Zika Fever : Symptoms, Transmission and Prevention Measures

Zika Fever : Symptoms, Transmission and Prevention Measures

The medical world has recently become interested in the Zika virus infection. Although the disease does not have a high death rate and does not have significant clinical manifestations in adult instances, infection with the...

The medical world has recently become interested in the Zika virus infection. Although the disease does not have a high death rate and does not have significant clinical manifestations in adult instances, infection with the Zika virus can affect foetal development and result in serious neuro developmental problems.

Several significant human diseases, including Dengue, West Nile and Yellow fevers, Japanese encephalitis, Tick-borne encephalitis, and Zika fever, are caused by flaviviruses. Arthropod vectors are the primary means of transmission for the majority of Flaviviruses, and the most common clinical results include hemorrhagic fevers and harm to the central nervous system. Zika virus infections have captured the attention of the global medical community in recent years, primarily because of its link to microcephaly and other neurological disorders that result from maternal infections.

Even though Zika virus infection is a worldwide problem, we have focused primarily on findings from nations in the Eastern Mediterranean Region (EMRO) in the epidemiology section. The final section of this paper presents a thorough analysis of ethical aspects of Zika virus infection, taking into account ethical issues pertaining to fete-maternal and neurodevelopmental dimensions of the viral infection.


The Flaviviridae family of viruses, which the Zika virus is a member of, is a recent addition. The Flavivirus, Hepacivirus, Pegivirus, and Pestivirus genera make up this family . According to phylogenetic and antigenic analyses, the Spondweni virus and the Flavivirus genus are related to each other . This genus contains a variety of significant human infections, including the viruses that cause Dengue, West Nile, Yellow Fever, tick-borne Japanese, Murray Valley, and St. Louis encephalitis, as well as the West Nile, Yellow Fever, and other encephalitises. From asymptomatic or self-limiting febrile illnesses to some lethal conditions like haemorrhage, shock, meningitis, and encephalitis, these viruses are linked to a variety of infections.

All members of the Flaviviridae family are enveloped viruses that have a single-stranded RNA genome with positive polarity and one open reading frame (ORF) and two flanking noncoding sections (at the 5′ and 3′ ends). Without a 3′ poly (A) tail, the genomes are 5′ capped

The ORF codes for a polyprotein, which is then broken down into seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5) and three structural proteins (the envelope, capsid, and precursor of the membrane, or prM). The nucleocapsid is enclosed by a membrane formed from the host that contains two viral glycoproteins. The icosahedral capsid is made of 12-kDa protein blocks.


Only occasional cases and serological evidence of the Zika virus were documented in western and central Africa and south-east Asia prior to the first major epidemic of the disease on Yap Island, Federated States of Micronesia, but in 2007 the Zika virus began to gain importance as a human pathogen.

Following a more widespread outbreak of Zika virus infection in French Polynesia in 2013, an increase in the prevalence of Guillain-Barré syndrome (GBS) cases was noted. From February to July of 2014, Easter Island (Chile) experienced autochthonous transmission of the Zika virus infection.

Zika virus was discovered by reverse transcription polymerase chain reaction (RT-PCR) assay in early 2015 after numerous patients showing a "dengue-like syndrome" studied in Brazil (a non-Dengue virus and non-Chikungunya virus infection).


Studies on the Zika virus' pathogenesis have revealed parallels with the pathogenesis of other Flavivirus infections. Skin keratinocytes, dermal fibroblasts, and dendritic cells (DCs) are just a few of the cell types that the Zika virus can infect after being spread by a mosquito bite.

Studies conducted in vitro on fibroblasts exposed to the Zika virus revealed high rates of infection in these cells 24 to 48 hours after infection. According to flow cytometric examinations of DCs exposed to the virus, up to 60% of DCs exhibit viral antigens 24 hours after infection.Numerous cell surface receptors, including as Tyro3 molecules, AXL, and DC-SIGN, have been proposed as mediating Zika infection of permissive cells.

The Zika virus enters cells and causes potent interferon reactions in infected cells. Interferon-beta transcripts were significantly up-regulated 24 to 48 hours after Zika virus infection, according to studies on human primary fibroblasts infected with the virus.

Interferon-alpha has been shown to have a milder reaction. Initial immune response to the virus appears to be heavily dependent on up-regulation of intracellular "pattern recognition receptors" (PRRs) that detect non-self-nucleic acids.

RIG-I and MDA-5 transcripts are strongly induced, according to studies on fibroblasts infected with the Zika virus. When intracytoplasmic viral RNA molecules are found, both of these molecules have the ability to start a signalling pathway. Adaptive immunological processes, such as the activation of T cells, follow innate immune responses.

Zika virus viremia, which explains the vague clinical signs that could continue for a few days, is mainly caused by productive infection of dermal fibroblasts and dendritic cells combined with poor control of infection by innate and adaptive immune mechanisms. Foetal viremia in a pregnant woman could result from maternal viremia. After foetal viremia has been established, it is unclear how the virus is transferred to the developing nervous system.

Foetal monocytes may become infected with the Zika virus while in the bloodstream, and these monocytes may then spread the infection to the growing neural system. Studies on foetal brain tissue from moms who had abortions and had the Zika virus found viral particles in neural cells, showing that the virus can multiply inside neural cells in a developing brain.


Zika virus laboratory diagnosis can be carried out by virus isolation, antigen detection, viral RNA detection with molecular assays, and anti-Zika virus antibody detection with serological assays, depending on the goal of the inquiry.


Through intracerebral mouse inoculation, which is regarded as the standard method for isolating arboviruses, the Zika virus was first isolated.Blood, urine, saliva, and semen are among the clinical samples from humans that the Zika virus can be cultivated from.


To confirm Zika virus infection in postmortem tissues, antigen detection is a useful test. Zika virus antigen has been discovered using the immunohistochemistry (IHC) approach in the brain and placental tissues of congenitally infected neonates with microcephaly and miscarriages . Recent developments in Zika virus antigen detection methods, such as the identification of the NS3 protein by flow cytometry in whole blood.


The "gold standard" for diagnosing ZIKV is reverse transcriptase PCR (RT-PCR), which is extremely sensitive and specific (55). Numerous traditional and real-time RT-PCR assays targeting the prM, E, NS1, NS3, NS4, and NS5 genes have been created for the Zika virus.To the best of our knowledge, however, only one commercial assay, such as Roche's Cobas Zika Test, a qualitative nucleic acid test for detecting Zika virus RNA in blood donors, has received FDA approval.


Zika virus infection falls under the category of "newly emerging" infectious diseases, along with Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS), both of which have the potential to have major negative effects on public health. Zika infection does not pose a significant threat to infected adults, and its risk is more due to the potential to cause foetal abnormalities, provided that the infection occurs during pregnancy.

This is in contrast to other "newly emerging" infections that can cause severe morbidity and mortality in infected adults or paediatric hosts. Indeed, of the four most recent PHEIC announcements made by WHO (i.e., the 2009 Swine Flu announcement, the 2014 Polio and Ebola announcements, and the 2016 Zika announcement).