Zika virus (ZIKV) was first isolated in 1947. From its isolation until 2007, symptoms of ZIKV-caused disease were limited (e.g., fever, hives, and headache); however, during the epidemic in Brazil in 2014, ZIKV infection caused Guillain-Barré syndrome in adults and microcephaly in fetuses and infants of women infected during pregnancy. The neurovirulence of ZIKV has been studied using neural progenitor cells (NPCs), brain organoids, neurons, and astrocytes. NPCs and astrocytes appear to be the most susceptible cells of the Central Nervous System to ZIKV infection. In this work, we aimed to develop a culture of astrocytes derived from a human NPC cell line. We analyze how ZIKV affects human astrocytes and demonstrate that 1) ZIKV infection reduces cell viability, increases the production of Reactive Oxygen Species (ROS), and results in high viral titers; 2) there are changes in the expression of genes that facilitate the entry of the virus into the cells; 3) there are changes in the expression of genes involved in the homeostasis of the glutamatergic system; and 4) there are ultrastructural changes in mitochondria and lipid droplets associated with production of virions. Our findings reveal new evidence of how ZIKV compromises astrocytic functionality, which may help understand the pathophysiology of ZIKV-associated congenital disease.

The genome of Alphaviruses can be modified to produce self-replicating RNAs and virus-like particles, which are useful virological tools. In this work, we generated three plasmids for the transfection of mammalian cells: an infectious clone of Chikungunya virus (CHIKV), one that codes for the structural proteins (helper plasmid), and another one that codes nonstructural proteins (replicon plasmid). All of these plasmids contain a reporter gene (mKate2). The reporter gene in the replicon RNA and the infectious clone are synthesized from subgenomic RNA. Co-transfection with the helper and replicon plasmids has biotechnological/biomedical applications because they allow for the delivery of self-replicating RNA for the transient expression of one or more genes to the target cells.

Infections caused by the Hepatitis A virus (HAV) occur worldwide. Molecular epidemiology is crucial to understanding the transmission dynamics; however, the current genotype assignment fails to provide useful epidemiologic information. We classified HAV sequences available in GenBank based on 460 bp of the VP1/2A region in clades. Additionally, we associated the site of isolation of the strains with the country's HAV endemicity. We analyzed 1369 sequences available in GenBank up to December 2023 which fulfilled inclusion criteria for our study. The collection date ranged from 1957 to 2023, and genotypes IA (n = 986) and IB (n = 290) comprised the majority of sequences. Sequences were assigned to 70 different clades; sequences from most clades (n = 36) were detected in one country or a few countries within a single continent, while sequences of only 9 clades were detected in more than two continents. Countries with lower HAV endemicity showed higher diversity of clades compared with countries with higher HAV endemicity. In addition, multinational HAV outbreaks were associated with specific clades. In conclusion, characterization of HAV strains below the genotype level should be helpful to analyze transmission patterns within and between countries.