Zika virus disease is caused by a virus from the Flavivirus genus, Flaviviridae family, from the Spondweni group. It was first isolated in 1947 from a monkey in the Zika forest, Uganda, then in mosquitoes (Aedes africanus) in the same forest in 1948, and in a human in Nigeria in 1952.
Virus assembly occurs at the endoplasmic reticulum. The virion buds at the endoplasmic reticulum and is transported to the Golgi apparatus. The prM protein is cleaved in the Golgi, thereby maturing the virion which is fusion competent.
Indeed, it was shown that Zika-related arthropod-borne flaviviruses, such as West Nile and Dengue viruses, actively recruit cellular fatty acid synthase, an enzyme that provides long chain fatty acids necessary for membrane lipid synthesis, to the replication sites [48,49,50].
Zika virus was first discovered in 1947 and is named after the Zika Forest in Uganda. In 1952, the first human cases of Zika were detected and since then, outbreaks of Zika have been reported in tropical Africa, Southeast Asia, and the Pacific Islands. Zika outbreaks have probably occurred in many locations.
Zika is spread mostly by the bite of an infected Aedes species mosquito (Ae. aegypti and Ae. albopictus).
Where Did Zika Go (And Will It Come Back)? In 1947, researchers isolated a new virus from a rhesus monkey in a tropical forest near Entebbe, Uganda. The virus, of the Flavivirus genus, was named Zika after the forest in which it was discovered.
In summary, the ZIKV uses a cell-type specific paracellular pathway to cross the placenta monolayer barrier by disrupting cellular tight junction. In addition, the ZIKV can also cross both the placenta barrier and the BBB by transcytosis.
So far, neither Zika virus latency (the dormant virus is present within a cell in a lysogenic life cycle and can be reactivated) nor a chronic clinical course of infection have been observed. To date, there is neither a vaccine to prevent Zika virus infections nor is there a specific antiviral treatment.
Pathogenesis in humans. Following a mosquito bite from a ZIKV-infected mosquito, ZIKV infects and replicates in dendritic cells, spreading through the blood to other parts of the human body. In most cases, the virus is self-limiting; however, infections in pregnant women result in teratogenic effects [17.
Zika virus entry receptorAXL is a key receptor being responsible for Zika virus entry. The ZIKV permissiveness of human skin fibroblasts was confirmed by the use of a neutralizing antibody and specific RNA silencing.
To replicate, animal viruses divert the host cell's metabolism into synthesizing viral building blocks, which then self-assemble into new virus particles that are released into the environment. Animal viruses are not susceptible to the action of antibiotics.
Classical skin tropic viruses such as herpes simplex virus (HSV), vaccinia virus (VACV), molluscum contagiosum virus (MCV), and varicella zoster virus (VZV) have tropism to skin epidermis where keratinocytes are the predominant cell type.
By preferentially destroying radial glial cells, Zika virus can produce severe microcephaly. Evolutionary changes such as mutations or recombination events might be responsible for the increased virulence and a new spectrum of Zika disease. Recombination events were reported to occur in different Zika viral strains.
Zika virions are comprised of an envelope and a nucleocapsid. The virus particles are spherical and small in size (approximately 50 nm in diameter) with an electron-dense core approximately 30 nm in diameter. The virion surface contains envelope protein (E) dimers and membrane (M) proteins in icosahedral-like symmetry.
Zika virus infects human blood mononuclear cells.
Zika virus can also be transmitted through sex and has been detected in semen, blood, urine, amniotic fluids, saliva as well as body fluids found in the brain and spinal cord.
Other viral diseases transmitted by vectors include chikungunya fever, Zika virus fever, yellow fever, West Nile fever, Japanese encephalitis (all transmitted by mosquitoes), tick-borne encephalitis (transmitted by ticks).
Zika outbreaks have been reported in the Pacific region, South and Central America, the Caribbean, Africa, and parts of south and southeast Asia. If you plan to travel to an affected area, seek travel health advice before your trip.
