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Dallas County Health and Human Services (DCHHS) is reporting the 31st case of Zika virus in Dallas County in 2016. This case was confirmed through testing in the DCHHS lab. DCHHS has submitted the case for review to the Texas Department of State Health Services. The 51 year-old resident of Dallas was infected with the virus during recent travel to Mexico.

References Rasmussen SA, Jamieson DJ, Honein MA, Petersen LR. Zika virus and birth defects—reviewing the evidence for causality. N Engl J Med 2016;374:1981–7. CrossRef PubMed Schuler-Faccini L, Ribeiro EM, Feitosa IML, et al. . Possible association between Zika virus infection and microcephaly—Brazil, 2015. MMWR Morb Mortal Wkly Rep 2016;65:59–62. CrossRef PubMed Aragao MFV, Van der Linden V, Brainer-Lima AM, et al. Clinical features and neuroimaging (CT and MRI) findings in presumed Zika virus related congenital infection and microcephaly: retrospective case series study. BMJ 2016;353:i1901. http://www.bmj.com/content/353/bmj.i1901CrossRef PubMed Microcephaly Epidemic Research Group1. Microcephaly in infants, Pernambuco State, Brazil, 2015. Emerg Infect Dis 2016;22:1090–3. CrossRefPubMed Ventura CV, Maia M, Bravo-Filho V, Góis AL, Belfort R . Zika virus in Brazil and macular atrophy in a child with microcephaly. Lancet 2016;387:228.http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(16)00006-4/abstract CrossRef PubMed Goderis J, De Leenheer E, Smets K, Van Hoecke H, Keymeulen A, Dhooge I. Hearing loss and congenital CMV infection: a systematic review. Pediatrics 2014;134:972–82. http://pediatrics.aappublications.org/content/134/5/972 CrossRef PubMed Cohen BE, Durstenfeld A, Roehm PC. Viral causes of hearing loss: a review for hearing health professionals. Trends Hear 2014;18. pii: 2331216514541361. Brazilian Ministry of Health. Protocol for monitoring and response to microcephaly occurrence relating to ZikaV infection [Portuguese].http://www.combateaedes.saude.gov.br/images/sala-de-situacao/Microcefalia-Protocolo-de-vigilancia-e-resposta-10mar2016-18h.pdf Cordeiro MT, Pena LJ, Brito CA, Gil LH, Marques ET. Positive IgM for Zika virus in the cerebrospinal fluid of 30 neonates with microcephaly in Brazil. Lancet 2016;387:1811–2. CrossRef PubMed American Academy of Pediatrics, Joint Committee on Infant Hearing. Year 2007 position statement: Principles and guidelines for early hearing detection and intervention programs. Pediatrics 2007;120:898–921. CrossRef PubMed

TABLE. Number of infants with microcephaly and laboratory evidence of congenital Zika virus infection (N = 70), by hearing test status, and selected characteristics — Brazil, November 2015–May 2016 Characteristic (number with information available) No hearing loss or conductive hearing loss (n = 65) No. (%) Sensorineural hearing loss (n = 5) No. (%) Gestational age at birth (n = 59) (n = 5) 37–41 weeks (term) 50 (85) 5 (100) <37 weeks (preterm) 8 (14) 0 (—) ≥42 weeks (postterm) 1 (2) 0 (—) Self-reported rash during pregnancy (n = 58) (n = 5) Yes 49 (84) 5 (100) No 9 (16) 0 (—) Timing of rash during pregnancy (n = 49) (n = 5) First trimester 37 (76) 4 (80) Second trimester 10 (20) 1 (20) Third trimester 2 (4) 0 (—) Infant sex (n = 65) (n = 5) Male 36 (55) 3 (60) Female 29 (45) 2 (40) Degree of microcephaly (n = 60) (n = 5) Severe (>3 SD below mean for gestational age) 39 (65) 4 (100) Other (≤3 SD below mean for gestational age) 21 (35) 0 (—) Age at testing (days) (n = 70) (n = 5) Mean 114 105 Median 98 60 SD 59 57 Range 16–315 36–171 Abbreviation: SD = standard deviation.

Discussion In this report of complete auditory function evaluation in a series of 70 children with microcephaly and laboratory evidence of congenital Zika virus infection, five (7.1%) infants had sensorineural hearing loss. The hearing loss varied in severity and laterality, which has been reported in hearing loss associated with other congenital infections (6,7). If the one infant with bilateral profound sensorineural hearing loss who had been treated with amikacin (a known ototoxic antibiotic) before the hearing testing is excluded, the proportion of infants with sensorineural hearing loss was 5.8% (four of 69). This proportion, although lower than the 9% reported from a small sample of newborns with microcephaly associated with presumed Zika-virus infection tested by otoacoustic emissions (4), is within the range (6%–65%) reported for other congenital viral infections (6,7). In the majority of cases of hearing loss associated with congenital viral infection, the damage to the auditory system is within the cochlea (7). It is likely that similar lesions account for the hearing deficit in children with congenital Zika virus infection, although histologic studies are needed to confirm this. However, a concomitant central origin cannot be discounted, and behavioral auditory evaluation might provide additional information. The findings in this report are subject to at least two limitations. First, auditory behavioral tests, in which an infant’s responses (e.g., quieting, eye-widening, or startle) to various calibrated sounds are recorded, and which can complement the hearing evaluation and provide information about processing of auditory signals, were not used. Second, this series includes only children with microcephaly. It is possible that the full spectrum of congenital Zika virus infection includes children without microcephaly, but with auditory deficits, as occurs in congenital rubella and CMV infections, in which children born with no apparent structural anomaly can be found to have hearing loss at birth or later in life. Although no statistically significant associations of hearing loss with timing of rash during pregnancy and degree of microcephaly were detected, sensorineural auditory impairment occurred predominantly in infants whose mothers had a rash illness during the first trimester of pregnancy, and all the infants with sensorineural hearing loss had severe microcephaly. Therefore, severe microcephaly in infants with evidence of congenital Zika virus infection should be considered a risk factor for auditory impairment. The prevalence of progressive hearing loss associated with congenital Zika virus infection is not known. To elucidate the full spectrum of hearing loss in infants with congenital Zika virus infection, testing and follow-up of all children born to women who had Zika virus infection during pregnancy, including infants with no apparent anomalies at birth, is needed. Sensorineural hearing loss should be considered part of the spectrum of clinical findings associated with congenital Zika virus infection, and congenital Zika virus infection should be considered a risk factor for hearing loss in auditory screening programs. Children with evidence of congenital Zika virus infection who have normal initial screening tests should receive regular follow-up, because onset of hearing loss could be delayed and the loss could be progressive. Top Acknowledgments Marli Tenório, MD, Ernesto Marques, MD, Virology and Experimental Therapy Department, Oswaldo Cruz Foundation, Pernambuco, Brazil.

Congenital infection with Zika virus causes microcephaly and other brain abnormalities (1). Hearing loss associated with other congenital viral infections is well described; however, little is known about hearing loss in infants with congenital Zika virus infection. A retrospective assessment of a series of 70 infants aged 0–10 months with microcephaly and laboratory evidence of Zika virus infection was conducted by the Hospital Agamenon Magalhães in Brazil and partners. The infants were enrolled during November 2015–May 2016 and had screening and diagnostic hearing tests. Five (7%) infants had sensorineural hearing loss, all of whom had severe microcephaly; however, one child was tested after receiving treatment with an ototoxic antibiotic. If this child is excluded, the prevalence of sensorineural hearing loss was 5.8% (four of 69), which is similar to that seen in association with other congenital viral infections. Additional information is needed to understand the prevalence and spectrum of hearing loss in children with congenital Zika virus infection; all infants born to women with evidence of Zika virus infection during pregnancy should have their hearing tested, including infants who appear normal at birth. The most well-described feature of congenital Zika syndrome is microcephaly (2,3). Clinical aspects appear to be predominantly neurologic, with neuroimaging showing calcifications between cortical and subcortical zones, cortical development errors, and pachygyria/agyria (2–4). In addition to the neurologic manifestations, ophthalmic (5) and orthopedic (1) lesions have been described as a component of the syndrome. A single study in Brazil investigated auditory function among 23 neonates with microcephaly and presumed congenital Zika virus infection, using otoacoustic emissions testing without a confirmatory examination, and found 9% with auditory deficits (4). In all of the studies described, Zika virus infection was a diagnosis of exclusion because, at the time, specific testing for Zika virus was not readily available. Hearing loss is a well established feature of other congenital infections, including cytomegalovirus (CMV), rubella, toxoplasmosis, herpes simplex, and syphilis. In these syndromes, the hearing loss is sensorineural, usually bilateral, and severe or profound; it is often undetectable at birth, and sometimes it is progressive or fluctuating (6,7). During November 2015–May 2016, as part of the protocol for evaluation of children who were born with microcephaly during the Zika virus disease epidemic, 150 children were referred to Hospital Agamenon Magalhães, a reference center for diagnosis of hearing loss and hearing rehabilitation in Pernambuco, Brazil; the 23 children previously evaluated in Pernambuco (4) were not part of this cohort. This report is a retrospective analysis of hearing assessments in 70 infants aged 0–10 months with microcephaly and laboratory evidence of Zika virus infection evaluated during that time. Zika virus–associated microcephaly was defined as head circumference ≤32 cm for term newborns (gestational age at birth 37 weeks to 41 weeks and 6 days), or at least two standard deviations below the mean for gestational age and sex using the Fenton curve for preterm newborns (8), with the characteristic radiologic findings from cranial computerized tomography or magnetic resonance imaging, and laboratory confirmation of Zika virus by a positive Zika virus-specific immunoglobulin M (IgM) capture enzyme-linked immunosorbent assay (ELISA) performed on cerebrospinal fluid (9).* Other infectious causes of congenital sensorineural hearing loss, including CMV, toxoplasmosis, herpes simplex, and syphilis, were excluded by serologic testing of infants and their mothers. Information was collected concerning the presence and timing of rash during pregnancy and on maternal or perinatal risk factors for congenital hearing loss, such as alcohol consumption, familial hearing loss, ototoxic drug exposure, birth trauma, and postnatal infections. The degree of microcephaly was evaluated, with severe microcephaly defined as head circumference at birth of at least three standard deviations below the mean for gestational age and sex. Auditory evaluation was carried out by screening and diagnostic tests as recommended by the American Academy of Pediatrics’ Joint Committee on Infant Hearing (10). The screening test consisted of measurement of the short latency auditory brainstem response (ABR) to click stimuli, and was considered to be normal when wave V (the fifth and most prominent and consistent wave) was identified in two consecutive averaged waveforms at 35 decibels normal hearing level (dB nHL). If the first screening test was not normal, it was repeated approximately 1 month later. If the second test also indicated hearing loss, a diagnostic confirmatory frequency-specific ABR was conducted, in which the stimuli were tone bursts at frequencies of 500 and 2,000 Hz. The diagnosis of hearing loss was confirmed if hearing thresholds exceeded 25 dB nHL. No behavioral auditory testing was performed. Conductive hearing loss was not considered to be related to Zika virus infection because the hearing impairment caused by congenital viral infections is sensorineural. All children considered normal on hearing evaluation will be regularly assessed for evidence of late-onset hearing impairment. Associations between sensorineural hearing loss and presence of maternal rash during pregnancy, timing of maternal rash during pregnancy, and severe microcephaly were analyzed using contingency tables and tested using Fisher’s exact test, with statistical significance defined as p<0.05. Although all investigations were carried out as part of routine clinical care, and human subjects review was not required, the protocol was submitted for ethical review and approved by Hospital Agamenon Magalhães. The mean age at the first auditory testing was 114 ± 59.1 days (range = 16–315 days, median = 97 days). Among all 70 infants, 16 (22.8%) failed the first screening test in at least one ear; among these, eight failed the repeat test and were evaluated by frequency-specific ABR. The diagnosis of hearing impairment was confirmed by ABR in seven (10%) children, including two with conductive hearing loss and five with sensorineural hearing loss. Sensorineural hearing loss was bilateral in three children and unilateral in two. One child with bilateral profound sensorineural hearing loss had been treated for sepsis with intravenous amikacin, an antibiotic with known ototoxicity, before the first test. A second child with bilateral profound sensorineural hearing loss had a twin brother with normal head circumference and cerebrospinal fluid negative for Zika-specific IgM. A third infant with sensorineural hearing loss had moderate impairment on the left and profound impairment on the right. One of the two infants with unilateral sensorineural hearing loss had mild impairment, and the other had profound impairment. Information on presence of rash during pregnancy was obtained from 63 mothers, 54 (86%) of whom reported a rash during pregnancy (Table). Among these 54 mothers, 41 (76%) experienced the rash during the first trimester. The mothers of four infants with confirmed sensorineural hearing loss, including the one infant treated with amikacin, reported having had a rash during the first 3 months of pregnancy; the mother of the fifth infant with confirmed sensorineural hearing loss reported having had a rash in the fourth month of pregnancy. Timing of maternal rash during pregnancy did not differ between infants with and without sensorineural hearing loss (p = 0.64). Information needed to determine the degree of microcephaly was available for 65 (93%) infants, among whom 44 (68%) had severe microcephaly; all five children with sensorineural hearing loss were in this group; however, no significant association was detected between the presence of sensorineural hearing loss and severe microcephaly (p = 0.55).

Mariana C. Leal, PhD1,2; Lilian F. Muniz, PhD2; Tamires S.A. Ferreira, MD1; Cristiane M. Santos, MD1; Luciana C. Almeida2; Vanessa Van Der Linden, MD3,4; Regina C.F. Ramos, MD5; Laura C. Rodrigues, PhD5; Silvio S. Caldas Neto, PhD2 Corresponding author: Mariana C. Leal, [email protected]. Top 1Hospital Agamenon Magalhães; 2Federal University of Pernambuco; 3Association for Assistance of Disabled Children; 4Oswaldo Cruz University Hospital; 5London School of Hygiene and Tropical Medicine.

Summary What is already known about this topic? Congenital Zika virus infection is characterized by microcephaly and other abnormalities of the brain and eye; orthopedic lesions have also been documented. While the full clinical spectrum of the syndrome is not yet known, the neurologic damage and corresponding radiologic brain imaging have been well described. Other congenital infections can cause hearing loss, which is diagnosed at birth or during later follow-up; however, few data exist regarding hearing loss associated with confirmed congenital Zika virus infection. What is added by this study? Congenital infection with Zika virus appears to be associated with sensorineural hearing loss. Among 70 children with microcephaly and laboratory evidence of congenital Zika virus infection, four of 69 (5.8%) were found to have sensorineural hearing loss without other potential cause. What are the implications for public health practice? Congenital infection with Zika virus should be considered a risk factor for hearing loss. Children with evidence of congenital Zika virus infection who have normal initial screening tests should receive regular follow-up, because onset of hearing loss associated with other congenital viral infections can be delayed and the loss can be progressive.

Hearing Loss in Infants with Microcephaly and Evidence of Congenital Zika Virus Infection — Brazil, November 2015–May 2016 Early Release / August 30, 2016 / 65 http://www.cdc.gov/mmwr/volumes/65/wr/mm6534e3.htm?s_cid=mm6534e3_w

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Number of cases reported County/Area Today Year to Date (8/26-29/16) Albany 0 4 Broome 0 3 Clinton 0 1 Columbia 0 1 Delaware 0 1 Dutchess 0 5 Erie 0 4 Lewis 0 1 Monroe 4 12 Nassau 3 40 Niagara 0 1 Oneida 0 3 Onondaga 1 6 Ontario 0 3 Orange 0 6 Otsego 0 1 Putnam 0 1 Rockland 0 8 Saratoga 1 2 St Lawrence 0 1 Schenectady 0 1 Suffolk 4 43 Tompkins 0 2 Wayne 0 2 Westchester 0 21 NYS (ex NYC) 13 173 NYC 11 539 NYS Total Confirmed 24 712 NYS Pregnant Registry 0 25 NYS Total 23 737

First victim of local Zika infection is Tampa firefighter living in Pinellas By Christopher O'DonnellTimes Staff Writer Tuesday, August 30, 2016 10:48am Print 0 At the Pinellas County Mosquito Control laboratory, researchers have been studying the Aedes Aegypti mosquito that can carry the Zika virus. [JIM DAMASKE | Times] At the Pinellas County Mosquito Control laboratory, researchers have been studying the Aedes Aegypti mosquito that can carry the Zika virus. [JIM DAMASKE | Times] TAMPA — The single victim of a locally transmitted Zika virus infection in the Tampa Bay area is a firefighter with Tampa Fire Rescue who lives in Pinellas County, an agency spokesman said today. RELATED NEWS/ARCHIVE The location of Pinellas County's first local Zika case is a secret. Good idea or bad? 15 Hours Ago Zika infections late in pregnancy led to no defects in study 2 Months Ago Zika Q&A: What you need to know now that a locally transmitted case is in Pinellas County 6 Days Ago Personnel at the station where the firefighter works also were tested for Zika and the results were negative, said Jason Penny, Tampa Fire Rescue spokesman. KEEPING ZIKA SECRET: Is it a good or badidea? The firefighter who was infected no longer has the virus, Penny said. The firefighter works at Station No. 3, Kennedy Boulevard at Willow Avenue. No personal information of about the firefighter is being released, Penny said, because of the federal Health Insurance Portability and Accountability Act, or HIPPA, which protects the privacy and security of health information. Gov. Rick Scott announced Aug. 23 that Pinellas had its first locally transmitted Zika case. State and local health officials are conducting a door-to-door outreach effort and have tested people known to be in direct contact with the infected resident. Mosquito spraying in areas where the resident spent time outdoors was conducted on both sides of Tampa Bay. Surgeon General Celeste Philip had declined to divulge where the infected resident lives or works until officials could confirm the virus is being spread in those locations. But that could take up to two weeks and leaves residents and local governments too much in the dark, some local leaders have said. This is a developing story. Stay with tampabay.com for updates. First victim of local Zika infection is Tampa firefighter living in Pinellas 08/30/16 [Last modified: Tuesday, August 30, 2016 10:48am] http://www.tampabay.com/news/health/first-victim-of-local-zika-infection-is-tampa-firefighter-living-in/2291469?utm_source=dlvr.it&utm_medium=twitter

An additional 18 pregnant women with laboratory criteria for possible Zika infection have been reported to CDC for US Zika Pregnancy Registry surveillance, 4 of whom had symptoms.m Pregnant Women with Possible Zika Infection m 0 1 0 0 0 2 4 18 http://www.dallascounty.org/department/hhs/documents/DCHHSEpiWNVWeeklyReport_8_29_2016.pdf

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States States CDC States States 24-Aug 25-Aug 25-Aug 26-Aug 29-Aug AK 1 1 0 1 1 AL 29 29 15 29 29 AR 9 9 9 9 9 AZ 24 24 20 26 26 CA 170 170 152 189 189 CO 21 24 24 24 24 CT 71 74 50 74 74 DE 12 12 11 12 12 DC 16 17 11 17 18 FL 636 647 471 662 663 GA 58 65 54 65 65 HI 10 11 11 11 11 ID 1 1 1 1 1 IL 56 58 49 58 58 IN 32 32 28 32 32 IA 13 13 13 13 13 KS 9 11 11 11 11 KY 11 19 19 19 19 LA 23 26 25 26 26 MD 77 77 77 77 77 MA 59 59 63 59 59 ME 9 9 10 9 9 MI 25 31 31 31 31 MN 31 31 31 31 31 MO 18 20 20 20 20 MS 17 17 17 17 17 MT 4 4 4 4 4 NC 36 36 35 36 36 ND 3 3 1 3 3 NE 6 7 7 7 7 NH 8 8 8 8 8 NJ 102 102 91 102 102 NM 3 3 3 3 3 NV 13 13 13 13 13 NY 691 714 601 714 714 OH 42 42 33 42 42 OK 19 20 20 20 20 OR 27 27 19 27 27 PA 82 82 77 82 95 RI 25 28 28 28 28 SC 33 33 31 33 33 SD 0 1 1 1 1 TN 33 35 35 35 35 TX 177 177 125 177 179 UT 8 8 7 8 8 VA 63 69 66 69 69 VT 6 7 7 7 7 WA 31 31 21 31 31 WI 31 31 21 31 31 WV 11 11 11 11 11 2891 2978 2488 3014 3031

26 more local Zika infections confirmed on Tuesday: MOH, NEA Posted 30 Aug 2016 21:11 Updated 30 Aug 2016 21:32 File photo of a mosquito (Photo: AFP/Marvin Recinos) ENLARGE CAPTION ? Email More A A SINGAPORE: 26 more cases of locally transmitted Zika virus infection have been confirmed in Singapore, the Ministry of Health (MOH) and National Environment Agency (NEA) said in a joint statement on Tuesday (Aug 30). This is on top of the15 cases confirmed on Monday and the 41 cases on Sunday, bringing the total number of confirmed cases in Singapore to 82. In their media release on Tuesday, the agencies gave more details of the new cases: 17 of them live or work in the Sims Drive/ Aljunied Crescent area and five live or work in Kallang Way and Paya Lebar Way, north of Sims Drive/Aljunied. The authorities are investigating the remaining four cases for their links to the affected area. The agencies added that another 111 individuals were tested negative over the last 24 hours. 5,000 OF 6,000 ALJUNIED/SIMS PREMISES CHECKED: NEA NEA added that as of Monday, it has inspected about 5,000 premises out of an estimated 6,000 premises in the Aljunied Crescent/Sims Drive cluster to check for mosquito breeding, and also conducted ground checks in the vicinity. 39 breeding habitats – comprising 23 in homes and 16 in common areas/other premises - have been detected and destroyed. NEA also said it served notices on more than 400 inaccessible premises in the Aljunied Crescent/Sims Drive cluster to require the owners to contact NEA to arrange for an inspection, failing which NEA will proceed with forced entry. NEA has also inspected the on-site workers' quarters at the construction site at Sims Drive, where a number of cases work. The stop-work order on the construction site at Sims Drive is still in force. NEA officers and grassroots volunteers have completed the first round of outreach efforts in the Aljunied Crescent/Sims Drive cluster, to distribute Zika information leaflets, and will be continuing with outreach in the areas of concern to raise general awareness of Zika, reiterate need for source reduction to prevent mosquito breeding, and advise residents to apply repellent as precaution. NEA said it would also begin vector control operations and outreach efforts in Kallang Way and Paya Lebar Way. INSPECTING CONSTRUCTION SITES, DORMITORIES In addition to inspecting homes and their common areas, NEA is also inspecting construction sites and engages dormitory operators. It said: "The latter plays an important role in helping to prevent and stem Zika transmission in their premises by ensuring a clean and hygienic environment. Some good practices include engaging dedicated pest control operator(s) for mosquito control, ensuring and sustaining proper housekeeping, and ensuring that all workers/residents apply insect repellent regularly." - CNA http://www.channelnewsasia.com/news/singapore/26-more-local-zika/3085542.html

Allegheny County Residents Approved for Zika Testing: 172 CDC Confirmed Cases: 10 Unspecified Flavivirus Infections: 1* (as of August 29) *- specific virus (dengue/zika) cannot be identified

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Zika virus cases in Ohio: https://www.odh.ohio.gov/odhprograms/bid/zdp/diseases/zika.aspx

Zika virus cases in Ohio:

Sequences producing significant alignments: Select:AllNone Selected:0 AlignmentsDownloadGenBankGraphicsDistance tree of resultsShow/hide columns of the table presenting sequences producing significant alignments Sequences producing significant alignments: Select for downloading or viewing reports Description Max score Total score Query cover E value Ident Accession Select seq gb|KX702400.1| Zika virus strain Zika virus/Homo sapiens/VEN/UF-1/2016, complete genome 18969 18969 100% 0.0 100% KX702400.1 Select seq gb|KX247646.1| Zika virus isolate Zika virus/Homo sapiens/COL/UF-1/2016, complete genome 18936 18936 100% 0.0 99% KX247646.1 Select seq gb|KU820897.5| Zika virus isolate FLR polyprotein gene, complete cds 18925 18925 100% 0.0 99% KU820897.5 Select seq gb|KX087102.1| Zika virus strain ZIKV/Homo sapiens/COL/FLR/2015, complete genome 18925 18925 100% 0.0 99% KX087102.1 Select seq gb|KX198135.1| Zika virus strain ZIKV/Homo sapiens/PAN/BEI-259634_V4/2016, complete genome 18881 18881 100% 0.0 99% KX198135.1 Select seq gb|KX156776.1| Zika virus strain ZIKV/Homo sapiens/PAN/CDC-259364_V1-V2/2015, complete genome 18870 18870 100% 0.0 99% KX156776.1 Select seq gb|KX156774.1| Zika virus strain ZIKV/Homo sapiens/PAN/CDC-259359_V1-V3/2015, complete genome 18864 18864 100% 0.0 99% KX156774.1 Select seq gb|KX156775.1| Zika virus strain ZIKV/Homo sapiens/PAN/CDC-259249_V1-V3/2015, complete genome 18859 18859 100% 0.0 99% KX156775.1 Select seq gb|KU647676.1| Zika virus strain MRS_OPY_Martinique_PaRi_2015 polyprotein gene, complete cds 18831 18831 100% 0.0 99% KU647676.1 Select seq gb|KX548902.1| Zika virus isolate ZIKV/COL/FCC00093/2015 polyprotein gene, complete cds 18825 18825 100% 0.0 99% KX548902.1 Select seq gb|KU922960.1| Zika virus isolate MEX/InDRE/Sm/2016, complete genome 18809 18809 100% 0.0 99% KU922960.1 Select seq gb|KU922923.1| Zika virus isolate MEX/InDRE/Lm/2016, complete genome 18803 18803 100% 0.0 99% KU922923.1 Select seq gb|KX447510.1| Zika virus isolate 1_0049_PF polyprotein gene, complete cds 18792 18792 100% 0.0 99% KX447510.1 Select seq gb|KU991811.1| Zika virus isolate Brazil/2016/INMI1 polyprotein gene, complete cds 18787 18787 100% 0.0 99% KU991811.1 Select seq gb|KX447512.1| Zika virus isolate 1_0181_PF polyprotein gene, complete cds 18781 18781 100% 0.0 99% KX447512.1 Select seq gb|KX369547.1| Zika virus strain PF13/251013-18, complete genome 18781 18781 100% 0.0 99% KX369547.1 Select seq gb|KU509998.3| Zika virus strain Haiti/1225/2014, complete genome 18781 18781 100% 0.0 99% KU509998.3 Select seq gb|KX447509.1| Zika virus isolate 1_0087_PF polyprotein gene, complete cds 18776 18776 100% 0.0 99% KX447509.1 Select seq gb|KJ776791.1| Zika virus strain H/PF/2013 polyprotein gene, complete cds 18776 18776 100% 0.0 99% KJ776791.1 Select seq gb|KX447515.1| Zika virus isolate 1_0030_PF polyprotein gene, complete cds 18770 18770 100% 0.0 99% KX447515.1 Select seq gb|KX447513.1| Zika virus isolate 1_0134_PF polyprotein gene, complete cds 18770 18770 100% 0.0 99% KX447513.1 Select seq gb|KX447511.1| Zika virus isolate 1_0015_PF polyprotein gene, complete cds 18764 18764 100% 0.0 99% KX447511.1 Select seq gb|KX280026.1| Zika virus isolate Paraiba_01, complete genome 18764 18764 100% 0.0 99% KX280026.1 Select seq gb|KU707826.1| Zika virus isolate SSABR1, complete genome 18764 18764 100% 0.0 99% KU707826.1 Select seq gb|KU365779.1| Zika virus strain BeH819966 polyprotein gene, complete cds 18764 18764 100% 0.0 99% KU365779.1 Select seq gb|KU321639.1| Zika virus strain ZikaSPH2015, complete genome 18764 18764 100% 0.0 99% KU321639.1 Select seq gb|KX447514.1| Zika virus isolate 1_0035_PF polyprotein gene, complete cds 18759 18759 100% 0.0 99% KX447514.1 Select seq gb|KX051563.1| Zika virus isolate Haiti/1/2016, complete genome 18759 18759 100% 0.0 99% KX051563.1 Select seq gb|KX447516.1| Zika virus isolate 1_0111_PF polyprotein gene, complete cds 18753 18753 100% 0.0 99% KX447516.1 Select seq gb|KU729218.1| Zika virus isolate BeH828305 polyprotein gene, complete cds 18753 18753 100% 0.0 99% KU729218.1 Select seq gb|KX262887.1| Zika virus isolate 103451, complete genome 18748 18748 100% 0.0 99% KX262887.1 Select seq gb|KX197192.1| Zika virus isolate ZIKV/H.sapiens/Brazil/PE243/2015, complete genome 18748 18748 100% 0.0 99% KX197192.1 Select seq gb|KU365780.1| Zika virus strain BeH815744 polyprotein gene, complete cds 18748 18748 100% 0.0 99% KU365780.1 Select seq gb|KU497555.1| Zika virus isolate Brazil-ZKV2015, complete genome 18744 18744 99% 0.0 99% KU497555.1 Select seq gb|KU365777.1| Zika virus strain BeH818995 polyprotein gene, complete cds 18742 18742 100% 0.0 99% KU365777.1 Select seq gb|KX694534.1| Zika virus strain ZIKV/Homo sapiens/HND/R103451/2015, complete genome 18737 18737 100% 0.0 99% KX694534.1 Select seq gb|KU758877.1| Zika virus isolate 17271 polyprotein gene, complete cds 18737 18737 100% 0.0 99% KU758877.1 Select seq gb|KU926309.1| Zika virus isolate Rio-U1, complete genome 18737 18737 100% 0.0 99% KU926309.1 Select seq gb|KU940228.1| Zika virus isolate Bahia07, partial genome 18731 18731 100% 0.0 99% KU940228.1 Select seq gb|KX447517.1| Zika virus isolate 1_0038_PF polyprotein gene, complete cds 18726 18726 100% 0.0 99% KX447517.1 Select seq gb|KU501217.1| Zika virus strain 8375 polyprotein gene, complete cds 18726 18726 100% 0.0 99% KU501217.1 Select seq gb|KU365778.1| Zika virus strain BeH819015 polyprotein gene, complete cds 18726 18726 100% 0.0 99% KU365778.1 Select seq gb|KU312312.1| Zika virus isolate Z1106033 polyprotein gene, complete cds 18726 18726 100% 0.0 99% KU312312.1 Select seq gb|KU729217.2| Zika virus isolate BeH823339 polyprotein gene, complete cds 18720 18720 100% 0.0 99% KU729217.2 Select seq gb|KU527068.1| Zika virus strain Natal RGN, complete genome 18720 18720 100% 0.0 99% KU527068.1 Select seq gb|KU501216.1| Zika virus strain 103344 polyprotein gene, complete cds 18720 18720 100% 0.0 99% KU501216.1 Select seq gb|KX247632.1| Zika virus isolate MEX_I_7 polyprotein gene, complete cds 18715 18715 100% 0.0 99% KX247632.1 Select seq gb|KU937936.1| Zika virus isolate ZIKVNL00013 polyprotein gene, complete cds 18715 18715 100% 0.0 99% KU937936.1 Select seq gb|KU926310.1| Zika virus isolate Rio-S1, complete genome 18715 18715 100% 0.0 99% KU926310.1 Select seq gb|KU501215.1| Zika virus strain PRVABC59, complete genome 18715 18715 100% 0.0 99% KU501215.1 Select seq gb|KX601168.1| Zika virus strain ZIKV/Homo Sapiens/PRI/PRVABC59/2015, complete genome 18709 18709 100% 0.0 99% KX601168.1 Select seq gb|KX520666.1| Zika virus isolate HS-2015-BA-01 polyprotein gene, complete cds 18709 18709 100% 0.0 99% KX520666.1 Select seq gb|KX087101.2| Zika virus strain ZIKV/Homo sapiens/PRI/PRVABC59/2015, complete genome 18709 18709 100% 0.0 99% KX087101.2 Select seq gb|KX446951.1| Zika virus strain ZIKV/Aedes.sp/MEX/MEX_I-7/2016, complete genome 18703 18703 100% 0.0 99% KX446951.1 Select seq gb|KX377337.1| Zika virus strain PRVABC-59, complete genome 18703 18703 100% 0.0 99% KX377337.1 Select seq gb|KU820898.1| Zika virus isolate GZ01 polyprotein gene, complete cds 18703 18703 100% 0.0 99% KU820898.1 Select seq gb|KX446950.1| Zika virus strain ZIKV/Aedes.sp/MEX/MEX_2-81/2016, complete genome 18698 18698 100% 0.0 99% KX446950.1 Select seq gb|KU870645.1| Zika virus isolate FB-GWUH-2016, complete genome 18698 18698 100% 0.0 99% KU870645.1 Select seq gb|KX766028.1| Zika virus isolate R114916, complete genome 18694 18694 100% 0.0 99% KX766028.1 Select seq gb|KU853013.1| Zika virus isolate Dominican Republic/2016/PD2, complete genome 18692 18692 100% 0.0 99% KU853013.1 Select seq gb|KU853012.1| Zika virus isolate Dominican Republic/2016/PD1, complete genome 18691 18691 100% 0.0 99% KU853012.1 Select seq gb|KX056898.1| Zika virus isolate Zika virus/GZ02/2016 polyprotein gene, complete cds 18687 18687 100% 0.0 99% KX056898.1 Select seq gb|KU955590.1| Zika virus isolate Z16019 polyprotein gene, complete cds 18687 18687 100% 0.0 99% KU955590.1 Select seq gb|KU740184.2| Zika virus isolate GD01 polyprotein gene, complete cds 18681 18681 100% 0.0 99% KU740184.2 Select seq gb|KU761564.1| Zika virus isolate GDZ16001 polyprotein gene, complete cds 18681 18681 100% 0.0 99% KU761564.1 Select seq gb|KX766029.1| Zika virus isolate R116265, complete genome 18670 18670 100% 0.0 99% KX766029.1 Select seq gb|KX673530.1| Zika virus isolate PHE_semen_Guadeloupe, complete genome 18665 18665 100% 0.0 99% KX673530.1 Select seq gb|KX117076.1| Zika virus isolate Zhejiang04, complete genome 18665 18665 100% 0.0 99% KX117076.1 Select seq gb|KX185891.1| Zika virus isolate Zika virus/CN/SZ02/2016 polyprotein gene, complete cds 18654 18654 100% 0.0 99% KX185891.1 Select seq gb|KU963796.1| Zika virus isolate SZ-WIV01 polyprotein gene, complete cds 18654 18654 100% 0.0 99% KU963796.1 Select seq gb|KX253996.1| Zika virus isolate ZKC2/2016, complete genome 18648 18648 100% 0.0 99% KX253996.1 Select seq gb|KU955589.1| Zika virus isolate Z16006 polyprotein gene, complete cds 18648 18648 100% 0.0 99% KU955589.1 Select seq gb|KU820899.2| Zika virus isolate ZJ03, complete genome 18648 18648 100% 0.0 99% KU820899.2 Select seq gb|KX266255.1| Zika virus isolate ZIKV_SMGC-1, complete genome 18644 18644 100% 0.0 99% KX266255.1 Select seq gb|KU866423.2| Zika virus isolate Zika virus/SZ01/2016/China polyprotein gene, complete cds 18643 18643 100% 0.0 99% KU866423.2 Select seq gb|KU940224.1| Zika virus isolate Bahia09, partial genome 18633 18633 99% 0.0 99% KU940224.1 Select seq gb|KU744693.1| Zika virus isolate VE_Ganxian, complete genome 18499 18499 100% 0.0 99% KU744693.1 Select seq gb|KU681081.3| Zika virus isolate Zika virus/H.sapiens-tc/THA/2014/SV0127- 14, complete genome 18366 18366 100% 0.0 99% KU681081.3 Select seq gb|KX694532.1| Zika virus strain ZIKV/Homo sapiens/THA/PLCal_ZV/2013, complete genome 18233 18233 100% 0.0 99% KX694532.1 Select seq gb|KF993678.1| Zika virus strain PLCal_ZV from Canada polyprotein gene, partial cds 17996 17996 98% 0.0 99% KF993678.1 Select seq gb|JN860885.1| Zika virus isolate FSS13025 polyprotein gene, partial cds 17991 17991 99% 0.0 98% JN860885.1 Select seq gb|KU955593.1| Zika virus isolate Zika virus/H.sapiens-tc/KHM/2010/FSS13025, complete genome 17989 17989 100% 0.0 98% KU955593.1 Select seq gb|EU545988.1| Zika virus polyprotein gene, complete cds 17804 17804 100% 0.0 98% EU545988.1 Select seq gb|KU681082.3| Zika virus isolate Zika virus/H.sapiens-tc/PHL/2012/CPC-0740, complete genome 17612 17612 100% 0.0 98% KU681082.3 Select seq gb|KX447518.1| Zika virus isolate 1_0117_PF polyprotein gene, partial cds 16574 16574 88% 0.0 99% KX447518.1 Select seq gb|KX601167.1| Zika virus strain ZIKV/Aedes sp./MYS/P6-740/1966, complete genome 16388 16388 99% 0.0 95% KX601167.1 Select seq gb|HQ234499.1| Zika virus isolate P6-740 polyprotein gene, partial cds 16382 16382 99% 0.0 95% HQ234499.1 Select seq gb|KX694533.1| Zika virus strain ZIKV/Aedes aegypti/MYS/P6-740/1966, complete genome 16377 16377 99% 0.0 95% KX694533.1 Select seq gb|KX377336.1| Zika virus strain P6-740, complete genome 16371 16371 99% 0.0 95% KX377336.1

Mosquitoes carrying Zika can hand down virus to offspring, study shows By HELEN BRANSWELL @HelenBranswell AUGUST 29, 2016 Twitter Facebook LinkedIn Email Republish Print Like a physical trait or a family heirloom, the Zika virus can be handed down by an infected female mosquito to some of her offspring, a new study shows. The study, by scientists at the University of Texas Medical Branch in Galveston, confirms that so-called vertical transmission of the virus occurs in Aedes aegypti mosquitoes, the main species responsible for the spread of Zika. But vertical transmission doesn’t always happen. In fact, the research suggests it only occurs at a rate of 1 in every 300 mosquitoes. Still, given that mosquito populations are massive, that rate of transmission probably is frequent enough to allow the virus to persist in places where a period of adverse weather conditions — a stretch of dry or cold weather — kills off adult mosquitoes, said Dr. Robert Tesh, director of the World Reference Center for Emerging Viruses and Arboviruses, housed at the university. “I don’t think it’s going to change the epidemiology of the disease,” said Tesh, who is the senior author of the paper, published in the American Journal of Tropical Medicine and Hygiene. “The only thing it means is that it’s possible that the virus could survive [in a location] say from one season to the next.” Joseph Conlon, a retired Navy entomologist who is now technical adviser for theAmerican Mosquito Control Association, agreed with Tesh’s read of the situation. Conlon said in the United States, Zika’s spread is more likely to be driven by people returning home from Zika-affected cities and towns than by vertical transmission in mosquitoes. “We’re going to have continual reintroduction of this virus in people. They’re the main problem. People coming in,” he said. Many viruses related to Zika and spread by Aedes mosquitoes are transmitted from mother to offspring in this way. To test whether the same kind of transmission occurred with Zika, Tesh’s team injected the virus into the gut of female mosquitoes. After the mosquitoes mated and laid their eggs, the eggs were hatched and tested for the presence of the virus. The group studied both Aedes aegypti mosquitoes — in which vertical transmission was seen at a rate of one per 290 offspring — and Aedes albopictus mosquitoes. It’s not clear if the latter species plays a role in the transmission of Zika in a real world setting, though they can be infected with the virus in a lab. Tesh’s team did not see vertical transmission with albopictus mosquitoes, but tested fewer of them. He suggested, based on the numbers, scientists cannot rule out that vertical transmission could happen in that species. Conlon said the fact that vertical transmission occurs adds another layer of complexity to controlling these already hard-to-control mosquitoes. He suggested a multipronged approach is needed, one that is grounded in changing the public’s attitudes toward mosquitoes. “The fact is when we allow trash to accumulate and water to get into the trash to grow these Aedes aegypti mosquitoes, we’re part of the problem,” he said. “We have to make it socially unacceptable, kind of like we did with smoking.” Helen Branswell can be reached at [email protected] Follow Helen on Twitter @HelenBranswell https://www.statnews.com/2016/08/29/mosquito-zika-virus-transmission/

Abstract Previous experimental studies have demonstrated that a number of mosquito-borne flavivirus pathogens are vertically transmitted in their insect vectors, providing a mechanism for these arboviruses to persist during adverse climatic conditions or in the absence of a susceptible vertebrate host. In this study, designed to test whether Zika virus (ZIKV) could be vertically transmitted, female Aedes aegypti and Aedes albopictus were injected with ZIKV, and their F1 adult progeny were tested for ZIKV infection. Of 69 Ae. aegypti pools, six consisted of a total of 1,738 F1 adults, yielded ZIKV upon culture, giving a minimum filial infection rate of 1:290. In contrast, none of 803 F1 Ae. albopictus adults (32 pools) yielded ZIKV. The MFIR for Ae. aegypti was comparable to MFIRs reported for other flaviviruses in mosquitoes, including dengue, Japanese encephalitis, yellow fever, West Nile, and St. Louis encephalitis viruses. The results suggest that vertical transmission may provide a potential mechanism for the virus to survive during adverse conditions. Footnotes Financial support: This work was supported in part by NIH grant R24 AI 120942. Received June 6, 2016. Accepted August 1, 2016.