Zika  Virus:  Frequently  Asked  Questions    

} How  is  Zika  virus  transmitted?  o Zika  virus  is  an  arthropod-­‐borne  virus  transmitted  to  

humans  by  female  Aedes  mosquitoes  o Zika  may  also  be  transmitted  through  sexual  contact,  

blood  transfusion,  and  perinatal  exposure  } How  is  Zika  infection  confirmed?  

} Who  should  be  tested?  o Symptomatic  individuals  or  asymptomatic  individuals  

with  history  of:  § Recent  travel  to  endemic  area(s)  § Sexual  contact  with  a  potentially  infected  

partner  } Which  insect  repellents  are  most  effective?  

o EPA  approved  repellants  containing  DEET,  picaridin,  or  IR3535  

o Most  effective  against  Aedes  mosquitoes  (Consumer  Reports):  

} Does  Zika  cause  microcephaly  or  Guillain-­‐Barré  syndrome  (GBS)?  What  is  the  risk?  

o WHO:  Zika  virus  is  neurotropic.  It  is  highly  likely  that  Zika  virus  causes  microcephaly,  Guillain-­‐Barré  syndrome,  and  other  neurologic  conditions.  The  risk  of  these  conditions  has  not  yet  been  quantified,  and  the  

biologic  mechanism  is  not  yet  clear.  

 

Picaridin  20%    (Sawyer  Fisherman’s  Formula,  Natrapel  8  Hour)  DEET  25%    (Off!  Deepwoods  VIII)  

Status  Update  

Cases  as  of  March  16,  2016  

US  States  

Travel-­‐associated  Zika  virus  disease          cases  reported:  258    

Locally  acquired  vector-­‐borne  cases  reported:  0  

US  Territories  

Travel-­‐associated  cases  reported:  3  

Locally  acquired  cases  reported:  283  

Global  

Documented  transmission  in  59  countries  and  territories  since  2007  

Vaccine  Development  

14  companies  working  on  various  projects  in  US,  France,  Brazil,  India,  and  Austria  

Trials  expected  to  begin  Summer,  2016:  

DNA  vaccines:  NIH  (US),  Inovio  (Canada)  

Inactivated  virus:  Bharat  Biotech  (India)  

Blood  or  serum  samples  should  be  sent  directly  to  CDC  for  RT-­‐PCR  testing  

Additional  evidence  for  Zika  virus  association  with  microcephaly  and  Guillain-­‐Barre  Syndrome  

Zika  Virus:  Frequently  Asked  Questions  

Why  are  RNA  viruses  so  dangerous?  

Virally  coded  RNA  polymerases  do  not  perform  exonuclease  (proofreading)  functions  and  allow  for  a  multitude  of  genetic  mutations.  This  characteristic  provides  RNA  viruses  the  capability  to  rapidly  adapt  to  different  environments.  

All  flaviviruses  have  similar  antigenic  sites,  which  are  the  sites  recognized  by  antibodies.  However,  the  ability  of  an  antibody  to  recognize  and  bind  to  different  types  of  flaviviruses  depends  on  the  degree  of  similarity.  Cross-­‐neutralization  

and  cross-­‐protection  occurs  more  robustly  among  flaviviruses  with  very  similar  amino  acid  sequences,  called  a  “serocomplex”.  Antibody-­‐mediated  protection  lasts  longer  against  viruses  within  the  same  serocomplex  versus  those  of  greater  antigenic  variation.  Examples  of  highly  similar  flavivirus  antigens  include  those  of  the  dengue  viruses  whereas  the  

yellow  fever  virus  is  more  distantly  related.  

Vaccines  are  currently  available  for  yellow  fever,  tick-­‐borne  encephalitis,  and  Japanese  encephalitis.  A  vaccine  against  Dengue  virus  was  approved  in  Mexico  (Sanofi  Pasteur;  Dec.  2016)  

 

What  are  other  RNA  viruses?  

Ebola,  SARS,  Influenza,  Hepatitis  C,  West  Nile,  Polio,  Measles  

What  are  other  arboviral  diseases?  

West  Nile,  La  Crosse  encephalitis,  Eastern  equine  encephalitis  

FYI  Zika  virus  is  a  single-­‐stranded  RNA  virus.  It  is  an  arbovirus  from  the  flaviviridae  family.  There  are  over  70  different  flaviviruses  and  the  most  common  include:  Dengue,  yellow  fever,  Japanese  encephalitis,  tick-­‐borne  encephalitis,  and  West  Nile.  

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How  does  a  flavivirus  replicate  in  a  host?  A  flavivirus  gains  entrance  into  a  host  cell  by  binding  to  certain  proteins  on  the  cell  membrane  followed  by  

endocytosis  (1).  Fusion  of  the  viral  envelope  proteins  with  the  endosome  membrane  releases  the  viral  RNA,  which  is  then  replicated  and  translated  using  host  cellular  machinery  on  the  surface  of  the  endoplasmic  reticulum  (2).  The  new  viral  proteins  and  replicated  RNA  traffic  through  the  host  golgi  apparatus  and  to  the  cell  membrane  where  the  new  virus  leaves  the  cell  via  exocytosis  (3).  Host  antibodies  may  bind  to  and  neutralize  the  virus  (4)  or  may  facilitate  infection  

by  enhancing  entrance  into  host  cells  (5),  known  as  antibody-­‐dependent  enhancement  (ADE).