluripotent stem (iPS) cells — lab-created stem cells — which they coaxed into become immature brain cells. Zika virus infected and killed them, they report in the journal Science. When they directed these iPS cells to become little batches of brain cells, the virus slowed their growth and development by 40 percent. But when Garcez's team tried the same thing with dengue virus, they did not see the same effects. The virus, which is very closely related to Zika, infected the nerve and brain cells but did not kill them. "THOUGH OUR STUDY IS SMALL, IT MAY PROVIDE EVIDENCE THAT IN THIS CASE THE VIRUS HAS DIFFERENT EFFECTS ON THE BRAIN THAN THOSE IDENTIFIED IN CURRENT STUDIES."This helps explain why Zika's effects were so unexpected. Viruses such as rubella and those in the herpes family are well known to cause birth defects and sometimes severe neurological effects in adults and children. But not so-called flaviviruses such as Zika and its cousin dengue. Zika was once believed to cause little more than a rash and some achiness - and even then only in a small percentage of people infected. Now it's known it can have serious effects on developing fetuses and adults as well. A second study shows more startling neurological effects. Dr. Maria Lucia Brito Ferreira of Restoration Hospital in Recife, Brazil and colleagues described the cases of two Zika patients who developed a condition called acute disseminated encephalomyelitis. It's an inflammation of the brain and spinal cord that damages the protective fatty myelin layer that covers nerve cells. That's similar to what multiple sclerosis does, but it's usually temporary - although the recovery can take months. Four more patients developed Guillain-Barre syndrome, a paralyzing condition hat's also caused by nerve damage, Ferreira's team said in remarks released ahead of an annual meeting of the American Academy of Neurology. "Though our study is small, it may provide evidence that in this case the virus has different effects on the brain than those identified in current studies," said Ferreira. When they left the hospital, five of the six people still had problems with movement and coordination and one had memory problems. "This doesn't mean that all people infected with Zika will experience these brain problems. Of those who have nervous system problems, most do not have brain symptoms," said Ferreira. "However, our study may shed light on possible lingering effects the virus may be associated with in the brain." Zika's spreading in both Latin America and the South Pacific. The mosquito-borne virus is blamed for thousands of birth defects, notably one called microcephaly, marked by an underdeveloped brain and head. The World Health Organization and the Centers for Disease Control and Prevention both warn travelers going to Zika-affected regions to do what they can to avoid mosquito bites. They're telling pregnant women to stay away completely if they can. Both also warn travelers who may bring Zika back home to avoid infecting loved ones sexually and to watch out not to get bitten by mosquitoes at home. The CDC predicts small, localized outbreaks in the U.S. as warmer weather fuels the breeding of the mosquitoes that spread Zika. http://www.nbcnews.com/health/health-news/there-s-more-evidence-zika-goes-straight-brain-n554041

As of April 11, 2016 there are no confirmed cases of Zika virus in South Carolina.

Alabama Residents Tested for Zika Virus as of April 11, 2016 Number Tested PositiveNumber of SubmissionsNumber with Results Pending3 47 15

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Med. 2,862–870 (2013). doi:10.5966/sctm.2013-0080 pmid:24113065Abstract/FREE Full TextGoogle Scholar↵E. A. Henchal, M. K. Gentry, J. M. McCown, W. E. Brandt, Dengue virus-specific and flavivirus group determinants identified with monoclonal antibodies by indirect immunofluorescence. Am. J. Trop. Med. Hyg. 31, 830–836 (1982). pmid:6285749Abstract/FREE Full TextGoogle ScholarAcknowledgments: The authors thank the lab-crew members Marcelo Costa, Ismael Gomes, Gabriela Vitória, Jarek Sochacki and Matías Alloati for providing technical support, cultures of human iPS cells and brain organoids. We acknowledge Dr. Ortrud Monika Barth for comments on the electron micrographs. We also thank Dr Fabricio Pamplona for Mind the Graph assistance and Centro Nacional de Biologia Estrutural e Bioimagem (CENABIO) for the use of the Electron Microscopy. Funds (not specifically for Zika virus studies) were provided by the Brazilian Development Bank (BNDES); Funding Authority for Studies and Projects (FINEP); National Council of Scientific and Technological Development (CNPq); Foundation for Research Support in the State of Rio de Janeiro (FAPERJ); and fellowships from the São Paulo Research Foundation (FAPESP, grant #2014/21035-0) and Coordination for the Improvement of Higher Education Personnel (CAPES). All protocols and procedures were approved by the institutional research ethics committee of Hospital Copa D'Or (CEPCOPADOR) under # 727.269. The authors declare no competing financial interests.

Primary microcephaly is a severe brain malformation characterized by the reduction of the head circumference. Patients display a heterogeneous range of brain impairments, compromising motor, visual, hearing and cognitive functions (1). Microcephaly is associated with decreased neuronal production as a consequence of proliferative defects and death of cortical progenitor cells (2). During pregnancy, the primary etiology of microcephaly varies from genetic mutations to external insults. The so-called TORCHS factors (Toxoplasmosis, Rubella, Cytomegalovirus, Herpes virus, Syphilis) are the main congenital infections that compromise brain development in utero (3). The increase in the rate of microcephaly in Brazil has been associated with the recent outbreak of Zika virus (ZIKV) (4, 5), a flavivirus that is transmitted by mosquitoes (6) and sexually (7–9). So far, ZIKV has been described in the placenta and amniotic fluid of microcephalic fetuses (10–13), and in the blood of microcephalic newborns (11, 14). ZIKV had also been detected within the brain of a microcephalic fetus (13, 14), and recently, there is direct evidence that ZIKV is able to infect and cause death of neural stem cells (15). Here, we used human induced pluripotent stem (iPS) cells cultured as neural stem cells (NSC), neurospheres and brain organoids to explore the consequences of ZIKV infection during neurogenesis and growth with 3D culture models. Human iPS-derived NSCs were exposed to ZIKV (MOI 0.25 to 0.0025). After 24 hours, ZIKV was detected in NSCs (Fig. 1, A to D), when viral envelope protein was shown in 10.10% (MOI 0.025) and 21.7% (MOI 0.25) of cells exposed to ZIKV (Fig. 1E). Viral RNA was also detected in the supernatant of infected NSCs (MOI 0.0025) by qRT-PCR (Fig. 1F), supporting productive infection. Download high-res image Open in new tab Download PowerpointFig. 1ZIKV infects human neural stem cells.Confocal microscopy images of iPS-derived NSCs double stained for (A) ZIKV in the cytoplasm, and (B) SOX2 in nuclei, one day after virus infection. (C) DAPI staining, (D) merged channels show perinuclear localization of ZIKV. Bar = 100 μm. (E) Percentage of ZIKV infected SOX2 positive cells (MOI 0.25 and 0.025). (F) RT-PCR analysis of ZIKV RNA extracted from supernatants of mock and ZIKV-infected neurospheres (MOI 0.0025) after 3 DIV, showing amplification only in infected cells. RNA was extracted, qPCR performed and virus production normalized to 12h post-infection controls. Data presented as mean ± SEM, n=5, Student’s t test, *p < 0.05, **p < 0.01. To investigate the effects of ZIKV during neural differentiation, mock- and ZIKV-infected NSCs were cultured as neurospheres. After 3 days in vitro, mock NSCs generated round neurospheres. However, ZIKV-infected NSCs generated neurospheres with morphological abnormalities and cell detachment (Fig. 2B). After 6 days in vitro (DIV), hundreds of neurospheres grew under mock conditions (Fig. 2, C and E). Strikingly, in ZIKV-infected NSCs (MOI 2.5 to 0.025) only a few neurospheres survived (Fig. 2, D and E). Download high-res image Open in new tab Download PowerpointFig. 2ZIKV alters morphology and halts the growth of human neurospheres.(A) Control neurosphere displays spherical morphology after 3 DIV. (B) Infected neurosphere showed morphological abnormalities and cell detachment after 3 DIV. (C) Culture well-plate containing hundreds of mock neurospheres after 6 DIV. (D) ZIKV-infected well-plate (MOI 2.5-0.025) containing few neurospheres after 6 DIV. Bar = 250 μm in (A) and (B), and 1 cm in (C) and (D). (E) Quantification of the number of neurospheres in different MOI. Data presented as mean ± SEM, n=3, Student’s t test, ***p < 0.01. Mock neurospheres presented expected ultrastructural morphology of nucleus and mitochondria (Fig. 3A). ZIKV-infected neurospheres revealed the presence of viral particles, similarly to those observed in murine glial and neuronal cells (16). ZIKV was bound to the membranes and observed in mitochondria and vesicles of cells within infected neurospheres (Fig. 3, B and F, arrows). Apoptotic nuclei, a hallmark of cell death, were observed in all ZIKV-infected neurospheres analyzed (Fig. 3B). Of note, ZIKV-infected cells in neurospheres presented smooth membrane structures (SMS) (Fig. 3, B and F), similarly to those previously described in other cell types infected with dengue virus (17). These results suggest that ZIKV induces cell death in human neural stem cells and thus impairs the formation of neurospheres. Download high-res image Open in new tab Download PowerpointFig. 3ZIKV induces death in human neurospheres.Ultrastructure of mock- and ZIKV-infected neurospheres after 6 days in vitro. (A) Mock-infected neurosphere showing cell processes and organelles, (B) ZIKV-infected neurosphere shows pyknotic nucleus, swollen mitochondria, smooth membrane structures and viral envelopes (arrow). Arrows point viral envelopes on cell surface (C), inside mitochondria (D), endoplasmic reticulum (E) and close to smooth membrane structures (F). Bar = 1 μm in (A) and (B) and 0.2 μm in (C) to (F). m = mitochondria; n = nucleus; sms = smooth membrane structures. To further investigate the impact of ZIKV infection during neurogenesis, human iPS-derived brain organoids (18) were exposed with ZIKV, and followed for 11 days in vitro (Fig. 4). The growth rate of 12 individual organoids (6 per condition) was measured during this period (Fig. 4, A and D). As a result of ZIKV infection, the average growth area of ZIKV-exposed organoids was reduced by 40% when compared to brain organoids under mock conditions (0.624 mm2 ± 0.064 ZIKV-exposed organoids versus 1.051 mm2 ± 0.1084 mock-infected organoids normalized, Fig. 4E). Download high-res image Open in new tab Download PowerpointFig. 4ZIKV reduces the growth rate of human brain organoids.35 days old brain organoids were infected with (A) MOCK and (B) ZIKV for 11 days in vitro. ZIKV-infected brain organoids show reduction in growth compared with MOCK. Arrows point to detached cells. Organoid area was measured before and after 11 days exposure with (C) MOCK and (D) ZIKV in vitro. Plotted quantification represent the growth rate. (E) Quantification of the average of mock- and ZIKV-infected organoid area 11 days after infection in vitro. Data presented as mean ± SEM, n=6, Student’s t test, *p < 0.05. In addition to MOCK infection, we used dengue virus 2 (DENV2), a flavivirus with genetic similarities to ZIKV (11, 19), as an additional control group. One day after viral exposure, DENV2 infected human NSCs with a similar rate as ZIKV (fig. S1, A and B). However, after 3 days in vitro, there was no increase in caspase 3/7 mediated cell death induced by DENV2 with the same 0.025 MOI adopted for ZIKV infection (fig. S1, C and D). On the other hand, ZIKV induced caspase 3/7 mediated cell death in NSCs, similarly to the results described by Tang and colleagues (15). After 6 days in vitro, there is a significant difference in cell viability between ZIKV-exposed NSCs compared to DENV2-exposed NSCs (fig. S1, E and F). In addition, neurospheres exposed to DENV2 display a round morphology such as uninfected neurospheres after 6 days in vitro (fig. S1G). Finally, there was no reduction of growth in brain organoids exposed to DENV2 for 11 days compared to MOCK (1.023 mm2 ± 0.1308 DENV2-infected organoids versus 1.011 mm2 ± 0.2471 mock-infected organoids normalized, fig. S1, H and I). These results suggest that the deleterious consequences of ZIKV infection in human NSCs, neurospheres and brain organoids are not a general feature of the flavivirus family. Neurospheres and brain organoids are complementary models to study embryonic brain development in vitro (20, 21). While neurospheres present the very early characteristics of neurogenesis, brain organoids recapitulate the orchestrated cellular and molecular early events comparable to the first trimester fetal neocortex, including gene expression and cortical layering (18, 22). Our results demonstrate that ZIKV induces cell death in human iPS-derived neural stem cells, disrupts the formation of neurospheres and reduces the growth of organoids (fig. S2), indicating that ZIKV infection in models that mimics the first trimester of brain development may result in severe damage. Other studies are necessary to further characterize the consequences of ZIKV infection during different stages of fetal development. Cell death impairing brain enlargement, calcification and microcephaly is well described in congenital infections with TORCHS (3, 23, 24). Our results, together with recent reports showing brain calcification in microcephalic fetuses and newborns infected with ZIKV (10, 14) reinforce the growing body of evidence connecting congenital ZIKV outbreak to the increased number of reports of brain malformations in Brazil. Supplementary Materialswww.sciencemag.org/cgi/content/full/science.aaf6116/DC1 Materials and Methods Figs. S1 and S2 References (25–27)

AbstractSince the emergence of Zika virus (ZIKV), reports of microcephaly have increased significantly in Brazil; however, causality between the viral epidemic and malformations in fetal brains needs further confirmation. Here, we examine the effects of ZIKV infection in human neural stem cells growing as neurospheres and brain organoids. Using immunocytochemistry and electron microscopy, we show that ZIKV targets human brain cells, reducing their viability and growth as neurospheres and brain organoids. These results suggest that ZIKV abrogates neurogenesis during human brain development.

Zika virus impairs growth in human neurospheres and brain organoidsPatricia P. Garcez1,2,*, Erick Correia Loiola2,†, Rodrigo Madeiro da Costa2,†,Luiza M. Higa3,†, Pablo Trindade2,†, Rodrigo Delvecchio3, Juliana Minardi Nascimento2,4, Rodrigo Brindeiro3, Amilcar Tanuri3, Stevens K. Rehen2,1,*+ Author Affiliations ↵*Corresponding author. Email: [email protected] (P.P.G.); [email protected](S.K.R.)↵† These authors contributed equally to this work. Science 10 Apr 2016:DOI: 10.1126/science.aaf6116 http://science.sciencemag.org/content/early/2016/04/08/science.aaf6116.full

Zika virus impairs growth in human neurospheres and brain organoidsPatricia P. Garcez1,2,*, Erick Correia Loiola2,†, Rodrigo Madeiro da Costa2,†,Luiza M. Higa3,†, Pablo Trindade2,†, Rodrigo Delvecchio3, Juliana Minardi Nascimento2,4, Rodrigo Brindeiro3, Amilcar Tanuri3, Stevens K. Rehen2,1,*+ Author Affiliations ↵*Corresponding author. Email: [email protected] (P.P.G.); [email protected](S.K.R.)↵† These authors contributed equally to this work. Science 10 Apr 2016:DOI: 10.1126/science.aaf6116 http://science.sciencemag.org/content/early/2016/04/08/science.aaf6116.full

Apr 11, 2016Zika Virus Tied to MS-like Brain DisorderScientists report that the Zika virus may be associated with an autoimmune disorder that attacks the brain's myelin similar to multiple sclerosis. The investigators will discuss the results of their research at the upcoming American Academy of Neurology's 68th Annual Meeting in Vancouver, Canada. "Though our study is small, it may provide evidence that in this case the virus has different effects on the brain than those identified in current studies," said study author Maria Lucia Brito Ferreira, MD, with Restoration Hospital in Recife, Brazil. "Much more research will need to be done to explore whether there is a causal link between Zika and these brain problems." For the study, researchers followed people who came to the hospital in Recife from December 2014 to June 2015 with symptoms compatible with arboviruses, the family of viruses that includes Zika, dengue and chikungunya. Six people then developed neurologic symptoms that were consistent with autoimmune disorders and underwent exams and blood tests. The authors saw 151 cases with neurological manifestations during a period of December 2014 to December 2015. All of the people came to the hospital with fever followed by a rash. Some also had severe itching, muscle and joint pain and red eyes. The neurologic symptoms started right away for some people and up to 15 days later for others. Of the six people who had neurologic problems, two of the people developed acute disseminated encephalomyelitis (ADEM), an attack of swelling of the brain and spinal cord that attacks the myelin. In both cases, brain scans showed signs of damage to the brain's white matter. Unlike MS, acute disseminated encephalomyelitis usually consists of a single attack that most people recover from within six months. In some cases, the disease can reoccur. Four of the people developed Guillain-Barré syndrome (GBS), a syndrome that involves myelin of the peripheral nervous system and has a previously reported association with the Zika virus. When they were discharged from the hospital, five of the six people still had problems with motor functioning. One person had vision problems and one had problems with memory and thinking skills. Tests showed that the participants all had Zika virus. Tests for dengue and chikungunya were negative. "This doesn't mean that all people infected with Zika will experience these brain problems. Of those who have nervous system problems, most do not have brain symptoms," said Dr. Ferreira. "However, our study may shed light on possible lingering effects the virus may be associated with in the brain." "At present, it does not seem that ADEM cases are occurring at a similarly high incidence as the GBS cases, but these findings from Brazil suggest that clinicians should be vigilant for the possible occurrence of ADEM and other immune-mediated illnesses of the central nervous system," noted James Sejvar, MD, with the Centers for Disease Control and Prevention in Atlanta and a member of the American Academy of Neurology. "Of course, the remaining question is 'why'-why does Zika virus appear to have this strong association with GBS and potentially other immune/inflammatory diseases of the nervous system? Hopefully, ongoing investigations of Zika virus and immune-mediated neurologic disease will shed additional light on this important question." http://www.genengnews.com/gen-news-highlights/zika-virus-tied-to-ms-like-brain-disorder/81252591/

Zika virus may cause broader range of brain disorders than previously believedStudy says five patients who tested positive for virus in Brazil reported difficulty with motor functioning while another had trouble with vision and memory The Zika virus is spread by mosquitoes. Photograph: Daniel Becerril/ReutersAlan Yuhas @alanyuhasSunday 10 April 2016 16.00 EDTLast modified on Sunday 10 April 201616.12 EDT Share on PinterestShare on LinkedInShare on Google+Shares177 Save for laterThe Zika virus may cause a wider range of brain disorders than previously thought, according to a small study released on Sunday. Scientists already suspect the mosquito and sex-spread virus causes fetal brain disorder and temporary paralysis. Analysis Zika virus: its effects, how it is spread, and the possible threat to womenThe disease is believed to have infected 1.5 million people since its outbreak in Brazil and dramatic spread around the world Read moreThe study followed patients with symptoms of arboviruses, the family of infectious agents that includes Zika and dengue, who came to a hospital in Recife, Brazil, between December 2014 and June 2015. Six people developed neurological symptoms and two suffered attacks that swelled the brain and damaged its myelin, the fatty material that protects nerves there and at the spinal cord. The research was presented on Sunday at the annual conference for the American Academy of Neurology in Vancouver. Its abstract concluded that “there is strong evidence that this epidemic has different neurological manifestations” than those already documented. All the people arrived in the hospital with a fever, then a rash, and some suffered red eyes, itching and aching muscles and joints – the known symptoms of the Zika virus. The neurological symptoms sometimes began immediately, or as long as 15 days after patients first sought treatment. All six people tested positive for the Zika virus, and negative for dengue fever and chikungunya. After they left hospital, five reported problems with motor functioning; one reported trouble with vision and memory. “Though our study is small, it may provide evidence that in this case the virus has different effects on the brain than those identified in current studies,” said the study’s author, Dr Maria Lucia Brito Ferreira of the Restoration hospital in Recife, Brazil. Brito Ferreira repeated a common refrain of Zika research: the research is early and still inconclusive, and meant to add to the growing investigation to discover what the virus actually does. In all, her team documented 151 cases with neurological symptoms. “This doesn’t mean that all people infected with Zika will experience these brain problems,” Ferreira said. “Of those who have nervous system problems, most do not have brain symptoms. Advertisement“However, our study may shed light on possible lingering effects the virus may be associated with in the brain.” The brain swelling, called acute disseminated encephalomyelitis (ADEM), resembles multiple sclerosis in some symptoms but is not a permanent condition. ADEM usually consists of a single or occasional attack, from which most people can recover over several months. Four of the people followed for Ferreira’s research developed Guillain-Barré syndrome (GBS), a serious brain condition that enervates muscles, and can leave people temporarily paralyzed and breathing through ventilators. Like ADEM, the condition attacks myelin, and many people also recover from GBS after several months. Earlier this year, scientists published strong evidence that Zika is linked to GBS through a study on 42 cases in French Polynesia. Dr James Sejvar, a neurologist with the US Centers for Disease Control and Prevention, said that cases of ADEM do not appear to afflict people with Zika as often as cases of GBS. “But these findings from Brazil suggest that clinicians should be vigilant,” he said, for signs of ADEM and other central nervous system diseases. “Of course, the remaining question is ‘why,’” Sejvar said. “Why does Zika virus appear to have this strong association with GBS and potentially other immune-inflammatory diseases of the nervous system?” Experts at the World Health Organization also “implicated” Zika in a disorder called microcephaly, which causes babies to suffer brain damage and abnormally small heads. In February, a few days after experts warned that the virus could be a greater threat than Ebola, the organization declared a global public health emergency. Scientists have yet to confirm what conditions the virus actually causes, although research has raced to study the once rare pathogen, which emerged from a remote forest in Uganda. That the evidence is still inconclusive has many scientists cautioning the public and leaders not to fuel hysteria around it. http://www.theguardian.com/world/2016/apr/10/zika-virus-brain-disorders-brazil-study

Zika may be associated with other neurological diseaseBy: Robério SáMonday | 11.04.2016 at 09:23 error_outlinecommunicate error Estadão In addition to the microcephaly and Guillain-Barré syndrome, Zika virus may be associated with another neurological disease: acute disseminated encephalomyelitis (ADEM, in its English acronym), autoimmune syndrome that causes inflammation in the central nervous system. A study in Recife, which will be released on Friday at the annual meeting of the American Academy of Neurology, in Vancouver, Canada, found evidence of association between the virus and the ADEM in at least two cases. Scientists have suspected a connection between zika and ADEM, as shown by the newspaper O Estado de S. Paulo in February. But only now will present the scientific results of the study led by Maria Lucia Ferreira Brito, head of the Restoration Hospital Neurology Service in Recife. "Although it is a small study, it can provide evidence that the virus causes brain effects different from those that had been identified in the ongoing studies. But a lot of research still needs to be done to explore whether there is a causal relationship between zika and these brain problems, "said Maria Lucia. In the study, scientists followed between December 2014 and June 2015, all cases brought to the Restoration Hospital with symptoms of infection by arboviruses - the family of viruses that includes zika, dengue and chikungunya. All patients arrived at the hospital with fever and rash. Some also had itches, pains in muscles and joints, and red eyes. Some had neurological symptoms soon after and the other had about 15 days later. The authors recorded 151 cases with some type of neurological manifestation, but six of them developed typical neurological symptoms of autoimmune diseases - those in which the patient's immune system attacks and destroys healthy tissue cells of your own body. The six patients underwent blood tests and tests. Four had Guillain-Barré syndrome, as well as microcephaly, has been linked to infection zika. The other two were diagnosed with ADEM. The tests revealed that the six had been infected zika, but none of chikungunya or dengue. In patients with ADEM, according to experts, the defense cells of the body in the brain and spinal cord attack the myelin sheath a fat covering that surrounds nerve fibers and has function similar to the cover of a wire conductor of electricity. Guillain-Barré syndrome is also autoimmune and involves damage to the myelin sheath. damage In both reported cases, the brain scans showed that patients with ADEM had signs of damage in brain white matter. According to scientists, they are similar to the symptoms of a multiple sclerosis ADEM but in general causes a single attack which most patients recover in about six months. When discharged from hospital, five of the six patients continued with motor problems. One had vision problems and another had problems with memory and thinking ability. "This does not mean that all people infected with zika have this type of brain problem. Of those who had nervous system problems, most do not have cerebral symptoms. However, our study may help clarify possible lasting effects with which the virus can be associated in the brain, "said Maria Lucia. "Right now, it does not seem that cases of ADEM are occurring with an incidence as large as the cases of Guillain-Barré, but these findings in Brazil suggest that physicians should be vigilant about the possible occurrence of ADEM and other diseases autoimmune related to the central nervous system, "said James Sejvar, the Center for Disease Control and Prevention (CDC, its acronym in English) in Atlanta, USA. "The question is: why zika virus seems to have this strong association with Guillain-Barré syndrome and potentially other autoimmune and inflammatory diseases of the nervous system," questioned Sejvar. The information is the newspaper O Estado de S. Paulo. http://ancoradosertao.com.br/zika-pode-estar-associado-a-outra-doenca-neurologica/

Sequences producing significant alignments:Select:AllNone Selected:0 AlignmentsDownloadGenBankGraphicsDistance tree of resultsShow/hide columns of the table presenting sequences producing significant alignmentsSequences producing significant alignments:Select for downloading or viewing reportsDescriptionMax scoreTotal scoreQuery coverE valueIdentAccessionSelect seq gb|KU963796.1|Zika virus isolate SZ-WIV01 polyprotein gene, complete cds1852518525100%0.0100%KU963796.1Select seq gb|KU955589.1|Zika virus isolate Z16006 polyprotein gene, complete cds1852018520100%0.099%KU955589.1Select seq gb|KU820899.2|Zika virus isolate ZJ03, complete genome1852018520100%0.099%KU820899.2Select seq gb|KU866423.1|Zika virus isolate Zika virus/SZ01/2016 polyprotein gene, complete cds1839318393100%0.099%KU866423.1Select seq gb|KJ776791.1|Zika virus strain H/PF/2013 polyprotein gene, complete cds1839318393100%0.099%KJ776791.1Select seq gb|KU509998.2|Zika virus strain Haiti/1225/2014, complete genome1834818348100%0.099%KU509998.2Select seq gb|KU991811.1|Zika virus isolate Brazil/2016/INMI1 polyprotein gene, complete cds1832718327100%0.099%KU991811.1Select seq gb|KU321639.1|Zika virus strain ZikaSPH2015, complete genome1832718327100%0.099%KU321639.1Select seq gb|KU729218.1|Zika virus isolate BeH828305 polyprotein gene, complete cds1831818318100%0.099%KU729218.1Select seq gb|KU707826.1|Zika virus isolate SSABR1, complete genome1831818318100%0.099%KU707826.1Select seq gb|KU365779.1|Zika virus strain BeH819966 polyprotein gene, complete cds1831818318100%0.099%KU365779.1Select seq gb|KU926309.1|Zika virus isolate Rio-U1, complete genome1830318303100%0.099%KU926309.1Select seq gb|KU501217.1|Zika virus strain 8375 polyprotein gene, complete cds1830318303100%0.099%KU501217.1Select seq gb|KU365780.1|Zika virus strain BeH815744 polyprotein gene, complete cds1830318303100%0.099%KU365780.1Select seq gb|KU940228.1|Zika virus isolate Bahia07, partial genome1830018300100%0.099%KU940228.1Select seq gb|KU647676.1|Zika virus strain MRS_OPY_Martinique_PaRi_2015 polyprotein gene, complete cds1830018300100%0.099%KU647676.1Select seq gb|KU501216.1|Zika virus strain 103344 polyprotein gene, complete cds1830018300100%0.099%KU501216.1Select seq gb|KU365777.1|Zika virus strain BeH818995 polyprotein gene, complete cds1830018300100%0.099%KU365777.1Select seq gb|KU729217.2|Zika virus isolate BeH823339 polyprotein gene, complete cds1829118291100%0.099%KU729217.2Select seq gb|KU497555.1|Zika virus isolate Brazil-ZKV2015, complete genome182911829199%0.099%KU497555.1Select seq gb|KU527068.1|Zika virus strain Natal RGN, complete genome1829118291100%0.099%KU527068.1Select seq gb|KU820897.1|Zika virus isolate FLR polyprotein gene, complete cds1828518285100%0.099%KU820897.1Select seq gb|KU365778.1|Zika virus strain BeH819015 polyprotein gene, complete cds1828518285100%0.099%KU365778.1Select seq gb|KU312312.1|Zika virus isolate Z1106033 polyprotein gene, complete cds1828518285100%0.099%KU312312.1Select seq gb|KU922960.1|Zika virus isolate MEX/InDRE/Sm/2016, complete genome1828218282100%0.099%KU922960.1Select seq gb|KU926310.1|Zika virus isolate Rio-S1, complete genome1827618276100%0.099%KU926310.1Select seq gb|KU922923.1|Zika virus isolate MEX/InDRE/Lm/2016, complete genome1827618276100%0.099%KU922923.1Select seq gb|KU501215.1|Zika virus strain PRVABC59, complete genome1827618276100%0.099%KU501215.1Select seq gb|KU870645.1|Zika virus isolate FB-GWUH-2016, complete genome1827318273100%0.099%KU870645.1Select seq gb|KU853013.1|Zika virus isolate Dominican Republic/2016/PD2, complete genome1826718267100%0.099%KU853013.1Select seq gb|KU853012.1|Zika virus isolate Dominican Republic/2016/PD1, complete genome1826718267100%0.099%KU853012.1Select seq gb|KU820898.1|Zika virus isolate GZ01 polyprotein gene, complete cds1825818258100%0.099%KU820898.1Select seq gb|KU740184.2|Zika virus isolate GD01 polyprotein gene, complete cds1825818258100%0.099%KU740184.2Select seq gb|KU761564.1|Zika virus isolate GDZ16001 polyprotein gene, complete cds1825818258100%0.099%KU761564.1Select seq gb|KU955590.1|Zika virus isolate Z16019 polyprotein gene, complete cds1825418254100%0.099%KU955590.1Select seq gb|KU940224.1|Zika virus isolate Bahia09, partial genome182041820499%0.099%KU940224.1Select seq gb|KU744693.1|Zika virus isolate VE_Ganxian, complete genome1811018110100%0.099%KU744693.1Select seq gb|KU681081.3|Zika virus isolate Zika virus/H.sapiens-tc/THA/2014/SV0127- 14, complete genome1805618056100%0.099%KU681081.3Select seq gb|KU955593.1|Zika virus isolate Zika virus/H.sapiens-tc/KHM/2010/FSS13025, complete genome1775917759100%0.098%KU955593.1Select seq gb|JN860885.1|Zika virus isolate FSS13025 polyprotein gene, partial cds177571775799%0.098%JN860885.1Select seq gb|KF993678.1|Zika virus strain PLCal_ZV from Canada polyprotein gene, partial cds176941769498%0.099%KF993678.1Select seq gb|EU545988.1|Zika virus polyprotein gene, complete cds1761217612100%0.098%EU545988.1Select seq gb|KU681082.3|Zika virus isolate Zika virus/H.sapiens-tc/PHL/2012/CPC-0740, complete genome1744717447100%0.098%KU681082.3Select seq gb|HQ234499.1|Zika virus isolate P6-740 polyprotein gene, partial cds164381643899%0.096%HQ234499.1Select seq gb|KU720415.1|Zika virus strain MR 766 polyprotein gene, complete cds1328113281100%0.089%KU720415.1Select seq gb|KF383115.1|Zika virus strain ArB1362 polyprotein gene, complete cds1327513275100%0.089%KF383115.1Select seq gb|HQ234498.1|Zika virus isolate MR_766 polyprotein gene, partial cds132751327599%0.089%HQ234498.1Select seq gb|KF268949.1|Zika virus isolate ARB15076 polyprotein gene, complete cds1327013270100%0.089%KF268949.1Select seq gb|DQ859059.1|Zika virus strain MR 766 polyprotein gene, complete cds1327013270100%0.089%DQ859059.1Select seq gb|KU955595.1|Zika virus isolate Zika virus/A.taylori-tc/SEN/1984/41671-DAK, complete genome1326813268100%0.089%KU955595.1Select seq gb|KF383119.1|Zika virus strain ArD158084 polyprotein gene, complete cds1326313263100%0.089%KF383119.1Select seq gb|KU955592.1|Zika virus isolate Zika virus/A.taylori-tc/SEN/1984/41662-DAK, complete genome1325913259100%0.089%KU955592.1Select seq dbj|LC002520.1|Zika virus genomic RNA, complete genome, strain: MR766-NIID1325913259100%0.089%LC002520.1Select seq gb|KF268948.1|Zika virus isolate ARB13565 polyprotein gene, complete cds1325213252100%0.089%KF268948.1Select seq gb|KF268950.1|Zika virus isolate ARB7701 polyprotein gene, complete cds1324513245100%0.089%KF268950.1Select seq gb|KU963573.1|Zika virus isolate ZIKV/Macaca mulatta/UGA/MR-766_SM150-V8/1947 polyprotein (GP1) gene, complete cds1324313243100%0.089%KU963573.1Select seq gb|KU955594.1|Zika virus isolate Zika virus/M.mulatta-tc/UGA/1947/MR-766, complete genome1324313243100%0.089%KU955594.1Select seq gb|KU955591.1|Zika virus isolate Zika virus/A.africanus-tc/SEN/1984/41525-DAK, complete genome1324113241100%0.089%KU955591.1Select seq gb|HQ234501.1|Zika virus isolate ArD_41519 polyprotein gene, partial cds132181321899%0.089%HQ234501.1Select seq gb|KF383116.1|Zika virus strain ArD7117 polyprotein gene, complete cds1321613216100%0.089%KF383116.1Select seq gb|AY632535.2|Zika virus strain MR 766, complete genome1320013200100%0.089%AY632535.2Select seq gb|KF383117.1|Zika virus strain ArD128000 polyprotein gene, complete cds1314613146100%0.088%KF383117.1Select seq gb|KU963574.1|Zika virus isolate ZIKV/Homo sapiens/NGA/IbH-30656_SM21V1-V3/1968 polyprotein (GP1) gene, complete cds1312613228100%0.088%KU963574.1Select seq gb|HQ234500.1|Zika virus isolate IbH_30656 polyprotein gene, partial cds131261312699%0.088%HQ234500.1Select seq gb|KF383118.1|Zika virus strain ArD157995 polyprotein gene, complete cds1294513013100%0.088%KF383118.1Select seq gb|KF383121.1|Zika virus strain ArD158095 polyprotein gene, partial cds128611286197%0.089%KF383121.1Select seq gb|KF383120.1|Zika virus strain ArD142623 nonfunctional polyprotein gene, partial sequence108621086297%0.084%KF383120.1Select seq gb|KU940227.1|Zika virus isolate Bahia08, partial genome50341439987%0.095%KU940227.1Select seq gb|KU312314.1|Zika virus isolate Z1106031 polyprotein gene, partial cds4962496227%0.099%KU312314.1Select seq gb|KU312313.1|Zika virus isolate Z1106032 polyprotein gene, partial cds4935493527%0.099%KU312313.1Select seq gb|KU646828.1|Zika virus isolate Si322 polyprotein gene, partial cds4637463725%0.099%KU646828.1Select seq gb|KU646827.1|Zika virus isolate Si323 polyprotein gene, partial cds4628462825%0.099%KU646827.1Select seq gb|KU312315.1|Zika virus isolate Z1106027 polyprotein gene, partial cds3431343118%0.099%KU312315.1Select seq gb|KU740199.1|Zika virus isolate VE_Ganxian2016 polyprotein gene, partial cds3202320217%0.099%KU740199.1Select seq gb|DQ859064.1|Spondweni virus strain SM-6 V-1 polyprotein gene, complete cds2850419195%0.071%DQ859064.1Select seq gb|KJ634273.1|Zika virus strain CK-ISL 2014 E protein (E) gene, partial cds2695269514%0.099%KJ634273.1Select seq gb|KU686218.1|Zika virus isolate MEX/InDRE/14/2015 polyprotein gene, partial cds2042204211%0.099%KU686218.1Select seq gb|KU179098.1|Zika virus isolate JMB-185 nonstructural protein 5 gene, partial cds2008200811%0.099%KU179098.1Select seq gb|KM078936.1|Zika virus strain CHI1410214 NS5 protein gene, partial cds173717379%0.099%KM078936.1Select seq gb|KM078961.1|Zika virus strain CHI2612114 NS5 protein gene, partial cds173617369%0.099%KM078961.1Select seq gb|KM078930.1|Zika virus strain CHI2283714 NS5 protein gene, partial cds173417349%0.099%KM078930.1Select seq gb|KM078971.1|Zika virus strain CHI2613014 NS5 protein gene, partial cds173017309%0.099%KM078971.1Select seq gb|KM078970.1|Zika virus strain CHI2490414 NS5 protein gene, partial cds173017309%0.099%KM078970.1Select seq gb|KM078933.1|Zika virus strain CHI1058514 NS5 protein gene, partial cds173017309%0.099%KM078933.1Select seq gb|KM078929.1|Zika virus strain CHI1805214 NS5 protein gene, partial cds172817289%0.099%KM078929.1Select seq gb|KJ873160.1|Zika virus isolate NC14-03042014-3481 nonstructural protein 5 gene, partial cds158815888%0.099%KJ873160.1Select seq gb|KJ873161.1|Zika virus isolate NC14-02042014-3220 nonstructural protein 5 gene, partial cds140614067%0.099%KJ873161.1Select seq gb|KM851039.1|Zika virus strain SV0127/14 nonstructural protein 5 gene, partial cds137013707%0.098%KM851039.1Select seq gb|KM851038.1|Zika virus strain CPC-0740 nonstructural protein 5 gene, partial cds133313337%0.097%KM851038.1Select seq gb|KU985087.1|Zika virus isolate MEX/InDRE/Zika-2/2015 nonstructural protein 5 gene, partial cds133013307%0.099%KU985087.1Select seq gb|KU556802.1|Zika virus isolate MEX/InDRE/14/2015 NS5 protein gene, partial cds132413247%0.099%KU556802.1Select seq gb|AF013415.1|Zika virus strain MR-766 NS5 protein (NS5) gene, partial cds1283128310%0.088%AF013415.1Select seq gb|KT200609.1|Zika virus isolate BR/949/15 NS5 gene, partial cds123612366%0.099%KT200609.1Select seq gb|KU232300.1|Zika virus isolate 067ZV_PEBR15 NS5 protein gene, partial cds121612166%0.099%KU232300.1Select seq gb|KU232290.1|Zika virus isolate 036ZV_PEBR15 NS5 protein gene, partial cds120712076%0.099%KU232290.1Select seq gb|KU232297.1|Zika virus isolate 049ZV_PEBR15 NS5 protein gene, partial cds120512056%0.099%KU232297.1Select seq gb|KU232294.1|Zika virus isolate 061ZV_PEBR15 NS5 protein gene, partial cds119811986%0.099%KU232294.1Select seq gb|KU232292.1|Zika virus isolate 054ZV_PEBR15 NS5 protein gene, partial cds119511956%0.099%KU232292.1Select seq gb|KU232298.1|Zika virus isolate 050ZV_PEBR15 NS5 protein gene, partial cds119111916%0.099%KU232298.1Select seq gb|KU232293.1|Zika virus isolate 057ZV_PEBR15 NS5 protein gene, partial cds118911896%0.099%KU232293.1Select seq gb|KU232296.1|Zika virus isolate 045ZV_PEBR15 NS5 protein gene, partial cds118711876%0.099%KU232296.1Select seq gb|KU232295.1|Zika virus isolate 068ZV_PEBR15 NS5 protein gene, partial cds118411846%0.099%KU232295.1Select seq gb|KU232288.1|Zika virus isolate 001ZV_PEBR15 NS5 protein gene, partial cds117311736%0.099%KU232288.1Select seq gb|KU232289.1|Zika virus isolate 020ZV_PEBR15 NS5 protein gene, partial cds116911696%0.099%KU232289.1Select seq gb|KU232299.1|Zika virus isolate 015ZV_PEBR15 NS5 protein gene, partial cds116611666%0.099%KU232299.1Select seq gb|KU232291.1|Zika virus isolate 051ZV_PEBR15 NS5 protein gene, partial cds116211626%0.099%KU232291.1Select seq gb|KU758878.1|Zika virus polyprotein gene, partial cds113011306%0.098%KU758878.1Select seq gb|KF270886.1|Zika virus strain CCB-870 envelope glycoprotein gene, partial cds108110818%0.089%KF270886.1Select seq gb|AF372422.1|AF372422Zika virus envelope protein (E) gene, partial cds102310238%0.087%AF372422.1Select seq gb|KU867812.1|Zika virus isolate Jiangxi.CHN/01/2016 nonstructural protein 5 gene, partial cds100010005%0.099%KU867812.1Select seq gb|KF270887.1|Zika virus strain CCB-870 NS3 protein gene, partial cds9919917%0.088%KF270887.1Select seq gb|KF383022.1|Zika virus strain ArD127988 envelope protein gene, partial cds9849847%0.089%KF383022.1Select seq gb|KF383026.1|Zika virus strain ArD127994 envelope protein gene, partial cds9809807%0.089%KF383026.1Select seq gb|KF383032.1|Zika virus strain ArD30101 envelope protein gene, partial cds9719717%0.089%KF383032.1Select seq gb|EU303241.1|Zika virus note MR766 (p4 15/9/76) nonstructural protein 5 (NS5) gene, partial cds9679677%0.088%EU303241.1Select seq gb|EF158064.1|St. Louis encephalitis virus strain GML 902612 polyprotein gene, partial cds967197965%0.070%EF158064.1Select seq gb|KF383037.1|Zika virus strain ArA506 envelope protein gene, partial cds9669667%0.089%KF383037.1Select seq gb|KF383034.1|Zika virus strain ArD30156 envelope protein gene, partial cds9669667%0.088%KF383034.1Select seq gb|KF383029.1|Zika virus strain ArD165522 envelope protein gene, partial cds9669667%0.088%KF383029.1Select seq gb|KF383033.1|Zika virus strain AnD30332 envelope protein gene, partial cds9629627%0.088%KF383033.1Select seq gb|KF383036.1|Zika virus strain ArA975 envelope protein gene, partial cds9609607%0.088%KF383036.1Select seq gb|KF383028.1|Zika virus strain ArD165531 envelope protein gene, partial cds9449447%0.088%KF383028.1Select seq gb|KF383039.1|Zika virus strain HD78788 envelope protein gene, partial cds9429427%0.088%KF383039.1Select seq gb|KF383031.1|Zika virus strain ArD9957 envelope protein gene, partial cds9399397%0.088%KF383031.1Select seq gb|KF383038.1|Zika virus strain ArA986 envelope protein gene, partial cds9339337%0.088%KF383038.1Select seq gb|KF383046.1|Zika virus strain ArA982 envelope protein gene, partial cds9249247%0.087%KF383046.1Select seq gb|KT823415.1|St. Louis encephalitis virus strain RT 121B polyprotein gene, complete cds919191265%0.069%KT823415.1Select seq gb|FJ753286.2|St. Louis encephalitis virus strain CbaAr-4005, complete genome919193865%0.069%FJ753286.2Select seq gb|KF383045.1|Zika virus strain ArA27106 envelope protein gene, partial cds9119117%0.087%KF383045.1Select seq gb|EU566860.1|St. Louis encephalitis virus strain Hubbard, complete genome910200257%0.069%EU566860.1Select seq gb|KF383043.1|Zika virus strain ArA27443 envelope protein gene, partial cds9069067%0.087%KF383043.1Select seq gb|KF383035.1|Zika virus strain MR1429 envelope protein gene, partial cds9069067%0.086%KF383035.1Select seq gb|KF383041.1|Zika virus strain ArA27290 envelope protein gene, partial cds9029027%0.087%KF383041.1Select seq gb|EF158069.1|St. Louis encephalitis virus strain 72 V 4749 polyprotein gene, partial cds899198467%0.069%EF158069.1Select seq gb|KF383042.1|Zika virus strain ArA27096 envelope protein gene, partial cds8978977%0.087%KF383042.1Select seq gb|FJ753287.2|St. Louis encephalitis virus strain 79V-2533, complete genome886183463%0.069%FJ753287.2Select seq gb|AY632542.4|Rocio virus strain SPH 34675, complete genome883150266%0.069%AY632542.4Select seq gb|KF383103.1|Zika virus strain ArA986 nonstructural protein 5 gene, partial cds8748746%0.087%KF383103.1Select seq gb|KF383086.1|Zika virus strain ArA975 nonstructural protein 5 gene, partial cds8748746%0.087%KF383086.1Select seq gb|KF383040.1|Zika virus strain ArA27101 envelope protein gene, partial cds8728727%0.086%KF383040.1Select seq gb|KF383106.1|Zika virus strain ArA27443 nonstructural protein 5 gene, partial cds8478476%0.087%KF383106.1Select seq gb|KF383107.1|Zika virus strain ArA27407 nonstructural protein 5 gene, partial cds8438436%0.086%KF383107.1Select seq gb|KF383104.1|Zika virus strain ArA982 nonstructural protein 5 gene, partial cds8438436%0.086%KF383104.1Select seq gb|KF383085.1|Zika virus strain ArD9957 nonstructural protein 5 gene, partial cds8438436%0.086%KF383085.1Select seq gb|KF383114.1|Zika virus strain AnD30332 nonstructural protein 5 gene, partial cds8348346%0.086%KF383114.1Select seq gb|KF383088.1|Zika virus strain ArD30101 nonstructural protein 5 gene, partial cds8348346%0.086%KF383088.1Select seq gb|KF383087.1|Zika virus strain ArD30156 nonstructural protein 5 gene, partial cds8298296%0.086%KF383087.1Select seq dbj|AB908162.1|Zika virus gene for polyprotein, partial cds, strain: ZIKV Hu/Tahiti/01u/2014NIID8298294%0.099%AB908162.1Select seq gb|KF383089.1|Zika virus strain ArD165531 nonstructural protein 5 gene, partial cds8258256%0.086%KF383089.1Select seq gb|KU872850.1|Zika virus isolate Dominican Rep-Rus-2016, NS2 partial cds8208204%0.099%KU872850.1Select seq gb|KF383101.1|Zika virus strain ArD127710 nonstructural protein 5 gene, partial cds8208206%0.086%KF383101.1Select seq gb|KF383097.1|Zika virus strain ArD127994 nonstructural protein 5 gene, partial cds8208206%0.086%KF383097.1Select seq gb|KC754955.1|Usutu virus isolate HB81P08, complete genome820163059%0.068%KC754955.1Select seq gb|KC754954.1|Usutu virus isolate ArD19848, complete genome820161457%0.068%KC754954.1Select seq gb|KF383099.1|Zika virus strain ArD127987 nonstructural protein 5 gene, partial cds8168166%0.086%KF383099.1Select seq gb|KF383098.1|Zika virus strain ArD127988 nonstructural protein 5 gene, partial cds8108106%0.085%KF383098.1Select seq gb|KC754958.1|Usutu virus isolate ArB1803, complete genome791187654%0.068%KC754958.1Select seq gb|HM147824.1|West Nile virus from Democratic Republic of the Congo, complete genome776170153%0.068%HM147824.1Select seq gb|KF383084.1|Zika virus strain HD78788 nonstructural protein 5 gene, partial cds7747746%0.084%KF383084.1Select seq gb|KF383113.1|Zika virus strain ArA1465 nonstructural protein 5 gene, partial cds7717716%0.084%KF383113.1Select seq gb|DQ176636.2|West Nile virus strain Madagascar-AnMg798, complete genome760153450%0.068%DQ176636.2Select seq gb|EF429199.1|West Nile virus SA381/00, complete genome756161557%0.068%EF429199.1Select seq gb|KM203863.1|West Nile virus strain Cz 13-502, complete genome735166655%0.067%KM203863.1Select seq gb|KM203860.1|West Nile virus strain Cz 13-104, complete genome720163755%0.067%KM203860.1Select seq gb|KF383017.1|Zika virus strain ArD149938 envelope protein gene, partial cds7137137%0.081%KF383017.1Select seq gb|KF383016.1|Zika virus strain ArD147917 envelope protein gene, partial cds7087087%0.081%KF383016.1Select seq gb|KF383015.1|Zika virus strain ArD149810 envelope protein gene, partial cds7087087%0.081%KF383015.1Select seq gb|KF383021.1|Zika virus strain ArD132912 envelope protein gene, partial cds7027027%0.081%KF383021.1Select seq gb|KF383020.1|Zika virus strain ArA1465 envelope protein gene, partial cds7027027%0.081%KF383020.1Select seq gb|KF258813.1|Zika virus isolate Java non-structural protein 5 mRNA, partial cds6996993%0.099%KF258813.1Select seq gb|KF383019.1|Zika virus strain ArD132915 envelope protein gene, partial cds6866867%0.080%KF383019.1Select seq gb|JF262780.1|Dengue virus 4 isolate P73-1120, complete genome666174150%0.069%JF262780.1Select seq gb|JF262779.1|Dengue virus 4 isolate P75-514, complete genome666174150%0.069%JF262779.1Select seq gb|EF457906.1|Dengue virus type 4 isolate P75-215, complete genome663172150%0.069%EF457906.1Select seq gb|KF383092.1|Zika virus strain ArD147917 nonstructural protein 5 gene, partial cds6596596%0.081%KF383092.1Select seq gb|KF383093.1|Zika virus strain ArD149810 nonstructural protein 5 gene, partial cds6576576%0.081%KF383093.1Select seq gb|KF383095.1|Zika virus strain ArD132915 nonstructural protein 5 gene, partial cds6546546%0.080%KF383095.1Select seq gb|KU985088.1|Zika virus isolate MEX/InDRE/Zika-2/2015 envelope protein gene, partial cds6506503%0.0100%KU985088.1Select seq gb|KF383091.1|Zika virus strain ArD149938 nonstructural protein 5 gene, partial cds6486486%0.080%KF383091.1Select seq gb|FJ410250.1|Dengue virus 1 isolate DENV-1/VN/BID-V1917/2007, complete genome621157546%9e-17369%FJ410250.1Select seq gb|FJ410211.1|Dengue virus 1 isolate DENV-1/VN/BID-V1830/2007, complete genome621158144%9e-17369%FJ410211.1Select seq gb|FJ410204.1|Dengue virus 1 isolate DENV-1/VN/BID-V1809/2007, complete genome621157744%9e-17369%FJ410204.1Select seq gb|FJ410203.1|Dengue virus 1 isolate DENV-1/VN/BID-V1808/2007, complete genome621157744%9e-17369%FJ410203.1Select seq gb|JQ686088.2|Dengue virus 2 strain JHA1, partial genome618147760%1e-17169%JQ686088.2Select seq gb|JQ048541.1|Dengue virus 1 isolate DG14, complete genome612159748%4e-17069%JQ048541.1Select seq gb|KP406804.1|Dengue virus 2 isolate DENV-2/KBPV-VR-29, complete genome610145960%2e-16969%KP406804.1Select seq emb|FM210240.2|Dengue virus 2 isolate MD1273, complete genome594139659%1e-16469%FM210240.2Select seq gb|DQ181799.1|Dengue virus type 2 strain ThD2_0017_98, complete genome592162249%4e-16469%DQ181799.1Select seq gb|KR815989.1|Zika virus isolate 15095 envelope protein gene, partial cds5875873%2e-16299%KR815989.1Select seq gb|AF100462.1|AF100462Dengue virus type 2 strain C0390 polyprotein gene, complete cds587159052%2e-16269%AF100462.1Select seq gb|KJ918750.1|Dengue virus 2 isolate P23085 INDI-60, complete genome585163847%6e-16269%KJ918750.1Select seq gb|AY744150.1|Dengue virus type 2 vector p4(delta30)-4995, complete sequence581168549%8e-16169%AY744150.1Select seq gb|AY744149.1|Dengue virus type 2 vector p2(delta30), complete sequence581169049%8e-16169%AY744149.1Select seq gb|AY744148.1|Dengue virus type 2 vector p2, complete sequence581169049%8e-16169%AY744148.1Select seq gb|EU056812.1|Dengue virus type 2 isolate 1328, complete genome580160043%3e-16068%EU056812.1Select seq gb|FJ639711.1|Dengue virus 2 isolate DENV-2/KH/BID-V2045/2005, complete genome578138458%9e-16068%FJ639711.1Select seq gb|FJ639710.1|Dengue virus 2 isolate DENV-2/KH/BID-V2044/2005, complete genome578138458%9e-16068%FJ639710.1Select seq gb|GU131894.1|Dengue virus 1 isolate DENV-1/IPC/BID-V3786/2008, complete genome576143042%3e-15968%GU131894.1Select seq gb|GQ868633.1|Dengue virus 1 isolate DENV-1/IPC/BID-V3793/2008, complete genome576143542%3e-15968%GQ868633.1Select seq gb|AY744147.1|Dengue virus type 2, complete genome576168549%3e-15969%AY744147.1Select seq gb|GU131887.1|Dengue virus 1 isolate DENV-1/IPC/BID-V3775/2006, complete genome567153542%2e-15668%GU131887.1Select seq gb|HM582108.1|Dengue virus 2 strain D2/PF/UH50/1972, complete genome565159745%6e-15668%HM582108.1Select seq gb|HM582100.1|Dengue virus 2 strain D2/FJ/UH40/1971, complete genome565160645%6e-15668%HM582100.1Select seq gb|EU529701.1|Dengue virus 2 isolate DENV-2/US/BID-V1087/1991, complete genome563163648%2e-15568%EU529701.1Select seq gb|JN819408.1|Dengue virus 2 isolate DENV-2/VE/BID-V2161/2001, complete genome562155748%7e-15568%JN819408.1Select seq gb|HM582117.1|Dengue virus 2 strain D2/TO/UH04/1974, complete genome560165449%2e-15468%HM582117.1Select seq gb|HM582109.1|Dengue virus 2 strain D2/PF/UH57/1971, complete genome558159042%9e-15468%HM582109.1Select seq gb|HM582101.1|Dengue virus 2 strain D2/FJ/UH22/1971, complete genome558159345%9e-15468%HM582101.1Select seq gb|KF955369.1|Dengue virus 2 isolate DENV-2/NI/BID-V1226/2007, complete genome556158952%3e-15368%KF955369.1Select seq gb|KF955368.1|Dengue virus 2 isolate DENV-2/NI/BID-V1222/2007, partial genome556126842%3e-15368%KF955368.1Select seq gb|HM582116.1|Dengue virus 2 strain D2/TO/UH94/1974, complete genome556164749%3e-15368%HM582116.1Select seq gb|EU482580.1|Dengue virus 2 isolate DENV-2/US/BID-V1177/1989, complete genome554161848%1e-15268%EU482580.1Select seq gb|FJ898466.1|Dengue virus 2 isolate DENV-2/VE/BID-V2942/2000, complete genome553155248%4e-15268%FJ898466.1Select seq gb|FJ850050.1|Dengue virus 2 isolate DENV-2/NI/BID-V2356/2007, complete genome553157651%4e-15268%FJ850050.1Select seq gb|EU569702.1|Dengue virus 2 isolate DENV-2/NI/BID-V1228/2007, complete genome553159152%4e-15268%EU569702.1Select seq gb|JN819407.1|Dengue virus 2 isolate DENV-2/VE/BID-V2613/2007, complete genome547157346%2e-15068%JN819407.1Select seq gb|EU596483.1|Dengue virus 2 isolate DENV-2/NI/BID-V608/2006, complete genome547160052%2e-15068%EU596483.1Select seq gb|EU482687.1|Dengue virus 2 isolate DENV-2/NI/BID-V574/2006, complete genome547159150%2e-15068%EU482687.1Select seq gb|KR816334.1|Zika virus isolate BR/UFBA/LabViro/Ex1 envelope protein gene, partial cds5455452%5e-15099%KR816334.1Select seq gb|KR816333.1|Zika virus isolate BR/UFBA/LabViro/23 envelope protein gene, partial cds5445442%2e-14999%KR816333.1Select seq gb|KR816335.1|Zika virus isolate BR/UFBA/LabViro/18 envelope protein gene, partial cds5405402%2e-14899%KR816335.1Select seq gb|KM212965.1|Zika virus isolate NC13(FP)-20112013-22015 glycoprotein gene, partial cds5355352%1e-146100%KM212965.1Select seq gb|KM212966.1|Zika virus isolate NC13(FP)-26112013-22072 glycoprotein gene, partial cds5295292%4e-14599%KM212966.1Select seq gb|KM212964.1|Zika virus isolate NC14-17042014-4554 glycoprotein gene, partial cds5265262%5e-14499%KM212964.1Select seq gb|KM212963.1|Zika virus isolate NC14-23012014-250 glycoprotein gene, partial cds5265262%5e-14499%KM212963.1Select seq gb|JQ922552.1|Dengue virus 2 isolate DENV-2/IND/P23085/1960, complete genome526160346%5e-14468%JQ922552.1Select seq gb|KJ680134.1|Zika virus strain PF13-091213-121 polyprotein gene, partial cds5085082%1e-138100%KJ680134.1Select seq gb|KU844090.1|Zika virus isolate Moscow-2016 polyprotein gene, partial cds5025022%6e-13799%KU844090.1Select seq gb|KJ579441.1|Zika virus isolate PF13-CP221013c polyprotein gene, partial cds5025022%6e-13799%KJ579441.1Select seq gb|KF955392.1|Dengue virus 2 isolate DENV-2/NI/BID-V3001/2007, partial genome45282828%9e-12267%KF955392.1Select seq gb|KF955343.1|Dengue virus 2 isolate DENV-2/NI/BID-V1724/2007, partial genome45258922%9e-12267%KF955343.1Select seq gb|KF955341.1|Dengue virus 2 isolate DENV-2/NI/BID-V1231/2007, partial genome45264325%9e-12267%KF955341.1Select seq gb|KU954085.1|Zika virus isolate ZIKCOLSC67 polyprotein gene, partial cds4214212%2e-11299%KU954085.1Select seq gb|JQ922553.1|Dengue virus 2 isolate DENV-2/IND/803347/1980, complete genome421142744%2e-11267%JQ922553.1Select seq gb|KF383083.1|Zika virus strain AnD30332 3' UTR4164162%7e-11193%KF383083.1Select seq gb|KF383052.1|Zika virus strain ArD165531 3' UTR4164162%7e-11193%KF383052.1Select seq gb|KF383049.1|Zika virus strain ArD7117 3' UTR4164162%7e-11193%KF383049.1Select seq gb|KU926326.1|Zika virus isolate Zika 2235 Israel ex Colombia 2015 polyprotein gene, partial cds4124122%8e-11099%KU926326.1Select seq gb|KU926325.1|Zika virus isolate Zika 356 Israel ex Mexico 2016 polyprotein gene, partial cds4124122%8e-11099%KU926325.1Select seq gb|KU926324.1|Zika virus isolate Zika 352 Israel ex Vietnam 2016 polyprotein gene, partial cds4124122%8e-11099%KU926324.1Select seq gb|KU926323.1|Zika virus isolate Zika 269 Israel ex Colombia 2016 polyprotein gene, partial cds4124122%8e-11099%KU926323.1Select seq gb|KT381874.1|Zika virus strain Zika1697_BR-RJ/2015 envelope protein gene, partial cds4124122%8e-11098%KT381874.1Select seq gb|KM212961.1|Zika virus isolate NC14-17042014-4554 polyprotein gene, partial cds4084082%1e-108100%KM212961.1