species of virus
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- ... microcephaly is only one possible adverse outcome among a spectrum of conditions that may be part of congenital Zika syndrome. A population-level increase in central nervous system anomalies has been observed in both French Polynesia and Brazil.
- The current Zika virus (ZIKV) outbreak is associated with neurological malformations and disorders in neonates. Areas of increased incidence of malformations may overlap with dengue-hyperendemic areas. ZIKV infection is enhanced by antibodies against dengue virus (DENV) in cell culture and inbred mice. Sufficiently powered clinical studies or primate studies addressing the enhancement of fetal ZIKV infection after previous dengue infection are not available. The human placenta is susceptible to ZIKV in vitro, but it is unknown whether antibody-dependent enhancement of ZIKV infection occurs at the placental barrier. Here we studied ZIKV infection in placental tissue in the presence of DENV-immune sera. Explants from the amniochorionic membrane, the chorionic villi, and the maternal decidua were infected with ZIKV in the presence of DENV type 1-, 2-, or 4-immune sera, or controls. Presence of DENV antibodies of any type enhanced the percentage of successful infections of organ explants between 1.42- and 2.67-fold, and led to a faster replication as well as significantly increased virus production. No enhancement was seen with yellow fever or chikungunya virus control sera. Pre-existing DENV antibodies may pose an increased risk of trans-placental ZIKV transmission.
- Kyra Hermanns, Claudia Göhner, Anne Kopp, Andre Schmidt, Waltraut M. Merz, Odo R. Markert, Sandra Junglen, and Christian Drosten: (2018). "Zika virus infection in human placental tissue explants is enhanced in the presence of dengue virus antibodies in-vitro". Emerging Microbes & Infections 7 (1): 1–8. ISSN 2222-1751. DOI:10.1038/s41426-018-0199-6.
- Zika virus (ZIKV) was discovered in Africa in 1947 and was first detected in Asia in 1966, yet its potential effect on public health was not recognized until the virus caused outbreaks in the Pacific from 2007 to 2015 and began spreading throughout the Americas in 2015. ... The ability of ZIKV to cause congenital defects in fetuses and infants, as exemplified by the microcephaly epidemic in Brazil, is an unprecedented feature in a mosquito-borne viral infection. ... Although transmission of ZIKV has declined in the Americas, outbreaks and infection clusters continue to occur in some regions, such as India and Southeast Asia, where there are large populations of women of childbearing age who are susceptible to the virus.
- The Zika virus protease NS2B-NS3 catalyses the processing of the viral precursor polyprotein as an essential step during viral replication. Since the epidemic Zika virus outbreak in the Americas, several inhibitors of this protease have been reported. Substrate-derived peptides revealed important structural information about the active site, whilst more drug-like small molecules have been discovered as allosteric inhibitors.
- We recently developed a chimeric flavivirus vaccine technology based on the novel insect-specific Binjari virus (BinJV) and used this to generate a chimeric ZIKV vaccine (BinJ/ZIKA-prME) that protected IFNAR-/- dams and fetuses from infection. Herein, we show that a single vaccination of IFNAR-/- mice with unadjuvanted BinJ/ZIKA-prME generated neutralizing antibody responses that were retained for 14 months. At 15 months post vaccination, mice were also completely protected against detectable viremia and substantial body weight loss after challenge with ZIKVPRVABC59. BinJ/ZIKA-prME vaccination thus provided long-term protective immunity without the need for adjuvant or replication of the vaccine in the vaccine recipient, both attractive features for a ZIKV vaccine.