The host's immune response against dengue virus infections
| dc.contributor.author | Ghanem Mohammed Mahjaf | |
| dc.contributor.author | Tibyan Abd Almajed ALtaher | |
| dc.contributor.author | Mosab Nouraldein Mohammed Hamad | |
| dc.date.accessioned | 2023-11-21T09:23:36Z | |
| dc.date.available | 2023-11-21T09:23:36Z | |
| dc.date.issued | 2023 | |
| dc.description.abstract | One of the biggest global public health issues is dengue virus (DENV) infection, particularly in tropical areas of the world where 75% of dengue cases occur. While most DENV infections are moderate or asymptomatic, about 5% of cases go on to develop a severe version of the illness. This is primarily related to several infections with various DENV serotypes that occurred in succession. Numerous immunopathogenic pathways involving virus and host variables influence the severity of dengue. New research suggests that an inadequate immune response, by limiting viral clearance and causing severe inflammation, which ultimately results in dengue hemorrhagic fever and dengue shock syndrome, contributes to the progression and severity of the disease. The natural history of viral infections, notably dengue, is greatly influenced by the host's innate and adaptive immune responses. In this context, it has been noted that RNA interference (RNAi) is becoming more prevalent in viral infection processes and immune defense in recent years. The context microRNAs (miRNAs) go for stands out as their presence during viral infection, both in the replication of the virus and in the defense against these infections, becomes more noticeable. As a result, it is becoming more and more important to understand the role of these small RNAs within viral infection by DENV and what their consequences are in aggravating the consequences of patients affected by this disease. Additionally, DENV specifically targets immune mediators to inhibit antiviral signal transduction and invisibly hides to avoid immune surveillance. The initial line of defense against viral infections is innate immunity, where type I interferons are a key component. Many viruses manage to get past inherent defenses and infect the host. Numerous investigations have demonstrated that in order to circumvent the host's immunological response, viruses like DENV decrease type I IFN production. The 5 dengue virus has four widely recognized serotypes: DENV-1, DENV-2, DENV-3, and DENV-4. A fifth serotype was recently discovered in 2013. Although DENV serotypes are roughly 65% similar, infection with various serotypes causes a variety of clinical symptoms. In addition to the host cell's cellular machinery being used by the virus, a host cell also produces different antiviral reactions. The creation of interferon-dependent cytokines, the induction of inflammation, and cell death through inducing apoptosis or autophagy are just a few of the ways the host immune system fights virus infection. We go over processes that are essential for the Dengue virus reproduction cycle in mammalian cells, its pathogenicity, and several antiviral defenses put forth by the host cell in this overview. Understanding the Dengue virus replication cycle and the host proteins that the virus uses as a resource might be crucial for creating antiviral targets and is of utmost relevance for maintaining public health | |
| dc.identifier.uri | https://ds.eaeu.edu.sd/handle/10.58971/393 | |
| dc.language.iso | other | |
| dc.publisher | جامعة الشيخ عبدالله البدري | |
| dc.title | The host's immune response against dengue virus infections |