Zika virus tropism and pathogenesis: understanding clinical impacts and transmission dynamics

The Zika virus (ZIKV) is classified within the Flavivirus genus of the Flaviviridae family and is categorized as an arbovirus. The virus was initially identified in a rhesus monkey in Uganda in 1947 and later in a human in Nigeria in 1952. Since 2007, the prevalence of the virus has been on the rise, culminating in a major outbreak in the United States (US) in 2015. During this outbreak, the adult population was severely impacted, experiencing a range of symptoms, including organ failure, microcephaly, fetal death, and Guillain-Barré syndrome (GBS). Additionally, skin rash, limb swelling, fever, headache, and heightened sensitivity are found in most adults with Zika syndrome. Although the virus can be transmitted through blood, vertical transmission from mother to child, and sexual contact, the primary way of transmission of the virus is through the Aedes mosquito. Cells such as neurons, macrophages, peripheral dendritic cells, and placental cells are among the target cells that the virus can infect. The TAM AXL receptor plays a crucial role in infection. After the virus enters the body through the bloodstream, it spreads in the body with a latent period of 3 to 12 days. Currently, there is no specific treatment or publicly available vaccine for the ZIKV. Limited laboratory testing has been conducted, and existing drugs originally designed for other pathogens have been repurposed for treatment. Given the Aedes mosquito's role as a vector and the wide geographical impact of the virus, this study aims to comprehensively investigate Zika's pathogenesis and clinical symptoms based on existing knowledge and research. By doing so, we seek to enhance our understanding of the virus and inform future prevention and treatment strategies.