A Review on Zika Virus Infection

 

Akshay R. Yadav*, Shrinivas K. Mohite

Department of Pharmaceutical Chemistry, Rajarambapu College of Pharmacy, Kasegaon, Sangli,

Maharashtra, India-415404.

 

ABSTRACT:

In Uganda, in 1947, Zika virus was initially identified in monkeys through a method that detected yellow fever. It was subsequently distinguished among the people of Uganda and Tanzania in 1952. Zika infection has reported the primary substantial outbreak of disease from Island of Yap.Brazil describes a partnership between the Zika virus infection and Guillain-Barré disorder in the month of July 2015. In this review we discuss various basic and clinical aspects of infection with Zika virus including virology, epidemiology and disease pathogenesis. Laboratory methods required for disease diagnosis along with ethical issues associated with Zika virus infection will be discussed in detail as well. Zika virus disease is typically mild and needs no treatment. There is actually no vaccine for Zika Virus disease.

 

 

 

INTRODUCTION:

Zika virus is a mosquito-borne virus that belongs to the Flaviviridae virus family. This family consists of four generaFlavivirus, Hepacivirus, Pegivirus and Pestivirus, respectively¹. Zika virus is related to the Spondweni virus both antigenically and phylogenetically². Within this genus, a broad range of essential human pathogenes include: dengue, west nile, yellow fever, tickborne encephalitis, japanese encephalitis, murray valley encephalitis, St. Louis encephalitis viruses. Such viruses cause a variety of illnesses, ranging from asymptomatic or febrile illnesses to many fatal diseases such as vomiting, shock, meningitis and encephalitis.

 

 

Zika was first isolated from the rhesus macaque in 1947 in the Zika Forest of Uganda³. The presence of neutralizing antibodies against the virus revealed serological studies carried out on human serum samples in Uganda later providing the first proof that the Virus would infect humans. The infections in other regions of Africa and Asian countries were found in subsequent studies⁴. Until 2007, Zika viral infections have been considered mostly infected by limited geographical distribution, yet later infection outbreaks in Pacific Islands and South America combined with newborn reports that the virus could lead to abnormality of the nervous system attracted the attention of a wide range of people in the scientific community. The situation peaked in 2015 when zika virus infections in Brazil were reported to have been significantly higher⁵. The epidemic then spread to South, Central and North American nations. The infections were associated with a large rise in the number of cases in affected regions of microcephaly and Guillain-Barré syndrome, leading to a declaration in the early 2016 WHO of an International Public Health Emergency (PHEIC). There has since been a strong international study of the epidemiological, molecular, pathogenic, and clinical aspects of zika infections⁶.

 

Epidemiology:

Just sporadic cases and serological evidence of zika were identified in west and central africa and south-east asia before the first major outbreak in island of yap, federal States of Micronesia, but Zika virus emerged as an significant human pathogen in 2007⁷. An increased incidence of Guillain-Barre syndrome (GBS) cases was reported following a major outbreak of Zika virus infection in French Polynesia in 2013. In 2014, autochthonous transmission of Zika virus infection occurred in Easter Island (Chile) from February to July⁸.

 

Pathogenesis:

Zika virus studies have shown similarities with other flavivirus infections. After mosquito bite transmission, the Zika virus can infect various types of cells, including the skin of keratinocytes, dermal fibroblasts and dendritic cells⁹. The high rate of infection in these cells 24-48 hours after infection was shown in in vitro studies with Zika exposed fibroblasts. Flow-cytometric study of DCs exposed to the virus showed that about 24 hours after infection up to 60% of DCs express viral antigens. Various cell surface-receptors, including DC-SIGN, AXL, and Tyro3 molecules, have been suggested to promote Zika penetration of permissive cell. The zika virus induces strong interferon reactions in infected cells after cell infection. Studies on human primary Fibroblasts infected by Zika virus have shown strong interferonbeta upregulation 24 to 48 hours after infection¹⁰. For interferon alpha, a milder response has been reported. Upregulation of the non-self-nucleic acid sensing "Pattern Recognition Receptors" (PRRs) seems to be a key component of the initial immunosuppression response of the virus. Research on Zika virus-infected fibroblasts shows that RIG-I and MDA-5 transcripts are inductive¹¹. Both of these molecules can be used to initiate signaling after intracytoplasmic viral RNA molecules have been detected. Innate immune responses follow adaptive immune events like T cell activation; zika viral DCs migrate to the lymphatic region where T cell proliferation, differentiation and cytokine production are stimulated¹². The productive infection and insufficient control by infection of dermal fibroblasts and dendritic cells, by inherent and adaptive immune systems, lead to Zika virus viremia which underlies non-specific, potentially lasting clinical symptoms for a period of several days. Maternal viremia can lead to fetalviremia in a pregnant woman. How the virus is transmitted into the nervous system after fetalviremia has been established is not well known Zika virus can infect fetal monocytes in circulation, and those monocytes can contribute to the infection of the nervous system in development¹³. Studies of Zika-infected mothers who are subjected to abortion on fetal brain tissue have shown that neural cells are able to proliferate from viral particles, which suggest that the virus can proliferate within neural cells. Zika virus, like other flaviviruses, can be directly neuroviral in the CNS. Zika virus can also induce indirect neurovirulence by activating immune functions such as microglial activation and macrophage infiltration. Zika virus may in adults be an etiological factor for Acute disseminated encephalomyelitis, a CNS immunized disease that occurs subsequently to viral and non-viral infections. It remains an open question whether an ADEM-like mechanism will impact brain growth¹⁴.

 

Symptoms:

The most widely-recognized indications of zika virus disease include fever, rash, joint agony and red eyes, areas of pain including the back portion of the eyes, joints or muscles. Symptoms such as fatigue, high fever, chill, loss of appetite and sweat, eye-redness, brain pain, skin rash or vomiting are commonly seen¹⁵.

 

Laboratory diagnosis of Zika virus infection:

Laboratory diagnoses of Zika virus are antigen detection, viral detection of RNA with molecular assays and serological tests can be performed by anti-zikavirus detection depending on the purpose of the study¹⁶.

 

i.      Virus Isolation:

The first isolation of Zika virus was performed by intracerebral mouse inoculation considered as a reference assay for the isolation of arboviruses. Zika virus may be produced from blood, urine, saliva and semen by human clinical specimens¹⁷.

 

ii.    Antigen Detection:

Detection of antigen is a valuable check to permitted autopsy tissue in zika virus infection. In the brain and placental tissues of congenital infected newborns with microcephaly and miscarriages. Zika virus antigen was detected using the Immunohistochemistry (IHC) technique. New tests have been developed recently for zika virus antigen detection, including NS3 flow cytometry protein identification, aptamer based ELISA testing for targeting Zika virus NS1 protein, competing NS1, ELISA protein based, NS1 protein-based rapid test¹⁸.

 

iii.  Molecular Assays:

Molecular diagnosis of zika virus infection in humans normally performs within the first week after the beginning of clinical symptoms on plasma or serum specimens. While there is several lines of proof of urine benefit for zika Virus RNA detection in this easy to pick up specimen for the long duration of viral shedding, interesting evidence has been found for the shorter durability of ZIKV RNA in urine versus serum.

 

iv.   Serological Assays:

Different serological tests, including complementary fixing, inhibition of hemagglutinating, immunofluorescence (IF), ELISA and neutral testing, can detect anti-zika virus. During the first week following the onset of symptoms, antizika virus IgM antibody is usually detectable from day 5 to 12 weaks of illness. IgM antibody Anti Zika virus IgG antibody is traceable for months to years, just a few days after IgM¹⁹.

 

Treatment:

There is no treatment but many people with symptoms for them that over-the-counter medications are useful for pain and aches. The infection usually happens in a week. Persons with zika virus will take plenty of rest, drink enough water and use simple medicines to relieve the pain and fever. When the symptoms escalate further, medical treatment and adequate therapy should be taken²⁰.

 

CONCLUSION:

Zika virus is thought to replicate initially in dendritic cells and then spread to lymph nodes and the bloodstream. Risk for infection through blood transfusion, sexual practices and perinatal transmission exsists. During delivery, breastfeeding and cloe contact between the mother and the baby are possible routes of perinatal transmission. Clinical presentation varies from asymptomatic infections to self-limiting low grade febrile disease and headache etc. The clinical feature could be mistaken for dengue or chickengunya fevers. For the diagnosis of ZIKV infection, laboratory tests are required because there are no known clinical, biochemical, or radiological pathogenomic features. RT-PCR is a liked assay. There is no certified vaccine or therapeutic medication.

 

ACKNOWLEDGEMENT:

I express my sincere thanks to Vice-principal Prof. Dr. S. K. Mohite for providing me all necessary facilities and valuable guidance extended to me.

 

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Received on 08.06.2020         Modified on 06.07.2020

Accepted on 24.07.2020       ©A&V Publications All right reserved