Research Papers

The Zika Virus Research Paper

In humans, the lifecycle of the Zika virus infection starts when the Aedes female mosquito deposits its virus on the skin or the bloodstream. The keratinocytes and the fibroblasts are permissive of the infection. The pathogen recognition receptors (PRR) and the tool like receptors (TLR) trigger the expression of the IFN genes to begin the life cycle (McArthur, 2017). The IFNs that come in type1 and type2 are imperative for controlling the flaviviruses infections by inhibiting the viruses’ replication. Stimulated genes which include the MX-1 and the ISG-15 are triggered when the dermal fibroblasts are infected by the Zika Virus (Makhluf, 2018).

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Different types of cells including the dendritic cells, neurons, and the keratinocytes are targets of the flaviviruses. When the glycoprotein and the receptors on the viral particles and cell surfaces interact they allow the flaviviruses to enter into the target cells. Although researchers have carried out many investigations, they are yet to establish the role of the fundamental cellular receptors and their significance in viral entry. Other receptors that have been established to allow the entry of viruses include DENV and the arboviruses. DC-SIGN has been established to allow attachment and subsequently the infection of the virus that in turn fosters the dissemination of the Zika virus (Fernandez, 2017).

Immune Responses:
1. Innate Immune Response to ZIKV
Once a viral infection has been confirmed, body cells will trigger a broad range of antiviral responses in an attempt of limiting the virus from spreading. As observed by Richner & Diamond (2018), the primary defenses are the innate and the adaptive immune responses. The innate response is triggered by producing the type 1interferons (IFNS) (Hamel, et al., 2016). The body senses the detecting of the molecular patterns that are associated with the pathogen. The detection is mediated using the pattern recognition receptors (PRRS). After the pathogens have been detected, the body triggers the pathways that are used to send signals. This leads to the secretion of IFNS. It also triggers the expression of the stimulated genes whose integration triggers the induction of the antiviral cells.

The IFN response plays an imperative role in controlling the flaviviruses. This is revealed by the increased susceptibility of the hosts that lack the IFN pathways components to flaviviral infections. The broad range of mechanisms that are employed to counteract these control mechanisms by the flavivirus is also a demonstration of the significance of the IFN responses. Researchers have undertaken a series of in-vitro studies to examine the IFN responses to the ZIKV infection (McArthur, 2017). The results indicate that depending on the cell type, the infection produces type I (α, β), type II (γ). It also produced type III (λ) IFN among other stimulated genes (Makhluf, 2018). It is common for cellular processes to be hijacked by the flaviviruses as they attempt to evade the response of cells and trigger the replication of viruses. Soon after infection, the patient will start innate immune responses as he tries to overcome the infection. Some viruses are able to evade detection. Arboviruses also have the ability to subvert the entire autophagy process. This promotes replication as well as the dissemination of the arboviruses. The flaviviruses will reorganize the membranes of the host cell to create a suitable environment that will foster their replication. By reorganizing the membranes the protein response is activated.

2. Humoral Immunity
This type of immunity relies on the ability of the immune system to produce antibodies that can bind and inactivate the various forms of infectious agents. Once the innate immune system activates the adaptive immune system the humoral immune system triggers the B cells which start the development of the plasma cells (Beck & Barrett, 2015).

The plasma cells begin the secretion of large volumes of antibodies that circulate in the lymphatic system and the bloodstream (Beck & Barrett, 2015). The bacteria that result in the Zika infection multiply in the intercellular spaces. The movement of the pathogens from cell to cell ensures that they spread in the extracellular fluids. Since the humoral immune response protects these spaces the B cells that are produced by the antibodies destruct the microorganisms which ultimately prevent infections from spreading. To activate the B cells, the body requires antigens that differentiate them into the plasma cells that secrete the antibodies.

3. Active and Passive Immunity
The humoral immune responses can be categorized into the active and passive responses. Active immunity entails the creation of the antibody after they have been exposed to a foreign antigen. This type of immunity can be artificial or natural. Artificial immunity is obtained through vaccinations using either alive or an attenuated virus. On the other hand, natural immunity is obtained once the body is exposed to an organism that causes diseases. Passive immunity entails getting an antibody that has been created by a different person. It could be natural or artificial.

4. Role of Antibodies
The antibodies are tasked with invading the pathogens. The different types of antibodies serve different functions among which involved binding on the antigens and marking the pathogens that need to be destructed. There are antibodies that cause the complements to be activated to enable the serum proteins to destruct the pathogens. These are referred to as the complement-mediated antibodies (Fernandez, 2017). The other types of antibodies are the neutralizing antibodies that are bound on the antigens in such a way that they are unable to recognize the host cells. This has the effect of inhibiting the infection of the cells. Once the patient is infected with the Zika virus, the neutralizing antibodies will bind to the antigens and inhibit the virus from attaching on the cell receptors of the patient.

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