Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04
  • 2024-05
  • The ZIKV field is still

    2018-11-09

    The ZIKV field is still developing, and critics regarding the use of the original ZIKV strain are starting to emerge. There is currently no appropriate African and Asian reference strains to allow proper comparison of results between laboratories. At this stage, we cannot disregard that the differences observed in our study are due to intrinsic abilities or differences in infectivity of these two ZIKV strains. Whether this difference could be explained by envelope variants and/or receptor usage or later in the replication purchase apexbio dilution will be the aim of future studies. One caveat of our study is the few number of African and Asian strains used that did not allow us to address a general conclusion regarding differences between ZIKV lineages. However, our work address the important concern that circulating African ZIKV strains must be closely followed and that ZIKV strains could have different molecular patterns. Studies need to investigate the neurotropism and neurovirulence of more circulating ZIKV AF strains versus AS strains in order to establish their replication and cellular response abilities. It is not unlikely that ZIKV outbreaks occurred recently in Africa and remained undiscovered due to the very low capacities for detection of emerging or re-emerging pathogens in most of the continent (Meda et al., 2016). Understanding the basic mechanisms of ZIKV AF infection is therefore of crucial importance.
    Funding Resources This work was funded by REACTing through the ITMOs I3M and Neurosciences and La RĂ©gion Languedoc-Roussillon (LR 0001146).
    Conflict of Interest
    Author Contributions
    Acknowledgments
    Introduction Zika virus (ZIKV) used to be an obscure mosquito-borne flavivirus from Flavivirus genus within Flaviviridae family. Other flaviviruses of global importance include dengue virus (DENV), West Nile virus (WNV), yellow fever virus (YFV), Japanese encephalitis virus (JEV), and tick-borne encephalitis virus (TBEV). ZIKV is phylogenetically divided into two lineages: the African and Asian lineages (Haddow et al., 2012). Since 2007, the Asian lineage of ZIKV has caused epidemics in Polynesia, the South Pacific, and most recently the Americas, leading to global concerns about its association with microcephaly and severe neurologic disorders (Gulland, 2016). The causal linkage between ZIKV infection and microcephaly, initially indicated by clinical studies, has recently been recapitulated in mouse models. ZIKV can infect mouse fetus, resulting in intrauterine growth restriction, placental damage, microcephaly, and fetal demise (Cugola et al., 2016; Li et al., 2016; Miner et al., 2016; Wu et al., 2016). Despite the above progress, the pathogenesis and transmission of ZIKV remain largely unknown. Recent data suggested human dermal fibroblasts, epidermal keratinocytes, placental macrophages and neural progenitor cells were permissive to ZIKV infection (Hamel et al., 2015; Li et al., 2016; Quicke et al., 2016; Tang et al., 2016). Results from mouse model suggest that ZIKV replicates efficiently in embryonic mouse brain by directly targeting neural progenitor cells and causing apoptosis (Cugola et al., 2016; Li et al., 2016). In patients, infectious ZIKV particles have been detected in blood, urine (Zhang et al., 2016), saliva (Barzon et al., 2016), and breastmilk (Dupont-Rouzeyrol et al., 2016). There is increasing evidence of sexual transmission of ZIKV (D\'Ortenzio et al., 2016; Moreira et al., 2016), and ZIKV RNA and infectious particles have been detected in semen in ZIKV-infected patients (Atkinson et al., 2016; Mansuy et al., 2016) or testis in infected mice (Lazear et al., 2016; Miner et al., 2016). However, due to the highly correlated nature of sexual behaviors, sexual and close contact transmission by saliva or other body fluids can be difficult to distinguish, whether such unusual viral excretions contribute to non-mosquito-mediated transmission remains to be determined. The knowledge of in vivo replication, excretion kinetics, and target tissues/organs of ZIKV is urgently needed for understanding the disease and pathogenesis.