The virus was first traced in Uganda, where there was a low prevalence of the disease in Asia and Africa. In recent years, the infections of the zika virus have been evidenced in formerly unaffected areas, initially in Oceania and later in the USA as of 2015 (Heinz and Stiasny, 2017). The mosquito generally bites during the daytime, where infection results in mild symptoms such as headaches, joint pains, fever, or inflammation of the conjunctiva. In most cases of infections, the victim shows no symptoms, while in mild cases, the disease may result in subsequent paralysis or birth defects in pregnant women. The defects in the fetus may lead to the infants` birth with several malformations. The malformations include congenital malformations or microcephaly conditions on the newly born infant (Krauer et al., 2017). Also, an connection between the zika pathogenic virus and pregnancy may result in premature birth or miscarriage.
In humans, the Zika virus (ZIKV) is a neurotropic flavivirus caused by Aedes female mosquito. Descriptively, the ZIKV cycle begins when the Aedes female mosquito bites and deposits its virus on the bloodstream or skin. The fibroblasts and keratinocytes are permissive to the Zika virus infection. The Toll-like receptor (TLR) and pathogen recognition receptors (PRR) triggers the interferons (IFNs) genes to start the life of ZIKV (Ropidi et al., 2020). The interferons (IFNs) that come in type1 and type are essential for controlling the neurotropic flavivirus infections, primarily by suppressing the replication of the viruses. In the suppression infection process, other stimulated genes, such as the ISG-15 and MX-1, are triggered, especially when dermal fibroblasts are infected, to initiate protein signaling within the infected cells (Winkler et al., 2017). Markedly, cells, such as the keratinocytes, dendritic cells, and neurons, are the primary targets of the flaviviruses. Primarily, the flavivirus will enter the target cells if the receptors and the glycoprotein on the cell surfaces and viral particles interact. However, despite multiple research pieces, the experts have failed to establish the underlying role of cellular receptors and their essential role in viral entry (Lesteberg et al., 2019). According to Bosseboeuf (2018), experts and scientists have established that some cellular receptors also permit the entry of viruses, such as arboviruses and Dengue virus (DENV). Also, multiple research pieces have indicated that the CD209 (DC-SIGN) fosters the dissemination of the ZIKV (Prado Acosta et al., 2019).
Innate Immune Response
Once the body has confirmed the presence of viral infection (ZIKV), the body cells will start triggering a vast antiviral response, mainly in an attempt to prevent the virus from spreading. Winkler et al. (2017) stated that the primary defenses the body will use are innate and adaptive responses. The innate defense will be triggered if the body releases several types of interferons (IFNs) (Elshahawi et al., 2019). During viral infection, the body will sense and detect the molecular patterns related to the pathogen using a pattern recognition receptor (PRRS). After the body has identified the pathogen, it will trigger pathways specifically used to send signals. This will result in the interferons (IFNs) secretions, which will foster the production of natural killer cell functions. Additionally, the body response to trigger the pathway will also lead to the production of interferons-stimulated genes (ISG) that will trigger the induction of the antiviral cell. In other words, the interferon response will have a significant role in controlling flavivirus.
Winkler et al. (2017) explained the role of interferons as ‘hugely importance,’ as their role can be shown by the increased hosts’ susceptibility, especially to those hosts with no interferons pathways components to infections caused by a flavivirus. The multiple mechanisms that the body uses to counter or fight the infections caused by a flavivirus also significantly show the role of interferons (IFNs) responses in the body. In recent past years, researchers and field experts did a series of in-vitro researches to assess the interferons (IFNs) responses to Zika virus infection (ZIKV) (Bosseboeuf et al., 2018). The results from the in-vitro researches showed that secondary to the cell type, the infection would produce type II (γ) and type I (α, β).
Moreover, the results from the research also indicated that among other production of the stimulated gene, type III ((λ) IFN will be produced (Makhluf & Shresta, 2018). Based on several studies, it is actually common for flaviviruses to hijack the cellular process, particularly as they try to evade cell responses in order to trigger the viruses’ replication. After the infection, the infected patient will begin innate immune responses as they try to defeat the infection. In some cases, some viruses succussed evading the detection. Like the Zika virus, arboviruses also have the ability to subvert the whole process of autophagy. This fosters the replication and dissemination of the arboviruses. According to Makhluf & Shresta (2018), after the flavivirus subverts the entire autophagy process, they reorganize the host cell membrane to create a conducive environment that will encourage their replication. When the host cell membrane is reorganized, the protein response will be activated.
Humoral immunity is a type of immunity that depends on the ability of the immune system to generate antibodies that inactivate and bind several forms of infectious agents. Immediately after the innate immune response activates the adaptive immune system, the humoral immune system activates the B cells, which imperatively will begin the development of plasma cells (Elong Ngono et al., 2019). The plasma cells will stimulate the secretion of antibodies circulating in the bloodstream and lymphatic system in large volumes. The bacteria that result from infection caused by the Zika virus will proliferate in the intercellular spaces. Technically, pathogen movement from one cell to another cell will ensure pathogens spread in intercellular spaces and fluids. Since the humoral immune response primarily protects the intercellular spaces, the B cells will be generated by the antibodies that will destroy the micro-organisms within the spaces, hence, ultimately stopping the infection from spreading (Elong Ngono et al., 2019). Most importantly, to activate B cells, the body needs an antigen that will differentiate them from plasma cells, which generate the antibodies.
Active and Passive Immunity
The humoral immune response can be grouped into passive and active immune responses. Active immune response mainly involves the development of antibodies after they have been exposed to a foreign organism or antigen. Interestingly, this particular type of humoral immune response can be categorized into natural or artificial. The artificial immune responses are mainly generated through vaccination using either attenuated or live viruses. On the other hand, the natural immune response will be generated once the body is exposed to pathogens or organisms that cause infection or diseases (Richner & Diamond, 2018). According to Richner and Diamond (2018), the passive immune response is a humoral immune response that entails receiving an antibody created by the other person’s immune system. Like an active immune response, the passive response can also be categorized into artificial or natural.
T cell responses to flavivirus infection
The immune system reaction to flavivirus antigens may foster both defensive mechanism or pathogenesis, as backed by the Human HLA linkages and vulnerability of humans to infections. Biological experiments using mouse study designs of a number of the flaviviruses established a defensive function for the CD8+ cell. Several pedigrees of CD+ T lymphocytes have been supported to promote the defense through the ability to secrete pro-inflammatory cytokines and aid in antibody maturation. Dengue-reactive cytotoxic T-cells (CD4+) were discovered in humans, specifically in one who had experimented with multiple illnesses (Malafa et al., 2020). T-cells are crucial in the defensive mechanism of the body and understanding how they function in the defense to zika virus is of importance.
In the immunological field of vaccines, several vaccines have been discovered to counter the effectiveness of flavivirus infections. Vaccines successful in the prevention of flavivirus diseases include the tick-borne encephalitis, yellow fever vaccine (YF), and Japanese encephalitis vaccine (JE). Additionally, there have been the recent development and use of the dengue virus vaccine, commonly known as the CYD-TDV (Saron et al., 2018). The development of vaccines against the various disease caused by viruses and flavivirus proposes that the development of a zika virus vaccine is quite possible.
In the immunity by the body`s immunoglobulins to the primary antigenic flaviviruses, there is a hiked production of the IgM antibodies involved in the neutralizing of the flavivirus in activated compliment. The immunoglobulin M (IgM) is vital in the protection of the body against the flavivirus in the early infection stages. In the flavivirus pathogenicity, the levels of the IgM antibodies may decline or be hindered. Though the immunoglobulin E (IgE) antibodies function in the provision of long-lasting immunity against the infections by the flavivirus, they also contribute to the antibody-dependent enhancement of infection (Malafa et al., 2020). IgM is a vital antibody in the defense mechanism against the virus antigens.
As the use of yellow virus vaccination increases the level of IgM antibodies in the bloodstream, helping the immune system to counter the effect of the flaviviruses. The IgM helps in the neutralization of the flaviviruses pathogens. A pregnant woman who had received a yellow virus vaccine would have high chances of fighting the zika virus in conjunction with the prescribed meals compared to non-vaccinated women.
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