Rift Valley Fever Virus (RVFV) is an arbovirus that predominantly affects sheep, goats, and cattle, causing epizootics in livestock and epidemics in humans. Infection in pregnant livestock leads to high abortion rates and neonatal mortality. In humans, RVFV usually causes a self-limiting febrile illness, but severe forms can develop, such as hepatitis, hemorrhage, encephalitis, and death. In addition, the association between RVFV infection during pregnancy and miscarriages or stillbirths has been documented. RVFV is transmitted by a range of mosquito species, and, due to the diffusion of these insects, the virus has spread in several world regions, making possible the risk of a public health emergency. Nevertheless, research remains limited and cellular pathology is still poorly characterized. This work aimed to fill some knowledge gaps on the comprehension of RVFV pathogenesis. For this purpose, transmission electron microscopy (TEM) was used to analyze cellular modifications associated with RVFV morphogenesis in four human cell lines (HuH-7, LAN-5, A549, and HTR-8/SVneo) derived from liver, brain, lung, and placenta. Our results showed that all four cell lines are permissive to RVFV infection and highlighted differences in the cytopathogenesis associated with the cell type. These findings could have important implications in understanding disease mechanisms and developing antiviral strategies.

Mitochondria are central hubs of cellular metabolism, playing essential roles in energy production, lipid metabolism, calcium homeostasis, and redox signaling. Findings show that many of these activities are regulated by contact sites between mitochondria and the endoplasmic reticulum (ER) (mitochondria–ER contacts, MERCs). Several studies suggest that Hepatitis B Virus (HBV) can affect mitochondrial functions, inducing metabolic alterations and oxidative stress. This work aimed to investigate, at an ultrastructural level, whether HBV infection causes changes in mitochondrial architecture and MERC modulation. Using HepG2-NTCP cells as an in vitro model system, we analyzed mitochondrial modifications after HBV infection at 2, 5, and 10 days. Electron and confocal microscopy analyses highlighted changes in mitochondrial morphology with a progressive enlargement of mitochondrial size and a remodeling of the mitochondrial network, together with an increase in MERC establishment. Moreover, functional assays showed decreased ATP production, despite increased mitochondrial membrane potential and tight regulation of mitochondrial reactive oxygen species (mtROS) levels. These findings suggest that HBV does not cause irreversible mitochondrial damage but drives a dynamic and coordinated adaptation involving metabolism, ultrastructure, ER interaction, and network organization.