Search Results (3)

The Coronaviridae family has again demonstrated the potential for significant neurological complications in humans during the recent pandemic. In patients, these symptoms persist throughout the infection, often lasting for months. The consequences of most of these post-infection symptoms might be linked with abnormal cytokine production and reactive oxygen species (ROS) expression, resulting in neuron damage. We investigated the effect of infection with the Mouse Hepatitis Virus (MHV) JHM strain and Sialodacryoadenitis Virus (SDAV) on a primary microglia and astrocyte culture by analysing ROS production, cytokine and chemokine expression, and cell death during one month post infection. For this purpose, confocal microscopy, flow cytometry, and a high-throughput Luminex ProcartaPlex immunopanel for 48 cytokines and chemokines were utilised. The replication of MHV-JHM and SDAV in microglia and astrocytes has increased the production of pro-inflammatory cytokines and inhibited the production of anti-inflammatory cytokines. The cytokine expression induced by the two viruses differed, as did their detection after infection. SDAV infection resulted in a much broader cytokine response compared to that of MHV-JHM. Both viruses significantly increased ROS levels and induced apoptosis in a small percentage of the cells, but without necrosis. Full article

Sialodacryoadenitis virus (SDAV) has been identified as the etiological agent responsible for the respiratory system and salivary gland infections in rats. The existing literature on SDAV infections is insufficient to address the topic adequately, particularly in relation to the central nervous system. In order to ascertain how SDAV gains access to neuronal cells and subsequently exits, our attention was focused on the small molecule valosin-containing protein (VCP), which is an ATPase. VCP is acknowledged for its function in the ubiquitin-mediated proteasomal degradation of proteins, including those of viral origin. To ascertain the potential influence of VCP on SDAV replication and egress, high-content screening was employed to determine the viral titer and protein content. Western blot analysis was employed to ascertain the relative expression of VCP. Real-time imaging of SDAV-infected cells and confocal imaging for qualitative morphological analysis were conducted. The Eeyarestatin I (EerI) inhibitor was employed to disrupt VCP involvement in the endoplasmic reticulum-associated protein degradation pathway (ERAD) in both pre- and post-incubation systems, with concentrations of 5 μM/mL and 25 μM/mL, respectively. We demonstrated for the first time that SDAV productively replicates in cultured primary neurons. VCP expression is markedly elevated during SDAV infection. The application of 5 μM/mL EerI in the post-treatment system yielded a statistically significant inhibition of the SDAV yield. It is likely that this modulates the efficacy of virion assembly by arresting viral proteins in the submembrane area. Full article

Sialodacryoadenitis virus (SDAV) is known to be an etiological agent, causing infections in laboratory rats. Until now, its role has only been considered in studies on respiratory and salivary gland infections. The scant literature data, consisting mainly of papers from the last century, do not sufficiently address the topic of SDAV infections. The ongoing pandemic has demonstrated, once again, the role of the Coronaviridae family as extremely dangerous etiological agents of human zoonoses. The ability of coronaviruses to cross the species barrier and change to hosts commonly found in close proximity to humans highlights the need to characterize SDAV infections. The main host of the infection is the rat, as mentioned above. Rats inhabit large urban agglomerations, carrying a vast epidemic threat. Of the 2277 existing rodent species, 217 are reservoirs for 66 zoonotic diseases caused by viruses, bacteria, fungi, and protozoa. This review provides insight into the current state of knowledge of SDAV characteristics and its likely zoonotic potential. Full article