Zika virus (ZIKV) is a flavivirus related to the Dengue, yellow fever and West Nile viruses. Since the explosive outbreaks of ZIKV in Latin America in 2015, a sudden increase in the number of microcephaly cases has been observed in infants of women who were pregnant when they contracted the virus. The severity of this condition raises grave concerns, and extensive studies on the possible link between ZIKV infection and microcephaly have been conducted. There is substantial evidence suggesting that there is a causal link between ZIKV and microcephaly, however, future studies are warranted to solidify this association. To summarize the most recent evidence on this issue and provide perspectives for future studies, we reviewed the literature to identify existing evidence of the causal link between ZIKV infection and microcephaly within research related to the epidemics, laboratory diagnosis, and possible mechanisms.

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Zika Virus Infection and Microcephaly: Evidence for a Causal Link

Up to 75 % of emerging human diseases are zoonoses, spread from animals to humans. Although bacteria, fungi and parasites can be causative agents, the majority of zoonotic infections are caused by viral pathogens. During the past 20 years many factors have converged to cause a dramatic resurgence or emergence of zoonotic diseases. Some of these factors include demographics, social changes, urban sprawl, changes in agricultural practices and global climate changes. In the period between 2014–2017 zoonotic viruses including ebola virus (EBOV), chikungunya virus (CHIKV), dengue virus (DENV) and zika virus (ZIKV), caused prominent outbreaks resulting in significant public health and economic burdens, especially in developing areas where these diseases are most prevalent. When a viral pathogen invades a new human host, it is the innate immune system that serves as the first line of defence. Myeloid cells are especially important to help fight viral infections, including those of zoonotic origins. However, viruses such as EBOV, CHIKV, DENV and ZIKV have evolved mechanisms that allow circumvention of the host’s innate immune response, avoiding eradication and leading to severe clinical disease. Herein, the importance of myeloid cells in host defence is discussed and the mechanisms by which these viruses exploit myeloid cells are highlighted. The insights provided in this review will be invaluable for future studies looking to identify potential therapeutic targets towards the treatment of these emerging diseases.

How myeloid cells contribute to the pathogenesis of prominent emerging zoonotic diseases.

Micronuclei (MN) are a strong cytogenetic indicator of a catastrophic change in the genetic structure and stability of a cell because they originate from either chromosome breaks or whole chromosomes that have been lost from the main nucleus during cell division. The resulting genetic abnormalities can to lead to cellular malfunction, altered gene expression and impaired regenerative capacity. Furthermore, MN are increased as a consequence of genetic defects in DNA repair, deficiency in micronutrients required for DNA replication and repair and exposure to genotoxic chemicals and ultraviolet or ionising radiation. For all of these reasons, the measurement of MN has become one of the best-established methods to measure DNA damage in humans at the cytogenetic level. This chapter is a narrative review of the current evidence for the association of increased MN frequency with developmental and degenerative diseases. In addition, important knowledge gaps are identified, and recommendations for future studies required to consolidate the evidence are provided. The great majority of published studies show a significant association of increased MN in lymphocytes and/or buccal cells with infertility, pregnancy complications, developmental defects, anaemias, inflammation, diabetes, cardiovascular disease, kidney disease, neurodegenerative diseases and cancer. However, the strongest evidence is from prospective studies showing that MN frequency in lymphocytes predicts cancer risk and cardiovascular disease mortality.

CHAPTER 4: Micronuclei and Their Association with Infertility, Pregnancy Complications, Developmental Defects, Anaemias, Inflammation, Diabetes, Chronic Kidney Disease, Obesity, Cardiovascular Disease, Neurodegenerative Diseases and Cancer

Zika virus (ZIKV) has attracted global attention after its first large-scale outbreak in Pacific, Micronesian island of Yap (Year 2007). The virus spreads rapidly and owes increased virulence than the ZIKV which appeared nearly six decades ago, where it was associated with sporadic cases and mild illness. The World Health Organization declared ZIKA as a „Public Health Emergency of International Concern” due to severe illness and associated several complications such as neurological disorders, autoimmune disorder, fetal anomalies, impaired central nervous system (CNS) of the fetus, microcephaly * Corresponding author KEYWORDS

/pdf/zika-virus-zika-fever-a-comprehensive-update-2ldjjsz3zm.pdf

Zika virus / zika fever : a comprehensive update

Zika virus is an arbovirus that is spreading at an alarming state in the American continents and now in Asian countries. The Aedes mosquitoes are the vectors for the spread of this virus beside other ways of transmission. Currently, there are no vaccines or drugs available for its treatment. The Zika virus–related microcephaly cases are reported in fetuses of pregnant women who got this viral infection. However, the exact mechanism of Zika virus and microcephaly is still not established. Here we review Zika virus epidemiology, its unusual relationship with microcephaly in fetuses and current scientific research progress on it.

/pdf/zika-virus-microcephaly-and-its-possible-global-spread-4pzfn9joms.pdf

Zika Virus, Microcephaly and its Possible Global Spread

Recently, an association between Zika virus infection and microcephaly/ocular findings was found to be reasonable e.g. because of the demonstration that the virus was found in the brain of a fetus after presumed maternal infection. Although there is no proof yet for a causal relationship, for an appropriate risk calculation efforts are urgently needed to either establish or disprove this assumption. On the basis of inherited syndromes combining microcephaly with ocular findings similar to those associated with Zika infections, we have hypothesized that the impairment of the proper function of the mitotic apparatus is a possible mechanism by which Zika can exert teratogenic effects. A bundle of well-known cytogenetic and molecular-cytogenetic methods (e.g. formation of micronuclei, chromosomal lagging, immunofluorescence of centrosomes) to evaluate proper function, maintenance, and establishment of the mitotic spindle poles can be applied on infected cells. Also, the viral proteins can be tested for their possible interaction with proteins encoded by genes involved in inherited syndromes with microcephaly and ocular findings resembling those in presumed cases of intrauterine ZIKV infection. Once proved, this hypothesis allows for a targeted approach into mechanisms of possible relevance as e.g. if different strains of the virus are implicated in the teratogenic effects to the same or a different extent.

/pdf/the-mitotic-spindle-linking-teratogenic-effects-of-zika-1c3wdx1k96.pdf

The mitotic spindle: linking teratogenic effects of Zika virus with human genetics?

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The mitotic spindle: linking teratogenic effects of Zika virus with human genetics?