niman

LOCUS KU729217 10624 bp RNA linear VRL 26-FEB-2016 DEFINITION Zika virus isolate BeH823339 polyprotein gene, complete cds. ACCESSION KU729217 VERSION KU729217.1 GI:998491030 KEYWORDS . SOURCE Zika virus ORGANISM Zika virus Viruses; ssRNA viruses; ssRNA positive-strand viruses, no DNA stage; Flaviviridae; Flavivirus. REFERENCE 1 (bases 1 to 10624) AUTHORS Faria,N.R., Azevedo,R.S.S., Kraemer,M.U.G., Souza,R., Cunha,M.S., Hill,S.C., Theze,J., Bonsall,M.B., Bodeng,T.A., Rissanen,I., Rocco,I.M., Nogueira,J.S., Maeda,A.Y., Vasami,F.G.S., Macedo,F.L.L., Suzuki,A., Rodrigues,S.G., Cruz,A.C.R., Diniz,B.T., Medeiros,D.B.A., Silva,E.V.P., Henriques,D.F., Travassos da Rosa,E.S., Oliveira,C.S., Martins,L.C., Vasconcelos,H.B., Casseb,L.M.N., Simith,D.B., Messina,J., Abade,L., Lourenco,J., Alcantara,L.C., Lima,M., Giovanetti,M., Hay,S.I., Oliveira,R.S., Lemos,P.S., Oliveira,L.F., Lima,C.P.S., Silva,S.P., Vasconcelos,J.M., Cardoso,J.F., Vianez-Junior,J.L.S.G., Mir,D., Bello,G., Delatorre,E., Khan,K., Creatore,M., Coelho,G.E., Oliveira,W.K., Tesh,R., Pybus,O.G., Nunes,M.R.T. and Vasconcelos,P.F.C. TITLE Zika virus in the Americas: early epidemiological and genetic findings JOURNAL Unpublished REFERENCE 2 (bases 1 to 10624) AUTHORS Nunes,M.R.T., Azevedo,R.S.S., Silva,S.P., Vasconcelos,J.M., Cardoso,J.F., Lemos,P.S., Lima,C.P.S., Oliveira,R.S., Faria,N.R., Vianez-Junior,J.L.S.G., Medeiros,D.B.A., Rodrigues,S.G., Diniz,B.T., Silva,E.V.P., Cruz,A.C.R. and Vasconcelos,P.F.C. TITLE Direct Submission JOURNAL Submitted (18-FEB-2016) Center for Technological Innovation, Evandro Chagas Institute, BR 316, Km 07, s/n, Ananindeua, Para 67030-000, Brazil COMMENT EMAIL: [email protected] ##Assembly-Data-START## Assembly method: Mira 4.0 and Geneious 7.0 Sequencing Technology: Ion and 454 ##Assembly-Data-END##. FEATURES Location/Qualifiers source 1..10624 /organism="Zika virus" /mol_type="genomic RNA" /isolate="BeH823339" /host="Homo sapiens" /db_xref="taxon:64320" /country="Brazil" /collection_date="2015"

Evandro Chagas Institute has released a full Zika sequence, BeH823339, at Genbank. http://www.ncbi.nlm.nih.gov/nuccore/KU729217 This sequence matches a sequence, ZikV|NA|BeH823343|Brazil_Ceara_microcephaly|18-11-2015 cited as from a microcephaly case in Ceara as described here http://virological.org/t/zika-virus-in-the-americas-early-epidemiological-and-genetic-findings/220

LOCUS KU729218 10729 bp RNA linear VRL 26-FEB-2016 DEFINITION Zika virus isolate BeH828305 polyprotein gene, complete cds. ACCESSION KU729218 VERSION KU729218.1 GI:998491032 KEYWORDS . SOURCE Zika virus ORGANISM Zika virus Viruses; ssRNA viruses; ssRNA positive-strand viruses, no DNA stage; Flaviviridae; Flavivirus. REFERENCE 1 (bases 1 to 10729) AUTHORS Faria,N.R., Azevedo,R.S.S., Kraemer,M.U.G., Souza,R., Cunha,M.S., Hill,S.C., Theze,J., Bonsall,M.B., Bodeng,T.A., Rissanen,I., Rocco,I.M., Nogueira,J.S., Maeda,A.Y., Vasami,F.G.S., Macedo,F.L.L., Suzuki,A., Rodrigues,S.G., Cruz,A.C.R., Diniz,B.T., Medeiros,D.B.A., Silva,E.V.P., Henriques,D.F., Travassos da Rosa,E.S., Oliveira,C.S., Martins,L.C., Vasconcelos,H.B., Casseb,L.M.N., Simith,D.B., Messina,J., Abade,L., Lourenco,J., Alcantara,L.C., Lima,M., Giovanetti,M., Hay,S.I., Oliveira,R.S., Lemos,P.S., Oliveira,L.F., Lima,C.P.S., Silva,S.P., Vasconcelos,J.M., Cardoso,J.F., Vianez-Junior,J.L.S.G., Mir,D., Bello,G., Delatorre,E., Khan,K., Creatore,M., Coelho,G.E., Oliveira,W.K., Tesh,R., Pybus,O.G., Nunes,M.R.T. and Vasconcelos,P.F.C. TITLE Zika virus in the Americas: early epidemiological and genetic findings JOURNAL Unpublished REFERENCE 2 (bases 1 to 10729) AUTHORS Nunes,M.R.T., Azevedo,R.S.S., Silva,S.P., Vasconcelos,J.M., Cardoso,J.F., Lemos,P.S., Lima,C.P.S., Oliveira,R.S., Faria,N.R., Vianez-Junior,J.L.S.G., Medeiros,D.B.A., Rodrigues,S.G., Diniz,B.T., Silva,E.V.P., Cruz,A.C.R. and Vasconcelos,P.F.C. TITLE Direct Submission JOURNAL Submitted (18-FEB-2016) Center for Technological Innovation, Evandro Chagas Institute, BR 316, Km 07, s/n, Ananindeua, Para 67030-000, Brazil COMMENT EMAIL: [email protected] ##Assembly-Data-START## Assembly method: Mira 4.0 and Geneious 7.0 Sequencing Technology: Ion and 454 Coverage: 659 ##Assembly-Data-END##. FEATURES Location/Qualifiers source 1..10729 /organism="Zika virus" /mol_type="genomic RNA" /isolate="BeH828305" /host="Homo sapiens" /db_xref="taxon:64320" /country="Brazil" /collection_date="2015" CDS 94..10365 /codon_start=1 /product="polyprotein" /protein_id="AMK49165.1" /db_xref="GI:998491033" /translation="MKNPKKKSGGFRIVNMLKRGVARVSPFGGLKRLPAGLLLGHGPI RMVLAILAFLRFTAIKPSLGLINRWGSVGKKEAMEIIKKFKKDLAAMLRIINARKEKK RRSADTSVGIVGLLLTTAMAAEVTRRGSAYYMYLDRNDAGEAISFPTTLGMNKCYIQI MDLGHMCDATMSYECPMLDEGVEPDDVDCWCNTTSTWVVYGTCHHKKGEARRSRRAVT LPSHSTRKLQTRSQTWLESREYTKHLIRVENWIFRNPGFALAAAAIAWLLGSSTSQKV IYLVMILLIAPAYSIRCIGVSNRDFVEGMSGGTWVDVVLEHGGCVTVMAQDKPTVDIE LVTTTVSNMAEVRSYCYEASISDMASDSRCPTQGEAYLDKQSDTQYVCKRTLVDRGWG NGCGLFGKGSLVTCAKFACSKKMTGKSIQPENLEYRIMLSVHGSQHSGMIVNDTGHET DENRAKVEITPNSPRAEATLGGFGSLGLDCEPRTGLDFSDLYYLTMNNKHWLVHKEWF HDIPLPWHAGADTGTPHWNNKEALVEFKDAHAKRQTVVVLGSQEGAVHTALAGALEAE MDGAKGRLSSGHLKCRLKMDKLRLKGVSYSLCTAAFTFTKIPAETLHGTVTVEVQYAG TDGPCKVPAQMAVDTQTLTPVGRLITANPVITESTENSKMMLELDPPFGDSYIVIGVG EKKITHHWHRSGSTIGKAFEATVRGAKRMAVLGDTAWDFGSVGGALNSLGKGIHQIFG AAFKSLFGGMSWFSQILIGTLLMWLGLNTKNGSISLMCLALGGVLIFLSTAVSADVGC SVDFSKKETRCGTGVFVYNDVEAWRDRYKYHPDSPRRLAAAVKQAWEDGICGISSVSR MENIMWRSVEGELNAILEENGVQLTVVVGSVKNPMWRGPQRLPVPVNELPHGWKAWGK SYFVRAAKTNNSFVVDGDTLKECPLKHRAWNSFLVEDHGFGVFHTSVWLKVREDYSLE CDPAVIGTAVKGKEAVHSDLGYWIESEKNDTWRLKRAHLIEMKTCEWPKSHTLWTDGI EESDLIIPKSLAGPLSHHNTREGYRTQMKGPWHSEELEIRFEECPGTKVHVEETCGTR GPSLRSTTASGRVIEEWCCRECTMPPLSFRAKDGCWYGMEIRPRKEPESNLVRSMVTA GSTDHMDHFSLGVLVILLMVQEGLKKRMTTKIIISTSMAVLVAMILGGFSMSDLAKLA ILMGATFAEMNTGGDVAHLALIAAFKVRPALLVSFIFRANWTPRESMLLALASCLLQT AISALEGDLMVLINGFALAWLAIRAMVVPRTDNITLAILAALTPLARGTLLVAWRAGL ATCGGFMLLSLKGKGSVKKNLPFVMALGLTAVRLVDPINVVGLLLLTRSGKRSWPPSE VLTAVGLICALAGGFAKADIEMAGPMAAVGLLIVSYVVSGKSVDMYIERAGDITWEKD AEVTGNSPRLDVALDESGDFSLVEDDGPPMREIILKVVLMTICGMNPIAIPFAAGAWY VYVKTGKRSGALWDVPAPKEVKKGETTDGVYRVMTRRLLGSTQVGVGVMQEGVFHTMW HVTKGSALRSGEGRLDPYWGDVKQDLVSYCGPWKLDAAWDGHSEVQLLAVPPGERARN IQTLPGIFKTKDGDIGAVALDYPAGTSGSPILDKCGRVIGLYGNGVVIKNGSYVSAIT QGRREEETPVECFEPSMLKKKQLTVLDLHPGAGKTRRVLPEIVREAIKTRLRTVILAP TRVVAAEMEEALRGLPVRYMTTAVNVTHSGTEIVDLMCHATFTSRLLQPIRVPNYNLY IMDEAHFTDPSSIAARGYISTRVEMGEAAAIFMTATPPGTRDAFPDSNSPITDTEVEV PERAWSSGFDWVTDHSGKTVWFVPSVRNGNEIAACLTKAGKRVIQLSRKTFETEFQKT KHQEWDFVVTTDISEMGANFKADRVIDSRRCLKPVILDGERVILAGPMPVTHASAAQR RGRIGRNPNKPGDEYLYGGGCAETDEDHAHWLEARMLLDNIYLQDGLIASLYRPEADK VAAIEGEFKLRTEQRKTFVELMKRGDLPVWLAYQVASAGITYTDRRWCFDGTTNNTIM EDSVPAEVWTRHGEKRVLKPRWMDARVCSDHAALKSFKEFAAGKRGAAFGVMEALGTL PGHMTERFQEAIDNLAVLMRAETGSRPYKAAAAQLPETLETIMLLGLLGTVSLGIFFV LMRNKGIGKMGFGMVTLGASAWLMWLSEIEPARIACVLIVVFLLLVVLIPEPEKQRSP QDNQMAIIIMVAVGLLGLITANELGWLERTKSDLSHLMGRREEGATIGFSMDIDLRPA SAWAIYAALTTFITPAVQHAVTTSYNNYSLMAMATQAGVLFGMGKGMPFYAWDFGVPL LMIGCYSQLTPLTLIVAIILLVAHYMYLIPGLQAAAARAAQKRTAAGIMKNPVVDGIV VTDIDTMTIDPQVEKKMGQVLLIAVAVSSAILSRTAWGWGEAGALITAATSTLWEGSP NKYWNSSTATSLCNIFRGSYLAGASLIYTVTRNAGLVKRRGGGTGETLGEKWKARLNQ MSALEFYSYKKSGITEVCREEARRALKDGVATGGHAVSRGSAKLRWLVERGYLQPYGK VIDLGCGRGGWSYYAATIRKVQEVKGYTKGGPGHEEPVLVQSYGWNIVRLKSGVDVFH MAAEPCDTLLCDIGESSSSPEVEEARTLRVLSMVGDWLEKRPGAFCIKVLCPYTSTMM ETLERLQRRYGGGLVRVPLSRNSTHEMYWVSGAKSNTIKSVSTTSQLLLGRMDGPRRP VKYEEDVNLGSGTRAVVSCAEAPNMKIIGNRIERIRSEHAETWFFDENHPYRTWAYHG SYEAPTQGSASSLINGVVRLLSKPWDVVTGVTGIAMTDTTPYGQQRVFKEKVDTRVPD PQEGTRQVMSMVSSWLWKELGKHKRPRVCTKEEFINKVRSNAALGAIFEEEKEWKTAV EAVNDPRFWALVDKEREHHLRGECQSCVYNMMGKREKKQGEFGKAKGSRAIWYMWLGA RFLEFEALGFLNEDHWMGRENSGGGVEGLGLQRLGYVLEEMSRIPGGRMYADDTAGWD TRISRFDLENEALITNQMEKGHRALALAIIKYTYQNKVVKVLRPAEKGKTVMDIISRQ DQRGSGQVVTYALNTFTNLVVQLIRNMEAEEVLEMQDLWLLRRSEKVTNWLQSNGWDR LKRMAVSGDDCVVKPIDDRFAHALRFLNDMGKVRKDTQEWKPSTGWDNWEEVPFCSHH FNKLHLKDGRSIVVPCRHQDELIGRARVSPGAGWSIRETACLAKSYAQMWQLLYFHRR DLRLMANAICSSVPVDWVPTGRTTWSIHGKGEWMTTEDMLVVWNRVWIEENDHMEDKT PVTKWTDIPYLGKREDLWCGSLIGHRPRTTWAENIKNTVNMVRRIIGDEEKYMDYLST QVRYLGEEGSTPGVL" ORIGIN 1 gtgaatcaga ctgcgacagt tcgagtttga agcgaaagct agcaacagta tcaacaggtt 61 ttattttgga tttggaaacg agagtttctg gtcatgaaaa acccaaaaaa gaaatccgga 121 ggattccgga ttgtcaatat gctaaaacgc ggagtagccc gtgtgagccc ctttgggggc 181 ttgaagaggc tgccagccgg acttctgctg ggtcatgggc ccatcaggat ggtcttggcg 241 attctagcct ttttgagatt cacggcaatc aagccatcac tgggtctcat caatagatgg 301 ggttcagtgg ggaaaaaaga ggctatggaa ataataaaga agttcaagaa agatctggct 361 gccatgctga gaataatcaa tgctaggaag gagaagaaga gacgaagcgc agatactagt 421 gtcggaattg ttggcctcct gctgaccaca gctatggcag cggaggtcac tagacgtggg 481 agtgcatact atatgtactt ggacagaaac gatgctgggg aggccatatc ttttccaacc 541 acattgggga tgaataagtg ttatatacag atcatggatc ttggacacat gtgtgatgcc 601 actatgagct atgaatgccc tatgctggat gagggggtgg aaccagatga cgtcgattgt 661 tggtgcaaca cgacgtcaac ttgggttgtg tacggaacct gccatcacaa aaaaggtgaa 721 gcacggagat ctagaagagc tgtgacgctc ccctcccatt ccactaggaa gctgcaaacg 781 cggtcgcaaa cctggttgga atcaagagaa tacacaaagc acttgattag agtcgaaaat 841 tggatattca ggaaccctgg cttcgcgtta gcagcagctg ccatcgcttg gcttttggga 901 agctcaacga gccaaaaagt catatacttg gtcatgatac tgctgattgc cccggcatac 961 agcatcaggt gcataggagt cagcaatagg gactttgtgg aaggtatgtc aggtgggact 1021 tgggttgatg ttgtcttgga acatggaggt tgtgtcaccg taatggcaca ggacaaaccg 1081 actgtcgaca tagagctggt tacaacaaca gtcagcaaca tggcggaggt aagatcctac 1141 tgctatgagg catcaatatc agacatggct tcggacagcc gctgcccaac acaaggtgaa 1201 gcctaccttg acaagcaatc agacactcaa tatgtctgca aaagaacgtt agtggacaga 1261 ggctggggaa atggatgtgg actttttggc aaagggagcc tggtgacatg cgctaagttt 1321 gcatgctcca agaaaatgac cgggaagagc atccagccag agaatctgga gtaccggata 1381 atgctgtcag ttcatggctc ccagcacagt gggatgatcg ttaatgacac aggacatgaa 1441 actgatgaga atagagcgaa ggttgagata acgcccaatt caccaagagc cgaagccacc 1501 ctggggggtt ttggaagcct aggacttgat tgtgaaccga ggacaggcct tgacttttca 1561 gatttgtatt acttgactat gaataacaag cactggttgg ttcacaagga gtggttccac 1621 gacattccat taccttggca cgctggggca gacaccggaa ctccacactg gaacaataaa 1681 gaagcactgg tagagttcaa ggacgcacat gccaaaaggc aaactgtcgt ggttctaggg 1741 agtcaagaag gagcagttca cacggccctt gctggagctc tggaggctga gatggatggt 1801 gcaaagggaa ggctgtcctc tggccacttg aaatgtcgcc tgaaaatgga taaacttaga 1861 ttgaagggcg tgtcatactc cttgtgtacc gcagcgttca cattcaccaa gatcccggct 1921 gaaacactgc acgggacagt cacagtggag gtacagtacg cagggacaga tggaccttgc 1981 aaggttccag ctcagatggc ggtggacacg caaactctga ccccagttgg gaggttgata 2041 accgctaacc ccgtaatcac tgaaagcact gagaactcta agatgatgct ggaacttgat 2101 ccaccatttg gggactctta cattgtcata ggagtcgggg agaagaagat cacccaccac 2161 tggcacagga gtggcagcac cattggaaaa gcatttgaag ccactgtgag aggtgccaag 2221 agaatggcag tcttgggaga cacagcctgg gactttggat cagttggagg cgctctcaac 2281 tcattgggca agggcatcca tcaaattttt ggagcagctt tcaaatcatt gtttggagga 2341 atgtcctggt tctcacaaat tctcattgga acgttgctga tgtggttggg tctgaacaca 2401 aagaatggat ctatttccct tatgtgcttg gccttagggg gagtgttgat cttcttatcc 2461 acagccgtct ctgctgatgt ggggtgctcg gtggacttct caaagaagga gacgagatgc 2521 ggtacagggg tgttcgtcta taacgacgtt gaagcctgga gggacaggta caagtaccat 2581 cctgactccc cccgtagatt ggcagcagca gtcaagcaag cctgggaaga tggtatctgc 2641 gggatctcct ctgtttcaag aatggaaaac atcatgtgga gatcagtaga aggggagctc 2701 aacgcaatcc tggaagagaa tggagttcaa ctgacggtcg ttgtgggatc tgtaaaaaac 2761 cccatgtgga gaggtccaca gagattgccc gtgcctgtga acgagctgcc ccacggctgg 2821 aaggcttggg ggaaatcgta cttcgtcaga gcagcaaaga caaataacag ctttgtcgtg 2881 gatggtgaca cactgaagga atgcccactc aaacatagag catggaacag ctttcttgtg 2941 gaggatcatg ggttcggggt atttcacact agtgtctggc tcaaggttag agaagattat 3001 tcattagagt gtgatccagc cgttattgga acagctgtta agggaaagga ggctgtacac 3061 agtgatctag gctactggat tgagagtgag aagaatgaca catggaggct gaagagggcc 3121 catctgatcg agatgaaaac atgtgaatgg ccaaagtccc acacattgtg gacagatgga 3181 atagaagaga gtgatctgat catacccaag tctttagctg ggccactcag ccatcacaat 3241 accagagagg gctacaggac ccaaatgaaa gggccatggc acagtgaaga gcttgaaatt 3301 cggtttgagg aatgcccagg cactaaggtc cacgtggagg aaacatgtgg aacaagagga 3361 ccatctctga gatcaaccac tgcaagcgga agggtgatcg aggaatggtg ctgcagggag 3421 tgcacaatgc ccccactgtc gttccgggct aaagatggct gttggtatgg aatggagata 3481 aggcccagga aagaaccaga aagcaactta gtaaggtcaa tggtgactgc aggatcaact 3541 gatcacatgg atcacttctc ccttggagtg cttgtgattc tgctcatggt gcaggaaggg 3601 ctgaagaaga gaatgaccac aaagatcatc ataagcacat caatggcagt gctggtagct 3661 atgatcctgg gaggattttc aatgagtgac ctggctaagc ttgcaatttt gatgggtgcc 3721 accttcgcgg aaatgaacac tggaggagat gtagctcatc tggcgctgat agcggcattc 3781 aaagtcagac cagcgttgct ggtatctttc atcttcagag ctaattggac accccgtgaa 3841 agcatgctgc tggccttggc ctcgtgtctt ttgcaaactg cgatctccgc cttggaaggc 3901 gacctgatgg ttctcatcaa tggttttgct ttggcctggt tggcaatacg agcgatggtt 3961 gttccacgca ctgataacat caccttggca atcctggctg ctctgacacc actggcccgg 4021 ggcacactgc ttgtggcgtg gagagcaggc cttgctactt gcggggggtt tatgctcctc 4081 tctctgaagg gaaaaggcag tgtgaagaag aacttaccat ttgtcatggc cctgggacta 4141 accgctgtga ggctggtcga ccccatcaac gtggtgggac tgctgttgct cacaaggagt 4201 gggaagcgga gctggccccc tagcgaagta ctcacagctg ttggcctgat atgcgcattg 4261 gctggagggt tcgccaaggc agatatagag atggctgggc ccatggccgc ggtcggtctg 4321 ctaattgtca gttacgtggt ctcaggaaag agtgtggaca tgtacattga aagagcaggt 4381 gacatcacat gggaaaaaga tgcggaagtc actggaaaca gtccccggct cgatgtggcg 4441 ctagatgaga gtggtgattt ctccctggtg gaggatgacg gtccccccat gagagagatc 4501 atactcaagg tggtcctgat gaccatctgt ggcatgaacc caatagccat accctttgca 4561 gctggagcgt ggtacgtata cgtgaagact ggaaaaagga gtggtgctct atgggatgtg 4621 cctgctccca aggaagtaaa aaagggggag accacagatg gagtgtacag agtaatgact 4681 cgtagactgc taggttcaac acaagttgga gtgggagtta tgcaagaggg ggtctttcac 4741 actatgtggc acgtcacaaa aggatccgcg ctgagaagcg gtgaagggag acttgatcca 4801 tactggggag atgtcaagca ggatctggtg tcatactgtg gtccatggaa gctagatgcc 4861 gcctgggacg ggcacagcga ggtgcagctc ttggccgtgc cccccggaga gagagcgagg 4921 aacatccaga ctctgcccgg aatatttaag acaaaggatg gggacattgg agcggttgcg 4981 ctggattacc cagcaggaac ttcaggatct ccaatcctag acaagtgcgg gagagtgata 5041 ggactttatg gcaatggggt cgtgatcaaa aatgggagtt atgttagtgc catcacccaa 5101 gggaggaggg aggaagagac tcctgttgag tgcttcgagc cttcgatgct gaagaagaag 5161 cagctaactg tcttagactt gcatcctgga gctgggaaaa ccaggagagt tcttcctgaa 5221 atagtccgtg aagccataaa aacaagactc cgtactgtga tcttagctcc aaccagggtt 5281 gtcgctgctg aaatggagga agcccttaga gggcttccag tgcgttatat gacaacagca 5341 gtcaatgtca cccactctgg aacagaaatc gtcgacttaa tgtgccatgc caccttcact 5401 tcacgtctac tacagccaat cagagtcccc aattataatc tgtatattat ggatgaggcc 5461 cacttcacag atccctcaag tatagcagca agaggataca tttcaacaag ggttgagatg 5521 ggcgaggcgg ctgccatctt catgaccgcc acgccaccag gaacccgtga cgcatttccg 5581 gactccaact caccaattac ggacaccgaa gtggaagtcc cagagagagc ctggagctca 5641 ggctttgatt gggtgacgga tcattctgga aaaacagttt ggtttgttcc aagcgtgagg 5701 aacggcaatg agatcgcagc ttgtctgaca aaggctggaa aacgggtcat acagctcagc 5761 agaaagactt ttgagacaga gttccagaaa acaaaacatc aagagtggga ctttgtcgtg 5821 acaactgaca tttcagagat gggcgccaac tttaaagctg accgtgtcat agattccagg 5881 agatgcctaa agccggtcat acttgatggc gagagagtca ttctggctgg acccatgcct 5941 gtcacacatg ccagcgctgc ccagaggagg gggcgcatag gcaggaatcc caacaaacct 6001 ggagatgagt atctgtatgg aggtgggtgc gcagagactg acgaagacca tgcacactgg 6061 cttgaagcaa gaatgctcct tgacaatatt tacctccaag atggcctcat agcctcgctc 6121 tatcgacctg aggccgacaa agtagcagcc attgagggag agttcaagct taggacggag 6181 caaaggaaga cctttgtgga actcatgaaa agaggagatc ttcctgtttg gctggcctat 6241 caggttgcat ctgccggaat aacctacaca gatagaagat ggtgctttga tggcacgacc 6301 aacaacacca taatggaaga cagtgtgccg gcagaggtgt ggaccagaca cggagagaaa 6361 agagtgctca aaccgaggtg gatggacgcc agagtttgtt cagatcatgc ggccctgaag 6421 tcattcaagg agtttgccgc tgggaaaaga ggagcggctt ttggagtgat ggaagccctg 6481 ggaacactgc caggacacat gacagagaga ttccaggaag ccattgacaa cctcgctgtg 6541 ctcatgcggg cagagactgg aagcaggcct tacaaagccg cggcggccca attgccggag 6601 accctagaga ccattatgct tttggggttg ctgggaacag tctcgctggg aatctttttc 6661 gtcttgatga ggaacaaggg catagggaag atgggctttg gaatggtgac tcttggggcc 6721 agcgcatggc tcatgtggct ctcggaaatt gagccagcca gaattgcatg tgtcctcatt 6781 gttgtgttcc tattgctggt ggtgctcata cctgagccag aaaagcaaag atctccccag 6841 gacaaccaaa tggcaatcat catcatggta gcagtaggtc ttctgggctt gattaccgcc 6901 aatgaactcg gatggttgga gagaacaaag agtgacctaa gccatctaat gggaaggaga 6961 gaggaggggg caaccatagg attctcaatg gacattgacc tgcggccagc ctcagcttgg 7021 gccatctatg ctgccttgac aactttcatt accccagccg tccaacatgc agtgaccact 7081 tcatacaaca actactcctt aatggcgatg gccacgcaag ctggagtgtt gtttggtatg 7141 ggcaaaggga tgccattcta cgcatgggac tttggagtcc cgctgctaat gataggttgc 7201 tactcacaat taacacccct gaccctaata gtggccatca ttttgctcgt ggcgcactac 7261 atgtacttga tcccagggct gcaggcagca gctgcgcgtg ctgcccagaa gagaacggca 7321 gctggcatca tgaagaaccc tgttgtggat ggaatagtgg tgactgacat tgacacaatg 7381 acaattgacc cccaagtgga gaaaaagatg ggacaggtgc tactcatagc agtagccgtc 7441 tccagcgcca tactgtcgcg gaccgcctgg gggtgggggg aggctggggc cctgatcaca 7501 gccgcaactt ccactttgtg ggaaggctct ccgaacaagt actggaactc ctctacagcc 7561 acttcactgt gtaacatttt taggggaagt tacttggctg gagcttctct gatctacaca 7621 gtaacaagaa acgctggctt ggtcaagaga cgtgggggtg gaacaggaga gaccctggga 7681 gagaaatgga aggcccgctt gaaccagatg tcggctctgg agttctactc ctacaaaaag 7741 tcaggcatca ccgaggtgtg cagagaagag gcccgccgcg ccctcaagga cggtgtggca 7801 acgggaggcc atgctgtgtc ccgaggaagt gcaaagctga gatggttggt ggagcgggga 7861 tacctgcagc cctatggaaa ggtcattgat cttggatgtg gcagaggggg ctggagttac 7921 tacgccgcca ccatccgcaa agttcaagaa gtgaaaggat acacaaaagg aggccctggt 7981 catgaagaac ccgtgttggt gcaaagctat gggtggaaca tagtccgtct taagagtggg 8041 gtggacgtct ttcatatggc ggctgagccg tgtgacacgt tgctgtgtga cataggtgag 8101 tcatcatcta gtcctgaagt ggaagaagca cggacgctca gagtcctctc catggtgggg 8161 gattggcttg aaaaaagacc aggagccttt tgtataaaag tgttgtgccc atacaccagc 8221 actatgatgg aaaccctgga gcgactgcag cgtaggtatg ggggaggact ggtcagagtg 8281 ccactctccc gcaactccac acatgagatg tactgggtct ctggagcgaa aagcaacacc 8341 ataaaaagtg tgtccaccac gagccagctc ctcttggggc gcatggacgg gcctaggagg 8401 ccagtgaaat atgaggagga tgtgaatctc ggctctggca cgcgggctgt ggtaagctgc 8461 gctgaagctc ccaacatgaa gatcattggt aaccgcattg aaaggatccg cagtgagcac 8521 gcggaaacgt ggttctttga cgagaaccac ccatatagga catgggctta ccatggaagc 8581 tatgaggccc ccacacaagg gtcagcgtcc tctctaataa acggggttgt caggctcctg 8641 tcaaaaccct gggatgtggt gactggagtc acaggaatag ccatgaccga caccacaccg 8701 tatggtcagc aaagagtttt caaggaaaaa gtggacacta gggtgccaga cccccaagaa 8761 ggcactcgtc aggttatgag catggtctct tcctggttgt ggaaagagct aggcaaacac 8821 aaacggccac gagtctgtac caaagaagag ttcatcaaca aggttcgtag caatgcagca 8881 ttaggggcaa tatttgaaga ggaaaaagag tggaagactg cagtggaagc tgtgaacgat 8941 ccaaggttct gggctctagt ggacaaggaa agagagcacc acctgagagg agagtgccag 9001 agttgtgtgt acaacatgat ggggaaaaga gaaaagaaac aaggggaatt tggaaaggcc 9061 aagggcagcc gcgccatctg gtatatgtgg ctaggggcta gatttctaga gttcgaagcc 9121 cttggattct tgaacgagga tcactggatg gggagagaga actcaggagg tggtgttgaa 9181 gggctgggat tacaaagact cggatatgtc ctagaagaga tgagtcgcat accaggagga 9241 aggatgtatg cagatgacac tgctggctgg gacacccgca tcagcaggtt tgatctggag 9301 aatgaagctc taatcaccaa ccaaatggag aaagggcaca gggccttggc attggctata 9361 atcaagtaca cataccaaaa caaagtggta aaggtcctta gaccagctga aaaagggaaa 9421 acagttatgg acattatttc gagacaagac caaaggggga gcggacaagt tgtcacttac 9481 gctcttaaca catttaccaa cctagtggtg caactcattc ggaatatgga ggctgaggaa 9541 gttctagaga tgcaagactt gtggctgctg cggaggtcag agaaagtgac caactggttg 9601 cagagcaacg gatgggatag gctcaaacga atggcagtca gtggggatga ttgcgttgtg 9661 aagccaattg atgataggtt tgcacatgcc cttaggttct tgaatgatat gggaaaagtt 9721 aggaaggaca cacaagagtg gaaaccctca actggatggg acaactggga agaagttccg 9781 ttttgctccc accacttcaa caagctccat ctcaaggacg ggaggtccat tgtggttccc 9841 tgccgccacc aagatgaact gattggccgg gcccgcgtct ctccaggggc gggatggagc 9901 atccgggaga ctgcttgcct agcaaaatca tatgcgcaaa tgtggcagct cctttatttc 9961 cacagaaggg acctccgact gatggccaat gccatttgtt catctgtgcc agttgactgg 10021 gttccaactg ggagaactac ctggtcaatc catggaaagg gagaatggat gaccactgaa 10081 gacatgcttg tggtgtggaa cagagtgtgg attgaggaga acgaccacat ggaagacaag 10141 accccagtta cgaaatggac agacattccc tatttgggaa aaagggaaga cttgtggtgt 10201 ggatctctca tagggcacag accgcgcacc acctgggctg agaacattaa aaacacagtc 10261 aacatggtgc gcaggatcat aggtgatgaa gaaaagtaca tggactacct atccacccaa 10321 gttcgctact tgggtgaaga agggtctaca cctggagtgc tgtaagcacc aatcttaatg 10381 ttgtcaggcc tgctagtcag ccacagcttg gggaaagctg tgcagcctgt gaccccccca 10441 ggagaagctg ggaaaccaag cctatagtca ggccgagaac gccatggcac ggaagaagcc 10501 atgctgcctg tgagcccctc agaggacact gagtcaaaaa accccacgcg cttggaggcg 10561 caggatggga aaagaaggtg gcgaccttcc ccacccttca atctggggcc tgaactggag 10621 atcagctgtg gatctccaga agagggacta gtggttagag gagacccccc ggaaaacgca 10681 aaacagcata ttgacgctgg gaaagaccag agactccatg agtttccac

LOCUS KU729218 10729 bp RNA linear VRL 26-FEB-2016 DEFINITION Zika virus isolate BeH828305 polyprotein gene, complete cds. ACCESSION KU729218 VERSION KU729218.1 GI:998491032 KEYWORDS . SOURCE Zika virus ORGANISM Zika virus Viruses; ssRNA viruses; ssRNA positive-strand viruses, no DNA stage; Flaviviridae; Flavivirus. REFERENCE 1 (bases 1 to 10729) AUTHORS Faria,N.R., Azevedo,R.S.S., Kraemer,M.U.G., Souza,R., Cunha,M.S., Hill,S.C., Theze,J., Bonsall,M.B., Bodeng,T.A., Rissanen,I., Rocco,I.M., Nogueira,J.S., Maeda,A.Y., Vasami,F.G.S., Macedo,F.L.L., Suzuki,A., Rodrigues,S.G., Cruz,A.C.R., Diniz,B.T., Medeiros,D.B.A., Silva,E.V.P., Henriques,D.F., Travassos da Rosa,E.S., Oliveira,C.S., Martins,L.C., Vasconcelos,H.B., Casseb,L.M.N., Simith,D.B., Messina,J., Abade,L., Lourenco,J., Alcantara,L.C., Lima,M., Giovanetti,M., Hay,S.I., Oliveira,R.S., Lemos,P.S., Oliveira,L.F., Lima,C.P.S., Silva,S.P., Vasconcelos,J.M., Cardoso,J.F., Vianez-Junior,J.L.S.G., Mir,D., Bello,G., Delatorre,E., Khan,K., Creatore,M., Coelho,G.E., Oliveira,W.K., Tesh,R., Pybus,O.G., Nunes,M.R.T. and Vasconcelos,P.F.C. TITLE Zika virus in the Americas: early epidemiological and genetic findings JOURNAL Unpublished REFERENCE 2 (bases 1 to 10729) AUTHORS Nunes,M.R.T., Azevedo,R.S.S., Silva,S.P., Vasconcelos,J.M., Cardoso,J.F., Lemos,P.S., Lima,C.P.S., Oliveira,R.S., Faria,N.R., Vianez-Junior,J.L.S.G., Medeiros,D.B.A., Rodrigues,S.G., Diniz,B.T., Silva,E.V.P., Cruz,A.C.R. and Vasconcelos,P.F.C. TITLE Direct Submission JOURNAL Submitted (18-FEB-2016) Center for Technological Innovation, Evandro Chagas Institute, BR 316, Km 07, s/n, Ananindeua, Para 67030-000, Brazil COMMENT EMAIL: [email protected] ##Assembly-Data-START## Assembly method: Mira 4.0 and Geneious 7.0 Sequencing Technology: Ion and 454 Coverage: 659 ##Assembly-Data-END##. FEATURES Location/Qualifiers source 1..10729 /organism="Zika virus" /mol_type="genomic RNA" /isolate="BeH828305" /host="Homo sapiens" /db_xref="taxon:64320" /country="Brazil" /collection_date="2015"

Evandro Chagas Institute has released a full Zika sequence, BeH828305, at Genbank. http://www.ncbi.nlm.nih.gov/nuccore/ku729218 This sequence matches a sequence, ZIkV|NA|BeH818305|Brazil_Maranhao|02-06-2015 cited as from a fatal case in Maranhao as described here http://virological.org/t/zika-virus-in-the-americas-early-epidemiological-and-genetic-findings/220

Tue Mar 1, 2016 10:40am ISTRelated: HEALTHMexico says 11 pregnant women infected with ZikaMEXICO CITY A state health worker walks towards a house to fumigate it as part of preventive measures against the Zika virus and other mosquito-borne diseases in Merida, Mexico, February 4, 2016.REUTERS/LORENZO HERNANDEZ Mexico has confirmed 11 pregnant women are infected with the Zika virus, out of a total of 121 cases, the government said on Monday. Most of the cases were identified in the southern Mexican states of Chiapas and Oaxaca, according to a health ministry report. Eight of the pregnant women are from Chiapas, two are from Oaxaca, and one is from the Gulf coast state of Veracruz, the health ministry reported. The number of cases of infected pregnant women has risen since mid-February, when the health ministry said there were 80 confirmed cases of Zika, including six cases of pregnant women with the virus. Much remains unknown about Zika, including whether the virus actually causes microcephaly, a condition marked by unusually small heads that can result in developmental problems. Brazil said it has confirmed more than 580 cases of microcephaly, and considers most of them to be related to Zika infections in the mothers. Brazil is investigating more than 4,100 additional suspected cases of microcephaly. (Reporting by Joanna Zuckerman Bernstein; Editing by Michael Perry)

Mexico has confirmed 11 pregnant women are infected with the Zika virus, out of a total of 121 cases, the government said on Monday. http://in.reuters.com/article/us-health-zika-mexico-idINKCN0W33CR?feedType=RSS&feedName=health&utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+reuters%2FINhealth+(News+%2F+IN+%2F+Health)

DiscussionThis is the first study to assess the role of Zika virus infection in a large number of patients with Guillain-Barré syndrome diagnosed during a Zika virus outbreak. The serological investigations done on the blood samples from the 42 patients who developed a Guillain-Barré syndrome during the Zika virus outbreak in French Polynesia confirm that all patients had experienced Zika virus infection. Moreover, the presence of IgM (93%) and the information that most patients (88%) reported a transient viral syndrome compatible with Zika virus disease in a median of 6 days before the onset of neurological symptoms, suggested a recent Zika virus infection. Patients with Guillain-Barré syndrome were no longer viraemic for Zika virus at the time of admission, consistent with previous data showing that Zika virus viraemia rarely exceeds 5 days after disease onset.25 However, detection of virus in the urine by RT-PCR could be a valuable alternative.26 Because dengue serotypes 1 and 3 were co-circulating at the time of the Zika virus epidemic,18 we investigated whether dengue infection could have contributed to the occurrence of Guillain-Barré syndrome. Analysis of dengue serology (immunofluorescent assay, microsphere immunoassay, and seroneutralisation) did not support recent dengue infection. Most patients (95%) with Guillain-Barré syndrome had pre-existing dengue immunity, but this did not differ significantly from the control groups. Guillain-Barré syndrome is an acute, immune-mediated polyradiculoneuropathy typically occurring after minor viral and bacterial infections. Motor function is usually affected, beginning distally and progressing proximally over up to a 4-week period.27 Patients have generalised weakness, areflexia, and a varying degree of sensory disturbances and involvement of cranial nerves.28 The risk of Guillain-Barré syndrome increases with age and men are more commonly affected than women.29The pathophysiology is incompletely understood, but is known to mostly occur 2–8 weeks after an infection. Guillain-Barré syndrome is the leading cause of non-traumatic paralysis, with a global incidence of 1–4 per 100 000 persons-years. The range of infections reported to have preceded Guillain-Barré syndrome include upper respiratory infections, notably influenza and pseudo-influenza, digestive tract infections, notably Campylobacter jejuni, as well as cytomegalovirus and Epstein-Barr virus infections.30, 31, 32 The incidence of Guillain-Barré syndrome cases during the French Polynesian outbreak was estimated to be 0·24 per 1000 Zika virus infections, at the lower range of the 0·25 to 0·65 per 1000 observed following C jejuni infections.33 It is unlikely that Guillain-Barré syndrome cases were missed during the study period, because routine procedures for systematic confirmation of diagnosis of Guillain-Barré syndrome pre-existed the Zika virus epidemic, and all cases were systematically referred to the CHPF for diagnosis confirmation. Although it is unknown whether attack rates of Zika virus epidemics will be as high in affected regions in Latin America than in the Pacific Islands (73% in Micronesia6 and 66% in French Polynesia24), high numbers of cases of Guillain-Barré syndrome might be expected in the coming months as the result of this association. The results of our study support that Zika virus should be added to the list of infectious pathogens susceptible to cause Guillain-Barré syndrome. Patients with Guillain-Barré syndrome in our study had electrophysiological findings compatible with the AMAN type. Electromyography assessments done during the first week of the disease showed substantial distal motor nerve conduction alterations, which explain the neuromuscular weakness. Prolonged distal latencies and reduced distal CMAP at admission could have been interpreted as demyelinating conduction slowing and block, leading to the classification of the Guillain-Barré syndrome pattern as acute inflammatory demyelinating neuropathy (AIDP) with possible axonal degeneration. However, the disappearance of the distal motor conduction alterations during the follow-up in a subset of patients, without development of abnormal temporal dispersion or conduction slowing in intermediate nerve segments, was consistent with “reversible conduction failure” already described in AMAN.34, 35 In patients with Guillain-Barré syndrome, such nodal or paranodal dysfunctions would be rather strictly localised in distal motor nerve endings.36The clinical outcome of these patients with Zika virus and Guillain-Barré syndrome was generally favourable, despite a rapid onset and short plateau phase, as has been seen in other patient groups with the AMAN type of Guillain-Barré syndrome.37 3 months after discharge, 24 (57%) patients were able to walk without assistance. Among the molecular mechanisms contributing to the pathogenesis of Guillain-Barré syndrome, a broad range of anti-glycolipid IgG antibodies, notably directed to gangliosides, has been previously described, particularly in axonal variants of the disease.38, 39 Results in this study, using both ELISA and combinatorial microarray techniques, found less than 50% of sera at admission with a significant autoimmune response against glycolipids, including gangliosides or glycolipid complexes (appendix p 10). This low detection rate for the AMAN clinical subtype could be a reflection of the unique nature of the preceding infection and study population, by contrast with more typical postCampylobacter Guillain-Barré syndrome AMAN clinical cohorts. These findings suggest that there might be autoantibodies in this post-Zika virus Guillain-Barré syndrome cohort that cannot be fully identified by current methods. Moreover, complementary analysis of sera with reactivity against GA1 did not show any competition between GA1 and Zika virus proteins, thus suggesting the absence of antigenic mimicry between Zika virus antigens and GA1 in these patients with Guillain-Barré syndrome and casting doubt on the relevance of the anti-GA1 antibodies to neuropathy pathogenesis. The disease might not be anti-glycolipid antibody mediated, but rather be mediated by other autoantibody specificities or unknown neurotoxic factors. Alternatively, viral neurotoxicity might contribute a more direct but as yet unexplained role. Because almost all of the patients with Guillain-Barré syndrome were of Polynesian origin and because distribution of HLA alleles has been previously described as being involved in certain forms of Guillain-Barré syndrome,40 a possible role of ethnicity in triggering Guillain-Barré syndrome was hypothesised. However, the high incidence of Guillain-Barré syndrome recently reported in Brazil, El Salvador, and Colombia during local Zika virus outbreaks11, 41 suggests that, whenever involved, such host factors might not be specific to the ethnic groups living in French Polynesia. In conclusion, this is the first study to document a large series of patients who developed a Guillain-Barré syndrome following Zika virus infection, a virus that previously used to be considered as causing only mild disease. Most (88%) of the patients with Guillain-Barré syndrome reported symptomatic Zika virus infection that preceded the occurrence of neurological symptoms by a median of 6 days. All patients with Guillain-Barré syndrome were of the AMAN type, characterised by distal motor nerve involvement, the absence of typical patterns and levels of anti-glycolipid antibodies, and faster recovery than usually observed in typical Guillain-Barré syndrome. Because Zika virus is spreading rapidly across the Americas, at risk countries need to be prepared to have adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome. Contributors V-MC-L, AB, VC, H-PM, DM, AF, JN, and FG conceived and designed the study. V-MC-L, SL, CR, JV, AT, J-CM, and PD developed, performed, and interpreted the virological analyses. VC, HJW, SKH, LM, and JN developed, performed, and interpreted the immunological analyses. SM, LB, PL, and FG provided care to the patients and designed the clinical report forms. A-LV, CD, AB, and H-PM designed the case report forms and collected the epidemiological data. FG and EF performed the electrophysiological assessments. AB, TD, H-PM, and AF performed the statistical analyses. V-MC-L, AB, VC, HJW, EF, AF, and JN wrote the first version of the report. All authors critically reviewed and approved the final version of the report. Declaration of interests We declare no competing interests. Acknowledgments We are grateful to Maite Aubry (Institut Louis Malardé, Papeete, French Polynesia) for implementing the seroneutralisation assay, and to Maria van Kerkhove and Rebecca Grant for critically reviewing the report. The study received funding from the French Government's Investissement d'Avenir Programme (Labex Integrative Biology of Emerging Infectious Diseases, IBEID, grant number ANR-10-LABX-62-IBEID) and the European Union Seventh Framework Programme (FP7/2007-2013) under grant agreement number 278433-PREDEMICS. The work of SKH and HJW was supported by the Wellcome Trust (grant number 092805). Jump to SectionIntroductionMethodsResultsDiscussionSupplementary MaterialReferencesSupplementary MaterialTitleDescriptionTypeSizeSupplementary appendix pdf1.09 MB

ResultsCases of Zika virus infection were reported weekly from October, 2013, to March, 2014 (figure). The first case of Guillain-Barré syndrome was reported on week 5 of the outbreak, while the peaks of the Zika epidemic and Guillain-Barré syndrome cases were reached on weeks 9 and 12, respectively. In total, 42 cases of Guillain-Barré syndrome were recorded during the Zika virus outbreak. Based on a 66% attack rate of Zika virus infection in the general population, the risk of Guillain-Barré syndrome was estimated to be 0·24 per 1000 Zika virus infections. FigureWeekly cases of suspected Zika virus infections and Guillain-Barré syndrome in French Polynesia between October, 2013, and April, 2014 View Large Image | View Hi-Res Image | Download PowerPoint SlideThe median age of the patients with Guillain-Barré syndrome was 42 years (IQR 36–56) years, 31 (74%) were men, and 38 (90%) were born in French Polynesia. The clinical characteristics of the patients in the Guillain-Barré syndrome group are shown in table 1. Most patients (88%) had a recent history of viral syndrome in a median of 6 days (IQR 4–10) before the onset of neurological manifestations. Rash (81%), arthralgia (74%), and fever (58%) were the most commonly reported symptoms (table 1). Table 1 Clinical characteristics of patients with Guillain-Barré syndrome (n=42) in French Polynesia 2013–14 The main characteristics of the Guillain-Barré syndrome were rapid progression to nadir (median of 6 days [IQR 4–9] between the onset of neurological symptoms to the nadir), and the short plateau phase (median of 4 days [IQR 3–10]). Clinical presentation at hospital admission was manifested by generalised muscle weakness (74%), with incapacity to walk (44%). Facial palsy was common (64%). 39 (93%) patients had increased (>0·52 g/L) protein concentration in the CSF obtained by lumbar puncture. 16 (38%) patients were admitted to intensive care units and 12 (29%) required respiratory assistance. All cases (100%) of Guillain-Barré syndrome received treatment by immunoglobulins, and one (2%) had plasmapheresis. The median duration of hospital stay was 11 days (IQR 7–20) for all patients, and 51 days (16–70) for the 16 patients who were admitted into intensive care. No patients died. 3 months after discharge, 24 (57%) patients were able to walk without assistance. Table 2, Table 3 display the results of virological analyses among patients with Guillain-Barré syndrome and the two control groups. Acute Zika virus infection, as confirmed by a positive RT-PCR result, was observed for all patients in control group 2, but for none of the 41 patients tested in the Guillain-Barré syndrome group (table 2); thus corroborating clinical observations, notably the absence of fever, suggesting that the patients in the Guillain-Barré syndrome group were no longer viraemic at admission. Table 2 Detection of Zika RNA (by RT-PCR), Zika and dengue IgM (by IFA), Zika IgG (MIA), and neutralising antibodies Data are n (%) or n. *RT-PCR was only done for 41 patients with Guillain-Barré syndrome; tested samples for patients with Guillain-Barré syndrome are late samples (around 3 months after admission), except for the RT-PCR (admission sample). ND=not done. IFA=immunofluorescent assay. MIA=microsphere immunoassay.Table 3 Dengue IgG (by microsphere-based immunoassay) and neutralising responses (neut) Data are n (%). *Tested samples for patients with Guillain-Barré syndrome are late samples (±3 months after admission).Recent infection by Zika virus was supported by the detection of anti-Zika virus IgM antibodies in 93% of patients in the Guillain-Barré syndrome group and 17% of patients in control group 1 (table 2). Because possible cross-reactivity between anti-dengue and anti-Zika virus IgM responses had previously been described, immunofluorescent assay was done using the two viruses. In the Guillain-Barré syndrome group, 74% of the patients had IgM against Zika virus but not against dengue. All 19% patients with anti-dengue IgM also had IgM against Zika virus, suggesting that the anti-dengue IgM response could result from cross-reactivity. When combining the results of both anti-Zika virus IgM and IgG, previous occurrence of a Zika virus infection was shown for 41 (98%) patients in the Guillain-Barré syndrome group and 35 (36%) in control group 1 (OR 59·7 [95% CI 10·4–+∞]; p<0·0001; table 4). Moreover, a neutralising response against Zika virus was observed for 100% of patients in the Guillain-Barré syndrome group and 56% in control group 1 (OR 34·1 [95% CI 5·8–+∞]; p<0·0001). Table 4 Zika virus and dengue virus serological patterns associated with Guillain-Barré syndrome Data are n (%), unless otherwise shown. *Tested samples for patients with Guillain-Barré syndrome are late samples (around 3 months after admission).†Adjusted for Zika virus IgG positivity. OR=odds ratio.The interpretation of anti-dengue IgM is difficult because of possible cross-reactivity with anti-Zika virus IgM. Still, there was no indication of increased recent infection with dengue among patients with Guillain-Barré syndrome when compared with the control group 1 (table 2; p>0·05). Past history of dengue was common among patients with Guillain-Barré syndrome (95% on the last sample available, away from the immunological boost associated with recent Zika virus infection) compared with the control group 1 (89%; OR 2·0 [95% CI 0·4–19·9]; p=0·62) and control group 2 (83%; OR 6·0 [95% CI 0·8–269·5]; p=0·10; table 4; appendix p 5). These non-significant differences were further attenuated after stratification by the presence of anti-Zika virus IgG, suggesting that the humoral responses elicited by Zika virus infection also triggered production of anti-dengue IgG (tables 3 and 4). This is corroborated by the examination of Zika virus and dengue IgG responses in the blood samples serially collected from the patients with Guillain-Barré syndrome. The number of patients with anti-Zika virus IgG increased from the earliest to the intermediate and then to the latest sample, whereas the reverse occurred for anti-dengue IgG (appendix pp 5, 6). A possible explanation could be that an anamnestic anti-dengue IgG response in the patients with Guillain-Barré syndrome might have been transiently boosted by the Zika virus infection. Serological tests for Campylobacter jejuni (n=41), HIV (n=42), cytomegalovirus (n=32), Epstein-Barr virus (n=32), and herpes simplex virus type 1 and 2 (n=8) were negative. 37 patients underwent electrophysiological examination during the first week of Guillain-Barré syndrome onset (table 5). Motor nerve conduction study showed the same pattern in all tested nerves, with prolonged distal latencies (p<0·0001) and marked reduction of the distal compound muscle action potential (CMAP) amplitude (p<0·0001), indicative of severe conduction alteration in the distal nerve segments. By contrast, there was no substantial conduction slowing or block in intermediate motor nerve segments (throughout forearm and legs; table 5). Amplitude and conduction velocity of sensitive potentials were not significantly altered in radial and sural nerves (sensory conduction velocity was 49 m/s and 42 m/s, and amplitude was 17·0 μV and 13·7 μV for radial and sural nerves, respectively; p>0·05 for comparison with reference values). Table 5 Evolution of motor nerve conduction parameters (mean values) after onset of Guillain-Barré syndrome 1st week values are compared with reference values; 4th month values are compared with 1st week values of the same subgroup (n=19). DML=distal motor latency. Ampli=amplitude of the distal compound muscle action potential. MCV=motor conduction velocity. *Reference values are as recommended by the American Association of Electrodiagnostic Medicine).†p<0·0001.‡p<0·001.§p<0·05.A second nerve conduction study was done 4 months later including 19 Guillain-Barré syndrome patients for whom a baseline assessment was available (there was no difference in baseline values of the 19 patients with follow-up compared with the 18 without follow-up). By comparison to the first study, results showed a clear improvement of the distal conduction abnormalities (p<0·05) with reduction of the prolonged distal latencies and near normalisation of CMAP amplitudes (table 5;appendix p 8). Together, these findings are suggestive of an acute motor axonal neuropathy (AMAN). By ELISA, at admission, sera from 13 (31%) patients with Guillain-Barré syndrome showed a positive reactivity (>50% binding) against different glycolipids (table 6; appendix p 7). Ten (24%) patients had an equivocal percentage of binding (30–50%). Among these 23 patients, 17 had a reactivity directed toward glycolipid GA1 (eight positive, nine equivocal) and it was either isolated or shared with other glycolipids (appendix p 7). At 3 months, the proportion of reactive sera had slightly increased (48%). Controls were negative (n=20). These results were heterogeneous and low intensity for 50% of them. Table 6 Positive (>50%) reactivity to glycolipids in sera of patients with Guillain-Barré syndrome (n=42) and controls (n=20) in French Polynesia 2013–14 Data are n (%). *Blood donors.Western blot was used to test the reactivity against Zika virus proteins in the serum from six patients with Guillain-Barré syndrome, four with high reactivity against GA1 (patients 6, 11, 20, and 29 as shown in the appendix [p 7]]), and two patients with no reactivity against GA1 (patients 13 and 27 as shown in the appendix [p 7]]). All sera showed intense reactivity with viral proteins regardless of their reactivity towards GA1 (appendix p 9). The reactivity of serum number 20 towards Zika virus proteins was not inhibited even at the highest GA1 amount (600 μg; appendix p 9). We further tested serum number 6 and did not observe any competition with a GA1 amount of 300 μg (data not shown). Combinatorial microarrays were used to screen glycolipid complexes as antigens. Most serum samples tested were negative or had low level binding to some single or heteromeric glycolipid complex. Notably, antibodies against GA1–sulphatide complex were frequently observed (19/41; 46%) in patient sera, with intermediate binding intensities, above the threshold of positivity (p=0·001). Additionally, a substantial number of patient sera had antibodies raised against GA1 in complex with cholesterol or phosphatidylserine or both, although most were of low binding intensity (appendix p 10).

MethodsStudy design and participantsIn this case-control study, cases were patients with Guillain-Barré syndrome who were diagnosed at the Centre Hospitalier de Polynésie Française (CHPF) in Papeete, Tahiti, French Polynesia, during the outbreak period. As routine, all patients with suspicion of Guillain-Barré syndrome in French Polynesia are referred to the CHPF for diagnosis confirmation. All patients included in this study were diagnosed as developing a Guillain-Barré syndrome by neurologists or staff in intensive care units according to international criteria.19 Clinical and demographic data were collected from medical records obtained during patients' hospital stay. The data recorded for all patients included patient's age, sex, island of residence, medical history and comorbidities, clinical signs and symptoms, and illness duration and severity. Electrophysiological assessment was done for all patients by standard electromyography techniques including motor nerve conduction studies of the median nerve (recording of the abductor pollicis brevis), the ulnar nerve (recording of the abductor digiti minimi), and the peroneal nerve (recording of the extensor digitorum brevis), as well as sensory nerve conduction studies in radial and sural nerves. To estimate the proportion of Zika virus infections in the general population, to be further compared with the series of Guillain-Barré syndrome, a first control group (control group 1; n=98) was recruited among patients in hospital or consulting for, non-febrile illness at the CHPF. Patients from the control group 1 were matched for age (within a 10-year margin), sex, and island of residence with patients in the Guillain-Barré syndrome group. Each patient in control group 1 had a blood sample taken about 7 days from the admission date of the matching Guillain-Barré syndrome case. To investigate a possible role of past dengue infection in developing Guillain-Barré syndrome in a Zika virus infected patient, a second control group (control group 2; n=70) was recruited among age-matched (within a 10-year margin) patients with RT-PCR-confirmed Zika virus infection, but who did not develop any neurological complication. The epidemic curve of Zika virus in French Polynesia was obtained by extrapolating data from a sentinel network of clinicians who have been reporting the number of suspected Zika virus cases on a weekly basis from October, 2013, until April, 2014, to the Bureau de Veille Sanitaire–Direction de la Santé de Polynésie Française (Papeete, Polynésie Française). The study protocol was approved by the Comité d'Ethique de la Polynésie Française (N°69/CEPF 2014), and all patients provided informed consent for their participation in the study. ProceduresIn the Guillain-Barré syndrome group, a first blood sample was collected at hospital admission and one to three additional blood samples were collected 3 weeks, 2 months, and 3 months later. In control group 1, the blood sample was collected within a 7-day period from the indexed Guillain-Barré syndrome case for 59 (60%) patients, and with a median period of 13 (IQR 9–16) days for the remaining controls. Diagnosis of Zika virus acute infection in patients in the Guillain-Barré syndrome group and control group 2 was done with a Zika virus specific RT-PCR protocol adapted from Lanciotti and colleagues.20 Serum was considered positive for Zika virus if the two distinct genomic regions targeted by the RT-PCR were amplified. Detection of IgM against Zika virus and dengue virus in blood samples from patients in the Guillain-Barré syndrome group and control group 1 was done with indirect immunofluorescent assay on Vero cells (African green monkey kidney cells) infected with either Zika virus [PF13-251013-18] or dengue virus [D1-Hawaii 1944]. Detection of IgG against Zika virus and each of the four dengue serotypes was done on blood samples from patients in the Guillain-Barré syndrome group, control group 1, and control group 2 using a recombinant-antigen-based microsphere immunoassay adapted from Beck and colleagues (appendix).21 Detection of neutralising antibodies against Zika virus and each of the four dengue serotypes was done for patients in the Guillain-Barré syndrome group and control group 1 by microseroneutralisation assay done on Vero cells inoculated with serial dilutions of each serum previously incubated with titrated Zika virus [PF13-251013-18] or dengue serotype 1 to 4 strains that were isolated during previous outbreaks in French Polynesia (appendix). The sera from patients in the Guillain-Barré syndrome group (n=42 at admission, n=31 at 3 months) and healthy blood donors (collected before April, 2013; n=20) were tested by ELISA (Bühlmann-Gangliocombi, Schönenbuch, Switzerland) for IgG or IgM reactivity to the glycolipids GM1, GA1, GM2, GD1a, GD1b, and GQ1b at 1:100 dilution. As per kit instructions, results were considered as positive, equivocal, and negative when showing more than 50%, 30–50%, and less than 30% binding, respectively. Sera (n=41 at admission, n=27 at 3 months) were also tested by a combinatorial microarray screening method based on a refinement and miniaturisation of previous published combinatorial glycoarray assay22 (appendix). The sera from six patients showing high reactivity towards GA1 were tested against Zika virus proteins by western blot (appendix). Molecular mimicry was assessed using the method by Neil and colleagues (appendix).23 Statistical analysisThe primary objectives of this study were to determine the association between Guillain-Barré syndrome and Zika virus infection in French Polynesia and to determine whether possible co-infection or pre-existing immunity to dengue (and a specific dengue serotype) seem to facilitate the development of Guillain-Barré syndrome. With two controls per case, and on the assumption that 70% of patients with Guillain-Barré syndrome and 40% of controls reported a recent Zika virus infection, the statistical power to detect a difference between the Guillain-Barré syndrome group and the control group was calculated to be 86%. The risk of developing Guillain-Barré syndrome per Zika virus infection was calculated by dividing the total estimated number of cases of Guillain-Barré syndrome reported in French Polynesia (n=42) by the total number of people infected by Zika virus during the epidemic period. This latter number was calculated by multiplying the attack rate (66%) estimated during a post-epidemic population-based serological survey24 by the total population of French Polynesia (268 270 inhabitants; 2012 census). The association between Zika virus positive serology, dengue positive serology, and Guillain-Barré syndrome was analysed with exact conditional logistic regression. Because the humoral response elicited by acute Zika virus infection might trigger production of anti-dengue virus IgG related to past dengue infections, we adjusted the odds ratio (OR) describing the association between anti-dengue IgG and Guillain-Barré syndrome for the presence of anti-Zika virus IgG. All ORs are given with 95% CIs. Motor nerve conduction parameter values were compared with reference values using one-sample ttests, and 1st week values were compared with 4th month values using Wilcoxon matched pairs signed rank sum tests. First week values of the 19 patients with electrophysiological measurements at 4th month were compared to those of the 18 patients without follow-up using a Mann-Whitney Utest. Data were collected with EpiData 3.1 software and were analysed with Stata 14 (StataCorp LP Lakeway, TX, USA). Role of the funding sourceThe funders had no role in the study design, data collection, data analysis, data interpretation, or writing of the report. The corresponding author had full access to all the data in the study, except for the results of the combinatorial microarray (SKH and HJW), and had final responsibility for the decision to submit the publication.

SummaryBackgroundBetween October, 2013, and April, 2014, French Polynesia experienced the largest Zika virus outbreak ever described at that time. During the same period, an increase in Guillain-Barré syndrome was reported, suggesting a possible association between Zika virus and Guillain-Barré syndrome. We aimed to assess the role of Zika virus and dengue virus infection in developing Guillain-Barré syndrome. MethodsIn this case-control study, cases were patients with Guillain-Barré syndrome diagnosed at the Centre Hospitalier de Polynésie Française (Papeete, Tahiti, French Polynesia) during the outbreak period. Controls were age-matched, sex-matched, and residence-matched patients who presented at the hospital with a non-febrile illness (control group 1; n=98) and age-matched patients with acute Zika virus disease and no neurological symptoms (control group 2; n=70). Virological investigations included RT-PCR for Zika virus, and both microsphere immunofluorescent and seroneutralisation assays for Zika virus and dengue virus. Anti-glycolipid reactivity was studied in patients with Guillain-Barré syndrome using both ELISA and combinatorial microarrays. Findings42 patients were diagnosed with Guillain-Barré syndrome during the study period. 41 (98%) patients with Guillain-Barré syndrome had anti-Zika virus IgM or IgG, and all (100%) had neutralising antibodies against Zika virus compared with 54 (56%) of 98 in control group 1 (p<0·0001). 39 (93%) patients with Guillain-Barré syndrome had Zika virus IgM and 37 (88%) had experienced a transient illness in a median of 6 days (IQR 4–10) before the onset of neurological symptoms, suggesting recent Zika virus infection. Patients with Guillain-Barré syndrome had electrophysiological findings compatible with acute motor axonal neuropathy (AMAN) type, and had rapid evolution of disease (median duration of the installation and plateau phases was 6 [IQR 4–9] and 4 days [3–10], respectively). 12 (29%) patients required respiratory assistance. No patients died. Anti-glycolipid antibody activity was found in 13 (31%) patients, and notably against GA1 in eight (19%) patients, by ELISA and 19 (46%) of 41 by glycoarray at admission. The typical AMAN-associated anti-ganglioside antibodies were rarely present. Past dengue virus history did not differ significantly between patients with Guillain-Barré syndrome and those in the two control groups (95%, 89%, and 83%, respectively). InterpretationThis is the first study providing evidence for Zika virus infection causing Guillain-Barré syndrome. Because Zika virus is spreading rapidly across the Americas, at risk countries need to prepare for adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome. FundingLabex Integrative Biology of Emerging Infectious Diseases, EU 7th framework program PREDEMICS. and Wellcome Trust. Jump to SectionIntroductionMethodsResultsDiscussionSupplementary MaterialReferencesIntroductionZika virus is an arthropod-borne virus (arbovirus) in the genus Flavivirus, family Flaviviridae.1 Zika virus was first isolated from a Rhesus macaque in 1947 in the Zika forest of Uganda;2 the monkey had been brought in the country by researchers as an experimental animal. The first human infection was reported in Nigeria in 1954.3 Like dengue virus and chikungunya viruses, Zika virus adapted from an ancestral transmission cycle involving non-human primates and a broad spectrum of canopy dwelling mosquito species as vectors to an urban–periurban cycle involving humans as reservoirs and the widely distributed Aedes (Stegomyia) mosquitoes as vectors.4 Since the 1950s, Zika virus has only been reported as circulating sporadically in Africa and southeast Asia.5 In 2007, Zika virus was isolated for the first time in the Pacific, on the Micronesian island of Yap.6 Between October, 2013, and April, 2014, French Polynesia experienced the largest Zika outbreak ever reported at that time.7 More than 32 000 patients were assessed for suspected Zika virus infection, with a weekly incidence peaking on week 9 of the outbreak.8 Since 2014, Zika virus has spread to other Pacific islands, notably Easter Island (Chile). In March, 2015, Brazil reported autochthonous transmission of Zika virus,9 and an outbreak was declared 6 months later.10 As of Feb 1, 2016, Zika virus had emerged in 25 countries and territories in South or Central America, with alarming reports of microcephaly cases among neonates in Brazil.11 Before the French Polynesian outbreak, Zika virus infection used to be described as a mild febrile illness with clinical symptoms including maculopapular rash, joint and muscle pain, headache, and non-purulent conjunctivitis.6 Between November, 2013, and February, 2014, in French Polynesia, 42 patients presented at hospital with Guillain-Barré syndrome, an autoimmune disease causing acute, or subacute flaccid paralysis, contrasting with reports of five, ten, three, and three, in 2009, 2010, 2011, and 2012, respectively.12 Other arboviral diseases like West Nile, Japanese encephalitis, chikungunya, and dengue had already been reported to sometimes cause Guillain-Barré syndrome,13, 14, 15, 16 but only during the outbreak in French Polynesia was this severe neurological complication first described to be associated with Zika virus infection.17 The temporal coincidence between the peaks in incidence of Zika virus and cases of Guillain-Barré syndrome, and also the concurrent circulation of dengue serotypes 1 and 318 suggested a possible causal relation between the three events. Using two control series, we address the hypothesis that Zika virus infection with or without dengue concurrent or sequential infection could be a risk factor for the development of Guillain-Barré syndrome.

Research in context Evidence before this study The ongoing Zika virus disease epidemic in Latin America is the largest epidemic ever recorded. On Feb 1, 2016, the WHO declared the suspected link between Zika virus and neurological disorders and neonatal malformations a Public Health Emergency of International Concern. The WHO Secretariat briefed the Emergency Committee convened by the Director General on the clusters of microcephaly and Guillain-Barré syndrome that have been temporally associated with Zika virus transmission in some settings, including French Polynesia, and urged further research to be conducted to confirm the link between Zika virus and these complications. We searched MEDLINE from Jan 1, 1990, to Feb 14, 2016, for evidence linking Zika virus and Guillain-Barré syndrome. The simultaneous occurrence of Zika virus and Guillain-Barré syndrome outbreaks has been reported in few studies in French Polynesia and Brazil, but only one case report provided serological evidence linking one patient with Guillain-Barré syndrome to recent Zika virus infection in French Polynesia in November, 2013. We provide here a complete description of a series of 42 cases of Guillain-Barré syndrome in French Polynesia, and serological evidence linking these cases to recent Zika virus infection. Added value of this study This is the first study to document a large series of patients who developed a Guillain-Barré syndrome following Zika virus infection, a virus that was previously considered to cause only mild disease. This study not only confirms the link between Zika virus infection and Guillain-Barré syndrome, but also provides useful findings regarding the clinical characteristics of the Guillain-Barré syndrome cases: most had electrophysiological findings compatible with the acute motor axonal neuropathy (AMAN) type of the syndrome, and had rapid evolution of the disease. The clinical outcome of these patients with Zika virus and Guillain-Barré syndrome was generally favourable, despite a rapid onset and short plateau phase, as may be seen in other patient groups suffering from the AMAN type of Guillain-Barré syndrome. No clear pathophysiological mechanism for the Guillain-Barré syndrome could be identified, because the typical AMAN-associated anti-ganglioside antibodies were rarely present. We also speculated whether past dengue history might have contributed to the development of Guillain-Barré syndrome, but could not find any evidence for it. Implications of all the available evidence The results of our study support that Zika virus should be added to the list of infectious pathogens susceptible to cause Guillain-Barré syndrome. As Zika virus is spreading rapidly across the Americas, at risk countries need to be prepared to have adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome.

Van-Mai Cao-Lormeau, PhD†, Alexandre Blake, MD†, Sandrine Mons, MSc, Stéphane Lastère, PharmD, Claudine Roche, MSc, Jessica Vanhomwegen, PhD, Timothée Dub, MPH, Laure Baudouin, MD, Anita Teissier, Philippe Larre, MD, Anne-Laure Vial, MSc, Christophe Decam, MD, Valérie Choumet, PhD, Susan K Halstead, PhD, Prof Hugh J Willison, PhD, Lucile Musset, PhD, Jean-Claude Manuguerra, PhD, Prof Philippe Despres, PhD, Prof Emmanuel Fournier, PhD, Henri-Pierre Mallet, MD, Didier Musso, MD, Prof Arnaud Fontanet, DrPH†, Jean Neil, MD†, Frédéric Ghawché, MD††Contributed equallyPublished Online: 29 February 2016

Guillain-Barré Syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control studyhttp://www.thelancet.com/journals/lancet/article/PIIS0140-6736(16)00562-6/fulltext

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2nd Zika case in N.J. confirmed; CDC expands travel warning 1 / 9 The mosquito is a vector for the proliferation of the Zika virus currently spreading throughout Latin America. The main type isn't native to the United States - but an invasive species, the Asian Tiger mosquito, is. (AP Photo/Felipe Dana)Kathleen O'Brien | NJ Advance Media for NJ.com PrintEmailBy Kathleen O'Brien | NJ Advance Media for NJ.com Email the author | Follow on Twitter on February 29, 2016 at 5:52 PM A second travel-related case of the Zika virus was confirmed by federal health officials late last week, the N.J. Department of Health said today. The newest case involved a woman in Hudson County who had acquired the virus while visiting Honduras. "There is no public health risk because the woman was exposed to mosquitoes in Honduras," the state department of health statement indicated. That statement did not indicate the woman's age or town. Several studies are underway in Zika outbreak countries to see if the mosquito-borne virus is the actual case. (AP Photo/Felipe Dana) The state's first travel-related case was last December, when a woman who had been exposed to the virus in Colombia got sick when she was visiting Bergen County. She fully recovered and returned Colombia. The Zika virus is mainly transmitted from mosquitoes. It is not spread from person-to-person except by sexual relations. In the meantime, the U.S. Centers for Disease Control and Prevention added two more Caribbean countriesto its list of destinations that pregnant women should avoid: St. Vincent and the Grenadines & Sint Maarten. The virus produces no symptoms in most of the people exposed to it. Those who do get sick usually have a mild illness with fever, rash, and "pink eye." However, the situation is far more dire for pregnant women, whose developing fetuses are now thought to be extremely vulnerable to the virus. A spike in the number of cases of microcephaly, or an abnormally small head, started turning up in Brazil at the end of last year. The CDC as well as other researchers are trying to determine whether the virus - relatively new to South America - definitively causes birth defects. State health officials, including Acting Commissioner Cathleen Bennett and State Epidemiologist Tina Tan will talk about the Zika virus later this week at Montclair State University, where a group is scheduled to travel to Brazil next month.1"New Jersey does not expect to see Zika outbreaks based on many years of mosquito control and monitoring in partnership with the New Jersey Department of Environmental Protection and local government," Tan said. If you cancel a trip over Zika fears, can you get a refund? Even though there is a health travel advisory urging pregnant women to avoid travel to countries where the Zika virus is being transmitted, that might not suffice for a vacation refund. The main mosquito that transmits Zika isn't prevalent in New Jersey - although it can make a limited appearance here during the summer. A second mosquito that is more common in New Jersey can also transmit Zika - but doesn't naturally prefer to bite humans, according to entomologists. Tan also pointed out that the United States' experience with other mosquito-borne viruses like dengue and chikungunya have been largely travel-imported cases that have not led to widespread outbreaks. Kathleen O'Brien may be reached at [email protected]. Follow her on Twitter @OBrienLedger. Find NJ.com on Facebook. http://www.nj.com/healthfit/index.ssf/2016/02/2nd_zika_case_in_nj_confirmed.html?utm_source=twitterfeed&utm_medium=twitter

A second travel-related case of the Zika virus was confirmed by federal health officials late last week, the N.J. Department of Health said today. The newest case involved a woman in Hudson County who had acquired the virus while visiting Honduras. http://www.nj.com/healthfit/index.ssf/2016/02/2nd_zika_case_in_nj_confirmed.html?utm_source=twitterfeed&utm_medium=twitter

Fifth Pennsylvanian diagnosed with Zika virusFebruary 29, 2016 4:21 PM James Gathany/Centers for Disease Control and Prevention via AP By Adam Smeltz / Pittsburgh Post-GazetteAnother person in Pennsylvania has been diagnosed with the Zika virus, marking five confirmed cases since the state Department of Health began releasing regular reports last month, health officials said this afternoon. The latest case appeared to be in Philadelphia, where the local health department announced the first known case of Zika in a city resident there. A woman more than 60 years old is recovering from the mosquito-borne virus after a trip to the Caribbean, where an epidemic of the virus is underway, the local department said. “She was not hospitalized for infection and is presently recovering without complications,” the Philadelphia Department of Public Health said in a statement. Nationwide, doctors have diagnosed more than 100 travel-associated Zika cases since early last year, according to the Atlanta-based Centers for Disease Control and Prevention. In the United States, the illness typically appears in people who have visited Central America, South America and other regions abroad affected by an outbreak that began last May. State health officials have not confirmed the locations of Zika patients in Pennsylvania, although the Allegheny County Health Department has reported none in the county. Lehigh University in Bethlehem announced Feb. 10 that a student there had recovered from the virus after traveling abroad. Meanwhile, 148 people in Pennsylvania are awaiting results from Zika blood tests, up from 124 at the same time last week, according to a weekly update from the state. Thirty-seven people in Allegheny County have been approved for the testing, up from 27 a week ago, said Kristen Mertz, a medical epidemiologist with the county. Although most people infected with the virus show no symptoms, the signs can include a fever, rash and joint pain that last about a week. Risks may be greater for infected pregnant women, who have seen rising rates of birth defects in outbreak-affected areas. “We really encourage pregnant women to postpone travel to Zika-affected areas,” Dr. Mertz said. She also advised pregnant women to abstain from unprotected sex from men who have traveled to those areas. Zika transmission through sexual intercourse and blood transfusions is possible, but researchers blame most human cases on bites from Zika-infected mosquitoes. No mosquitoes carrying the virus have been detected in the U.S. The CDC processes Zika blood tests for patients nationwide. It can take up to two weeks from the time of a blood drawing for test results to emerge. Adam Smeltz: [email protected], 412-263-2625 or on Twitter @asmeltz. http://www.post-gazette.com/news/health/2016/02/29/Fifth-Pennsylvanian-diagnosed-with-Zika-virus/stories/201602290173

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Eighth Zika virus case confirmed in Houston areaKHOU Staff, KHOU.com3:56 p.m. CST February 29, 2016(Photo: KHOU) CONNECTTWEETLINKEDINCOMMENTEMAILMOREHOUSTON -- Another case of the Zika virus has been confirmed in the Houston area, bringing the total to eight. Houston Health Department officials confirm a little girl who recently traveled to Honduras has been diagnosed with Zika. She is the fourth patient in Houston with the virus. Four other Zika virus cases have been confirmed in Harris County. http://www.khou.com/story/news/health/2016/02/29/eighth-zika-virus-case-confirmed-houston-area/81122650/

ZIKA VIRUS UPDATE http://www.houstontx.gov/health/Epidemiology/Zika_Virus.html Monday, February 29, 2016 GenderAge RangeTravel HistoryTravel MonthConfirmation DateCase Status by CDCFemale60-64Colombia11/1512/22/2015Confirmed PositiveMale35-39Honduras12/1501/28/2016Confirmed PositiveFemale40-45Honduras12/151/29/2016Confirmed PositiveFemale0-10HondurasUnknown2/22/2016Confirmed Positive

http://www.houstontx.gov/health/Epidemiology/Zika_Virus.html ZIKA VIRUS UPDATE Monday, February 29, 2016 GenderAge RangeTravel HistoryTravel MonthConfirmation DateCase Status by CDCFemale60-64Colombia11/1512/22/2015Confirmed PositiveMale35-39Honduras12/1501/28/2016Confirmed PositiveFemale40-45Honduras12/151/29/2016Confirmed PositiveFemale0-10HondurasUnknown2/22/2016Confirmed Positive

Zika Virus InformationAs of February 29, 2016 there are no confirmed cases of Zika virus in South Carolina.

Alabama Residents Tested for Zika Virus as of February 29, 2016 Number Tested PositiveNumber of SubmissionsNumber with Results Pending1 27 23

New tally page http://www.adph.org/mosquito/index.asp?id=7427